causal inference view markdown
Some good packages: msft econML, uber causalml, msft dowhy
classic studies
 Descriptive Representation and Judicial Outcomes in Multiethnic Societies (Grossman et al. 2016)
 judicial outcomes of arabs depended on whether there was an Arab judge on the panel
 Using Maimonides’ Rule to Estimate the Effect of Class Size on Scholastic Achievement (angrist & lavy 1999)
 reducing class size induces a signicant and substantial increase in test scores for fourth and 5th graders, although not for third graders.
 Smoking and Lung Cancer: Recent Evidence and a Discussion of Some Questions (cornfield et al. 1959)
 not a traditional statistics paper
 most of it is a review of various scientific evidence about smoking and cancer
 small methodology section that describes an early version of sensitivity analysis
 describes one of the most important contributions causal inference has made to science
 Attributing Effects to a ClusterRandomized GetOuttheVote Campaign (hansen & bowers 2009)
 about a randomized experiment
 proved complex to analyze and led to some controversy in political science
 resolves that controversy using wellchosen statistical tools.
 Because randomization is present in the design I think the assumptions are much less of a stretch than in many settings (this is also the case in the Angrist, Imbens, Rubin paper)
natural experiments
 John Snow on cholera  natural experiment  change of water pollution allowed for computing effect of the water pollution on cholera
 Who Gets a Swiss Passport? A Natural Experiment in Immigrant Discrimination (Hainmueller & Hangartner 2013)
 naturalization decisions vary with immigrants’ attributes
 is there immigration against immigrants based on country of origin?
 citizenship requires voting by municipality
 When Natural Experiments Are Neither Natural nor Experiments (sekhon & titunik 2012)
 even when natural interventions are randomly assigned, some of the treatment–control comparisons made available by natural experiments may not be valid
instrumental variables
 Identification of Causal Effects Using Instrumental Variables (angrist, imbens, & rubin 1996)
 bridges the literature of instrumental variables in econometrics and the literature of causal inference in statistics
 applied paper with delicate statistics
 carefully discuss the assumptions
 instrumental variables  regression w/ constant treatment effects
 effect of veteran status on mortality, using lottery number as instrument
matching
 Matching and thick description in an observational study of mortality after surgery. (rosenbaum & silber 2001)
 spends a lot of time discussing links between quantitative and qualitative analyses
 takes the process of checking assumptions very seriously, and it deals with an important scientific problem
“paradoxes”
 simpson’s paradox = yulesimpson paradox  trend appears in several different groups but disappears/reverses when groups are combined
 Sex Bias in Graduate Admissions: Data from Berkeley (bickel et al. 1975)
 e.g. overall men seemed to have higher acceptance rates, but in each dept. women seemed to have higher acceptance rates  explanation is that women selectively apply to harder depts.
graph LR A(Gender) >B(Dept Choice) B > C(Acceptance rate) A > C
 monty hall problem: why you should switch
graph LR A(Your Door) >B(Door Opened) C(Location of Car) > B
 berkson’s paradox  diseases in hospitals are correlated even when they are not in the general population
 possible explanation  only having both diseases together is strong enough to put you in the hospital
problems beyond ATE
causal mechanisms
 treatment effect variation?
 principal stratification
 interference
mediation analysis
Mediation analysis aims to identify a mechanism through which a cause has an effect. Direct effects measure when the treatment varies as mediators are held constant.

if there are multiple possible paths by which a variable can exert influence, can figure out which path does what, even with just observational data

cannot just condition on $M$! This can lead to spurious associations

which pathway do causes flow through from X to Y (direct/indirect?)

consider potential outcomes with hypothetical intervention on $T$:
 ${M(t), Y(t)}$

hypothetical intervention on $T$ and $M$:
 ${Y(t, m)}$
 hypothetical intervention on $T$ fixing $M$ to $M(t’) = M_{t’}$ (nested potential outcome, robs & greenland, 1992; pearl, 2001)
 ${Y(t, M_{t’})}$
 has also been called a priori counterfactual (frangakis & rubin, 2002)
 when $t \neq t’$, this can’t be observed and can’t be falsified

total effect $\tau=E{Y(1)Y(0)} = \textrm{NDE + NIE}$
 assumes composition assumption $Y(1, M_1) = Y(1)$, very reasonable

natural direct effect $\mathrm{NDE}=E\left{Y\left(1, M_{0}\right)Y\left(0, M_{0}\right)\right}$
 controlled direct effect $\mathrm{CDE}=E\left{Y\left(1, m\right)Y\left(0, m\right)\right}$ is simpler: sets mediator to some assumed value $m$ rather than the actual value seen in the data $M_0$
 w/ composition: $=E\left{Y\left(1, M_{0}\right)Y\left(0\right)\right}$

natural indirect effect $\mathrm{NIE}=E\left{Y\left(1, M_1\right)Y\left(1, M_{0}\right)\right}$

w/ composition: $=E\left{Y\left( 1 \right)Y\left(1, M_0\right)\right}$

mediation formula

can condition effects on $x$
 $\operatorname{NDE}(x)=E\left{Y\left(1, M_{0}\right)Y\left(0, M_{0}\right) \mid X=x\right}$
 $\operatorname{NIE}(x)=E\left{Y\left(1, M_{1}\right)Y\left(1, M_{0}\right) \mid X=x\right}$

estimators
 $\widehat{NDE}(x) = E\left{Y\left(t, M_{t^{\prime}}\right) \mid X=x\right}=\sum_{m} E(Y \mid T=t, M=m, X=x) \operatorname{pr}\left(M=m \mid T=t^{\prime}, X=x\right)$
 $\widehat{NIE}(x) = E\left{Y\left(t, M_{t^{\prime}}\right)\right}=\sum_{x} E\left{Y\left(t, M_{t^{\prime}}\right) \mid X=x\right} P(X=x)$

estimators depend on 4 assumptions

no treatmentoutcome confounding: $T \perp Y(t, m) \mid X$

no mediatoroutcome confounding: $M \perp Y(t, m) \mid (X, T)$

assumption 3: no treatmentmediator confounding: $T \perp M(t) \mid X$

no crossworld independence between potential outcomes and potential mdediators: $Y(t, m) \perp M(z’) \; \forall \; t, t’, m$

 assumption notes
 1 + 2 are equivalent to $T, M) \perp Y(t, m) \mid X$
 first three essentially assume that $T$ and $M$ are both randomized
 13 are very strong but hold with squentially randomized treatment + mediator
 4 cannot be verified
 baronkenny method (assumes linear models):

heterogenous treatment effects
Heterogenous treatment effects refer to effects which differ for different subgroups / individuals in a population and requires more refined modeling.

conditional average treatment effect (CATE)  get treatment effect for each individual conditioned on its covariates $\mathbb E [y x, t=1]  \mathbb E[y x, t=0]$ (different from ITE $Y^{T=1}_i  Y^{T=0}_i$)  metalearners  break down CATE into regression subproblems
 e.g. Slearner (hill 11)  “S” stands for “single” and fits a single statistical model for $\mu_1  \mu_0$
 can be biased towards 0
 e.g. Tlearner (foster et al. 2011)  “T” stands for “two” because we fit 2 models: one model for conditional expectation of each potential outcome: $\hat \mu_1(x), \hat \mu_0(x)$
 can have issues, e.g. different effects are regularized differently
 doesn’t do well with variation in the propensity score. If $e(x)$ varies considerably, then our estimates of $\hat \mu(0)$ will be driven by data in areas with many control units (i.e., with $e(x)$ closer to 0), and those of $\hat \mu (1)$ by regions with more treated units (i.e., with e(x) closer to 1).
 e.g. Xlearner (kunzel et al. 19)  “X” stands for crossing between estimates and conditional outcomes for each group
 first, fit $\hat \mu_1(x), \hat \mu_0(x)$
 second, compute effects using all the data $\begin{aligned} \hat{\tau}{1, i} &=Y{i}(1)\hat{\mu}{0}\left(x{i}\right) \ \hat{\tau}{0, i} &=\hat{\mu}{1}\left(x_{i}\right)Y_{i}(0) \end{aligned}$
 finally, combine effects $\hat{\tau}(x)=g(x) \hat{\tau}{0}(x)+(1g(x)) \hat{\tau}{1}(x)$
 $g(x)$ is weighting function, e.g. estimated propensity score
 e.g. Rlearner (robinson, 1988; niewager, 20)  regularized semiparametric learner
 $\hat{\tau}{R}(\cdot)=\operatorname{argmin}{\hat \tau}\left{\frac{1}{n} \sum_{i=1}^{n}\left(\underbrace{Y_{i}\hat \mu\left(X_{i}\right)}{\text{Y residual}}\left(T{i}\hat e\left(X_{i}\right)\right) \hat \tau\left(X_{i}\right)\right)^{2}\right. \left.+ \underbrace{\Lambda_{n}\left(\hat \tau(\cdot)\right)}_{\text{regularization}}\right}$

$\hat \mu(x) = E[Y_i X=x]$  use crossfitting to estimate $\hat \tau$ and $\hat \mu$
 $\tau$ takes a form, e.g. LASSO

 $\hat{\tau}{R}(\cdot)=\operatorname{argmin}{\hat \tau}\left{\frac{1}{n} \sum_{i=1}^{n}\left(\underbrace{Y_{i}\hat \mu\left(X_{i}\right)}{\text{Y residual}}\left(T{i}\hat e\left(X_{i}\right)\right) \hat \tau\left(X_{i}\right)\right)^{2}\right. \left.+ \underbrace{\Lambda_{n}\left(\hat \tau(\cdot)\right)}_{\text{regularization}}\right}$
 e.g. Slearner (hill 11)  “S” stands for “single” and fits a single statistical model for $\mu_1  \mu_0$
 treebased methods
 e.g. causal tree (athey & imbens, 16)  like decision tree, but change splitting criterion for differentiating 2 outcomes + compute effects for each leaf on outofsample data
 e.g. causal forest (wager & athey, 18)  extends causal tree to forest
 e.g. BART (hill, 12)  takes treatment as an extra input feature
 neuralnet based methods
 e.g. TARNet (shalit et al. 2017)  full notes below, use data from both groups
 metalearners  break down CATE into regression subproblems
 validation
 can crossvalidate CATE on Rloss (sampling variability is high, but may not always be an issue (wager, 2020))
 indirect approach  use CATE to identify subgroups, and then use outofsample data to evaluate these subgroups
 fit $\hat \tau$ then rerun semiparametric model and see if coefficient for $\hat \tau$ ends up close to 1
 more discussion in (athey & wager, 2019) and (chernozhukov et al. 2017)
 subgroup analysis  identify subgroups with treatment effects far from the average
 generally easier than CATE
 staDISC (dwivedi, tan et al. 2020)  learn stable / interpretable subgroups for causal inference
 CATE  estimate with a bunch of different models
 metalearners: T/X/R/Slearners
 treebased methods: causal tree/forest, BART
 calibration to evaluate subgroup CATEs
 main difficulty: hard to do model selection / validation (especially with imbalanced data)
 often use some kind of proxy loss function
 solution: compare average CATE within a bin to CATE on test data in bin
 actual CATE doesn’t seem to generalize
 but ordering of groups seems pretty preserved
 stability: check stability of this with many CATE estimators
 main difficulty: hard to do model selection / validation (especially with imbalanced data)
 subgroup analysis
 use CATE as a stepping stone to finding subgroups
 easier, but still linked to real downstream tasks (e.g. identify which subgroup to treat)
 main difficulty: can quickly overfit
 cellsearch  sequential
 first prune features using feature importance
 target: maximize a cell’s true positive  false positive (subject to using as few features as possible)
 sequentially find cell which maximizes target
 find all cells which perform close to as good as this cell
 remove all cells contained in another cell
 pick one randomly, remove all points in this cell, then continue
 stability: rerun search multiple times and look for stable cells / stable cell coverage
 CATE  estimate with a bunch of different models
 Estimating individual treatment effect: generalization bounds and algorithms (shalit, johansson, & sontag, 2017)
 bound the ITE estimation error using (1) generalization err of the repr. and (2) the distance between the treated and control distrs., e.g. MMD
reinforcement (policy) learning
 rather than estimating a treatment effect, find a policy that maximizes some expected utility (e.g. can define utility as the potential outcome $\mathbb E[Y_i(\pi(X_i))]$)
 in this case, policy is like an intervention
causal discovery
Causal discovery aims to identify causal relationships (sometimes under some smoothness / independence assumptions. This is often impossible in general. Also called causal relation learning, causal search.
 a lot of our science does not actually rest on experiments (e.g. physics, geology)
 hume (1739)  all we can observe is association, never actual counterfactuals or causes (“necesary connexion”)
 requires careful model selection
 rvw: Review of Causal Discovery Methods Based on Graphical Models
 constraintbased algorithms  use conditional indep. checks to determine graphs up to markov equivalence
 faithfulness means the statistical dependence between variables estimated from the data does not violate the independence defined by any causal graph which generates the data
 extensions to more general distrs., unobserved confounders
 peterclark (PC) algorithm  first learns undirected graph, then detects edge directions and returns equivalence class
 assumes that there is no confounder (unobserved direct common cause of two measured variables)
 fast causal inference (FCI) (spirtes et al. 200)
 can deal with confounders  instead of edge/no edge have 3 possibilities: edge, no edge, confounding by unobserved missing common cause (+possibly another possibility for “unknown”)
 scorebased algorithms  replace conditional indep. tests with godness of fit tests (e.g. BIC)
 assume there are no confounders
 still can only determine graphs up to markov equivalence
 optimizing goodness of fit is NPhard, so often use heuristics such as greedy equivalence search (GES) (chickering, 2002)
 functional causal models  assume a variable can be written as a function of its direct causes and some noise term
 can distinguish between different DAGs in same equivalence class

e.g. (hyavarinen & zhang, 2016) assume additive noise and that $p(E C)$ can be modeled while $P(C E)$ cannot  e.g. LiNGAM (Shimizu et al., 2006), ICALINGAM  linear relations between different variables and noise
 additive noise models ANM (Hoyer et al., 2009) relax the linear restriction
 ANMMM (Hu et al., 2018)
 postnonlinear models PNL (Zhang and Hyvarinen, 2009) expand the functional space with nonlinear relations between the variables and the noise

many models assume the generating cause distribution $p(C)$ is in some sense “independent” to the mechanism $P(E C)$  e.g. IGCI (Janzing et al., 2012) uses orthogonality in information space to express the independence between the two distributions
 e.g. KCDC (Mitrovic et al., 2018) uses invariance of Kolmogorov complexity of conditional distribution
 e.g. RECI (Blobaum et al., 2018) extends IGCI to the setting with small noise, and proceeds by comparing the regression errors in both possible directions
 check variables which reduce entropy the most
 Origo : causal inference by compression (budhathoki & vreekan, 2017)  similar intuition as ICM: causal directions are more easily compressible

Learning and Testing Causal Models with Interventions (acharya et al. 2018)
 given DAG, want to learn distribution on interventions with minimum number of interventions, variables intevened on, numper of samples draw per intervention
 Discovering Causal Signals in Images (lopezpaz et al. 2017)
 C(A, B)  count number of images in which B would disappear if A was removed
 we say A causes B when C(A, B) is (sufficiently) greater than the converse C(B, A)
 basics
 given joint distr. of (A, B), we want to know if A > B, B> A
 with no assumptions, this is nonidentifiable
 requires 2 assumptions
 ICM: independence between cause and mechanism (i.e. the function doesn’t change based on distr. of X)  this usually gets violated in anticausal direction
 causal sufficiency  we aren’t missing any vars
 ex.
 here noise is indep. from x (causal direction), but can’t be independent from y (noncausal direction)
 in (c), function changes based on input
 can turn this into binary classification and learn w/ network: given X, Y, does X>Y or YX?
 given joint distr. of (A, B), we want to know if A > B, B> A
 on images, they get scores for different objects (w/ bounding boxes)
 eval  when one thing is erased, does the other also get erased?
 link to iclr talk (bottou 2019)
 Visual Causal Feature Learning (chalupka, perona, & eberhardt, 2015)
 assume the behavior $T$ is a function of some hidden causes $H_i$ and the image
 Causal Coarsening Theorem  causal partition is coarser version of the observational partition

observational partition  divide images into partition where each partition has constant prediction $P(T I)$ 
causal partition  divide images into partition where each partition has constant $P(T man(I))$  $man(I)$ does visual manipulation which changes $I$, while keeping all $H_i$ fixed and $T$ fixed
 ex. turn a digit into a 7 (or turn a 7 into not a 7)
 $man(I)$ does visual manipulation which changes $I$, while keeping all $H_i$ fixed and $T$ fixed


can further simplify the problem into $P(T I) = P(T C, S)$  $C$ are the causes and $S$ are the spurious correlates

any other variable $X$ such that $P(T I) = P(T X)$ has Shannon entropy $H(X) \geq H(C, S)$  these are the simplest descriptions of $P(T I$)
 causal effect prediction

first, create causal dataset of $P(T man(I))$ and train, so the model can’t learn spurious correlations  then train on this  very similar to adversarial training

 assume the behavior $T$ is a function of some hidden causes $H_i$ and the image
 Visual Physics: Discovering Physical Laws from Videos
 3 steps
 Mask RCNN finds bounding box of object and center of bounding box is taken to be location
 $\betaVAE$ compresses the trajectory to some latent repr. (while also being able to predict heldout points of the trajectory)
 Eureqa package does eq. discovery on latent repr + trajectory
 includes all basic operations, such as addition, mult., sine function
 Rsquared value measures goodness of fit
 see also SciNet  Discovering physical concepts with neural networks (iten et al. 2020)
 see also the field of symbolic regression
 genetic programming is the most pervalent method here
 alternatives: sparse regression, dimensional function synthesis
 3 steps
 Causal Mosaic: CauseEffect Inference via Nonlinear ICA and Ensemble Method (wu & fukumizu, 2020)
 focus on bivariate case
stable/invariant predictors
Under certain assumptions, invariance to data perturbations (i.e. interventions) can help us identify causal effects.
invariance hierarchies
 The Hierarchy of Stable Distributions and Operators to Trade Off Stability and Performance (subbaswamy, chen, & saria 2019)
 different predictors learn different things
 only pick the stable parts of what they learn (in a graph representation)
 there is a tradeoff between stability to all shifts and average performance on the shifts we expect to see
 different types of methods
 transfer learning  given unlabelled test data, match training/testing representations
 proactive methods  make assumptions about possible set of target distrs.
 datadriven methods  assume independence of cause and mechanism, like ICP, and use data from different shifts to find invariant subsets
 explicit graph methods  assume explicit knowledge of graph representing the datagenerating process
 hierarchy

level 1  invariant conditional distrs. of the form $P(Y \mathbf Z)$ 
level 2  conditional interventional distrs. of the form $P(Y do(\mathbf W), \mathbf Z)$  level 3  distributions corresponding to counterfactuals

 Causality for Machine Learning (scholkopf 19)
 most of ml is built on the iid assumption and fails when it is violated (e.g. cow on a beach)
invariance algorithms
 algorithms overview (see papers for more details) + implementations
 ICP  invariant causal prediction  find feature set where, after conditioning, loss is the same for all environments
 fails when distr. of residuals varies across environments
 IRM  invariant risk minimization (v1)  find a feature repr. such that the optimal classifier, on top of that repr., is the identity function for all environments
 GroupDRO  distributionally robust optimization (e.g. encourage strict equality between err of each group)
 ERM  empirical risk minimization  minimize total training err
 domainadversarial techniques: find a repr. which does not differ across environments, then predict
 fails when distr. of causes changes across environments
 ANDmask  minimize the err only in directions where the sign of the gradient of the loss is the same for most environments
 IGA  interenvironmental gradient alignment  ERM + reduce variance of the gradient of the loss per environment: $\lambda \operatorname{trace}\left(\operatorname{Var}\left(\nabla_{\theta} L_{\mathcal{E}}(\theta)\right)\right)$
 ICP  invariant causal prediction  find feature set where, after conditioning, loss is the same for all environments
 Invariance, Causality and Robustness  ICP (buhlmann 18)
 predict $Y^e$ given $X^e$ such that the prediction “works well” or is “robust” for all $e ∈ \mathcal F$ based on data from much fewer environments $e \in \mathcal E$
 key assumption (invariance): there exists a subset of “causal” covariates  when conditioning on these covariates, the loss is the same across all environments $e$
 assumption: ideally $e$ changes only the distr. of $X^e$ (so doesn’t act directly on $Y^e$ or change the mechanism between $X^e$ and $Y^e$)
 when these assumptions are satisfied, then minimizing a worstcase risk over environments $e$ yields a causal parameter
 identifiability issue: we typically can’t identify the causal variables without very many perturbations $e$
 Invariant Causal Prediction (ICP) only identifies variables as causal if they appear in all invariant sets (see also Peters, Buhlmann, & Meinshausen, 2015)
 bruteforce feature selection
 anchor regression model helps to relax assumptions
 predict $Y^e$ given $X^e$ such that the prediction “works well” or is “robust” for all $e ∈ \mathcal F$ based on data from much fewer environments $e \in \mathcal E$
 Invariant Risk Minimization  IRM (arjovsky, bottou, gulrajani, & lopezpaz 2019)
 idealized formulation: $\begin{array}{ll}\min {\Phi: \mathcal{X} \rightarrow \mathcal{H}} & \sum{e \in \mathcal{E}{\mathrm{tr}}} R^{e}(w \circ \Phi) \ \text { subject to } & w \in \underset{\bar{w}: \mathcal{H} \rightarrow \mathcal{Y}}{\arg \min } : R^{e}(\bar{w} \circ \Phi), \text { for all } e \in \mathcal{E}{\mathrm{tr}}\end{array}$
 $\Phi$ is repr., $w \circ \Phi$ is predictor
 practical formulation: $\min {\Phi: \mathcal{X} \rightarrow \mathcal{Y}} \sum{e \in \mathcal{E}{\mathrm{tr}}} R^{e}(\Phi)+\lambda \cdot\left\nabla{w \mid w=1.0} R^{e}(w \cdot \Phi)\right^{2}$
 random splitting causes problems with our data
 what to perform well under different distributions of X, Y
 can’t be solved via robust optimization
 a correlation is spurious when we do not expect it to hold in the future in the same manner as it held in the past
 i.e. spurious correlations are unstable
 assume we have infinite data, and know what kinds of changes our distribution for the problem might have (e.g. variance of features might change)
 make a model which has the minimum test error regardless of the distribution of the problem
 adds a penalty inspired by invariance (which can be viewed as a stability criterion)
 idealized formulation: $\begin{array}{ll}\min {\Phi: \mathcal{X} \rightarrow \mathcal{H}} & \sum{e \in \mathcal{E}{\mathrm{tr}}} R^{e}(w \circ \Phi) \ \text { subject to } & w \in \underset{\bar{w}: \mathcal{H} \rightarrow \mathcal{Y}}{\arg \min } : R^{e}(\bar{w} \circ \Phi), \text { for all } e \in \mathcal{E}{\mathrm{tr}}\end{array}$
 Learning explanations that are hard to vary  ANDmask (parascandolo…sholkopf, 2020)
 basically, gradients should be consistent during learning
 after learning, they should be consistent within some epsilon ball
 practical algorithm: ANDmask
 like zeroing out those gradient components with respect to weights that have inconsistent signs across environments
 basically same complexity as normal GD
 previous works used cosine similarity between weights in different settings
 experiments
 real data is spiral but each env is linearly separable  still able to learn spiral
 cifar  with real labels, performance unaffected; with random labels, training acc drops significantly
 each example is its own environment
 with noisy labels, imposes good regularization
 rl  works well on coinrun
 like zeroing out those gradient components with respect to weights that have inconsistent signs across environments
 propose invariant learning consistency (ILC) measures expected consistency of the soln found by an algorithm given a hypothesis class
 consistency  what extent a minimum of the loss surface appears only when data from different envs are pooled
 given algorithm $\mathcal A$, maximize this: $\mathrm{ILC}\left(\mathcal{A}, p_{\theta^{0}}\right):= \underbrace{\mathbb{E}{\theta^{0} \sim p\left(\theta^{0}\right)}}{\text{expectation over reinits}}\left[\mathcal{I}^{\epsilon} (\underbrace{\mathcal{A}{\infty}(\theta^{0}, \mathcal{E}}{\hat \theta}) \right]$

inconsistency score for a solution $\hat \theta$ given environments $e$: $\mathcal{I}^{\epsilon}(\hat \theta):=\overbrace{\max {\left(e, e^{\prime}\right) \in \mathcal{E}^{2}} }^{\text{env. pairs}} \underbrace{\max _{\theta \in N{e, \hat \theta}^{\epsilon}}}{\text{lowloss region around $\hat \theta$}} \overbrace{\mid \mathcal{L}{e^{\prime}}(\theta)\mathcal{L}_{e}(\theta) }^{\text{loss between envs.}}$ 
$N_{e, \hat \theta}^{\epsilon}$ is pathconnected region around $\hat \theta$ where $\left{\theta \in \Theta\right.$ s.t. $\left \mathcal{L}{e}(\theta)\mathcal{L}{e}\left(\hat \theta\right)\right \leqslant \epsilon$


 basically, gradients should be consistent during learning

Invariant Risk Minimization Games (ahuja et al. 2020)  pose IRM as finding the Nash equilibrium of an ensemble game among several environments
 Invariant Rationalization (chang et al. 2020)  identify a small subset of input features – the rationale – that best explains or supports the prediction

key assumption: $Y \perp E Z$  $\max {\boldsymbol{m} \in \mathcal{S}} I(Y ; \boldsymbol{Z}) \quad$ s.t. $\boldsymbol{Z}= \overbrace{\boldsymbol{m}}^{\text{binary mask}} \odot \boldsymbol{X}, \quad \underbrace{Y \perp E \mid \boldsymbol{Z}}{\text{this part is invariance}}$
 solve this via 3 nets with adv. penalty to approximate invariance
 standard maximum mutual info objective is just $\max _{\boldsymbol{m} \in \mathcal{S}} I(Y ; \boldsymbol{Z}) \quad$ s.t. $\boldsymbol{Z}= \overbrace{\boldsymbol{m}}^{\text{binary mask}} \odot \boldsymbol{X}$ (see lei et al. 2016)
 ex. $X$ is text reviews for beer, $Y$ is aroma, $E$ could be beer brand

 Linear unittests for invariance discovery (aubin et al. 2020)  a set of 6 simple settings where current IRM procedures fail
 test 1 (colormniststyle linear regr): $x_{inv} \to \tilde y \to x_{spu}$
 $\tilde y \to y$
 test 2 (cows vs camels binary classification): $y=mean(x_{inv})>0$, but $x_{inv} \propto x_{spu}$
 test 3 (small invariant margin): $y_i\sim Bern(1/2)$, $x_{inv} = \pm 0.1+$noise, $x_{spu} = \pm \mu^e$ + noise, where $\mu^e ~ N(0, 1)$
 scrambling: apply random rotation matrix to inputs
 test 1 (colormniststyle linear regr): $x_{inv} \to \tilde y \to x_{spu}$
misc problems
 Incremental causal effects (rothenhausler & yu, 2019)
 instead of considering a treatment, consider an infinitesimal change in a continuous treatment
 use assumption of local independence and can prove some nice things
 local ignorability assumption states that potential outcomes are independent of the current treatment assignment in a neighborhood of observations

probability of necessity $PN(t, y) = P(Y^{T=t’}=y’ T=t, Y=y)$ = “probability of causation” (Robins & Greenland, 1989) 
find the probability that $Y$ would be $y′$ had $T$ been $t’$, given that, in reality, $Y$ is actually $y$ and $T$ is $t$

If $Y$ is monotonic relative to $T$ $i.e ., Y^{T=1}(x) \geq Y^{T=0}(x),$ then $\mathrm{PN}$ is identifiable whenever the causal effect $P(y \mid d o(t))$ is identifiable and, moreover, \(\mathrm{PN}=\underbrace{\frac{P(y \mid t)P\left(y \mid t^{\prime}\right)}{P(y \mid t)}}_{\text{excess risk ratio}}+\underbrace{\frac{P\left(y \mid t^{\prime}\right)P\left(y \mid d o\left(t^{\prime}\right)\right)}{P(t, y)}}_{\text{confounding adjustment}}\)


causal transportability  seeks to identify conditions under which causal knowledge learned from experiments can be reused in different domains with observational data only

Radical Empiricism and Machine Learning Research (pearl 2021)
 contrast the “data fitting” vs. “data interpreting” approaches to datascience
 current research is too empiricist (datafitting based)  should include manmade models of how data are generated
 3 reasons: expediency, transparency, explainability
 expediency: we often have to ask fast (e.g. covid) and use our knowledge to guide future experiments
 transparency: need repr.d with right level off abstraction
 explainability: humans must understand inferences
transferring outofsample
 Elements of External Validity: Framework, Design, and Analysis
 external validity  when do results from an RCT generalize to new settings?
 X, T, Y , and Cvalidity (units, treatments, outcomes, and contexts)
 two goals: effectgeneralization + signgeneralization
different assumptions / experimental designs

unconfoundedness $T_i \perp (Y_i(0), Y_i(1)) X_i$ is strong 
sometimes we may perfer $T_i \perp (Y_i(0), Y_i(1)) X_i, Z_i$ for some unobserved $Z_i$ that we need to figure out

 The Blessings of Multiple Causes (wang & blei, 2019)  having multiple causes can help construct / find all the confounders
 deconfounder algorithm
 fit a factor model of causes
 estimate a repr $Z_i$ of data point $A_i$  $Z_i$ renders the causes conditionally independent
 now, $Z_i$ is a substitute for unobserved confounders
 assumptions
 no causal arrows among causes $A_i$
 no unobserved singlecause confounders: any missing confounder affects multiple observed variables
 –> can check the fit of the factor model, but won’t check perfectly
 the substitute confounder: there is enough information in the data to learn the variable $Z$ which renders causes conditionally independent
 strong assumption!
 thm

with observed covariates X, weak unconfoundedness: $A_1, …A_m \perp Y(a) Z, X$ (i.e. $Z$ contains all multicause confounders, $X$ contains all singlecause confounders)

 replaces an uncheckable search for possible confounders with the checkable goal of building a good factor model of observed casts.
 controversial whether this works in general
 Towards Clarifying the Theory of the Deconfounder (wang & blei, 2020)
 On MultiCause Causal Inference with Unobserved Confounding: Counterexamples, Impossibility, and Alternatives (d’amour 2019)
 deconfounder algorithm
synthetic control/interventions
 synthetic control
 Using Synthetic Controls rvw paper (abadie 2020)
 setting: treatment occurs at time t0 on multiple units (e.g. policy in california)
 goal: estimate effect of treatment (e.g. effect of policy in california)
 approach: impute counterfactual (california timeseries without policy) by weighted combination on observed outcomes for other observations (e.g. average other “similar” states)
 perobservation weights are learned during preintervention period with crossvalidation procedure
 perfeature weights are also learned (bc matching on some features is more important than others)
 perobservation weights are learned during preintervention period with crossvalidation procedure
 The Economic Costs of Conflict: A Case Study of the Basque Country (Abadie & G, 2003)
 Synthetic Control Methods for Comparative Case Studies: Estimating the Effect of California’s Tobacco Control Program (abadie et al. 2010)
 Using Synthetic Controls rvw paper (abadie 2020)
solutions to basic problems
learning “causal representations”
 Learning Representations for Counterfactual Inference (johansson et al. 2016)

assumption similar to ignorability: the treatment assignment information (and any info which predicts it) should not influence the ITE: $T \perp !!! \perp { Y^{T=1}, Y^{T=0}} X$  often not the case, e.g. medical symptoms lead doctors to give a treatment more
 in this case, we will lose info that can help us predict the CATE
 also an extra loss: penalty that encourages counterfactual preds to be close to nearest observed outcome from the same set
 fit linear ridge regression on top of representation $\phi$
 not exactly the same as the setting in fair repr. learning or domain adversarial training  MMD or Wasserstein distance instead of classification
 same idea present in Training confounderfree deep learning models for medical applications (zhou et al. 2020)

 Estimating individual treatment effect: generalization bounds and algorithms (shalit et al. 2017)
 bound for estimating ITE $\tau(x)$ is uper bounded by error for learning $Y_1$ and $Y_0$ plus a term for the Integral Probability Metric (IPM)

IPM measures distance between $p(x T = 0)$ and $P(x T = 1)$, and requires that they overlap at $x$  In his foundational text about causality, Pearl (2009) writes: “Whereas in traditional learning tasks we attempt to generalize from one set of insteances to another, the causal modeling task is to generalize from behavior under one set of conditions to behavior under another set. Causal models should therefore be chosen by a criterion that challenges their stability against changing conditions...”
 Learning Weighted Representations for Generalization Across Designs (johansson et al. 2018)
 Counterfactual Representation Learning with Balancing Weights (assaad et al. 2020)
 combine balancing weights with representation learning: Balancing Weights Counterfactual Regression (BWCFR)
 representation learning has tradeoff between balance and predictive power (zhang, bellot, & van der Schaar, 2020)
 weights are from propensity scores, unlike johansson et al. 2018
 intuition: upweight regions with good overlap
 bounds on degree of imbalance as a function of propensity model
 combine balancing weights with representation learning: Balancing Weights Counterfactual Regression (BWCFR)
 Causal Effect Inference with Deep LatentVariable Models (louizos et al. 2017)  like vae but learn latent distr. that also changes based on treatment
 Invariant Representation Learning for Treatment Effect Estimation (shi, veitch, & blei, 2020)
 Nearly Invariant Causal Estimation  uses IRM to learn repr. that strips out bad controls but preserves sufficient information to adjust for confounding
 observe data from multiple environments
 covariates contain some causal variables
 covariates also contain some false confounders
 Nearly Invariant Causal Estimation  uses IRM to learn repr. that strips out bad controls but preserves sufficient information to adjust for confounding
 DeepMatch: Balancing Deep Covariate Representations for Causal Inference Using Adversarial Training (kallus, 2018)
 weighting and a discriminator network compete adversarially to minimize “discriminative discrepancy metric” for measuring covariate balance
 this metric goes beyond just the original feature space
limitations
 Limits of Estimating Heterogeneous Treatment Effects: Guidelines for Practical Algorithm Design (alaa & van der schaar, 2018)
 over enforcing balance can be harmful, as it may inadvertently remove information that is predictive of outcomes
 analyze optimal minimax rate for ITE using Bayesian nonparametric methods
 with small sample size: selection bias matters
 with large sample size: smoothness and sparsity of $\mathbb{E}\left[Y_{i}^{(0)} \mid X_{i}=x\right]$ and $\mathbb{E}\left[Y_{i}^{(1)} \mid X_{i}=x\right]$
 suggests smoothness of mean function for each group should be different, so better to approximate each individually rather than their difference directly
 algorithm: nonstationary Gaussian process w/ doublyrobust huperparameters