Let’s say we’re looking at the relationship between smoking and cardiac arrest. We might assume that smoking causes changes in cholesterol, which causes cardiac arrest:

The path from smoking to cardiac arrest is directed: smoking causes cholesterol to rise, which then increases risk for cardiac arrest. Cholesterol is an intermediate variable between smoking and cardiac arrest. Directed paths are also chains, because each is causal on the next. Let’s say we also assume that weight causes cholesterol to rise and thus increases risk of cardiac arrest. Now there’s another chain in the DAG: from weight to cardiac arrest. However, this chain is indirect, at least as far as the relationship between smoking and cardiac arrest goes.

We also assume that a person who smokes is more likely to be someone who engages in other unhealthy behaviors, such as overeating. On the DAG, this is portrayed as a latent (unmeasured) node, called unhealthy lifestyle. Having a predilection towards unhealthy behaviors leads to both smoking and increased weight. Here, the relationship between smoking and weight is through a forked path (weight <- unhealthy lifestyle -> smoking) rather than a chain; because they have a mutual parent, smoking and weight are associated (in real life, there’s probably a more direct relationship between the two, but we’ll ignore that for simplicity).

Forks and chains are two of the three main types of paths:

- Chains
- Forks
- Inverted forks (paths with colliders)

An inverted fork is when two arrowheads meet at a node, which we’ll discuss shortly.

There are also common ways of describing the relationships between nodes: parents, children, ancestors, descendants, and neighbors (there are a few others, as well, but they refer to less common relationships). Parents and children refer to direct relationships; descendants and ancestors can be anywhere along the path to or from a node, respectively. Here, smoking and weight are both parents of cholesterol, while smoking and weight are both children of an unhealthy lifestyle. Cardiac arrest is a descendant of an unhealthy lifestyle, which is in turn an ancestor of all nodes in the graph.

So, in studying the causal effect of smoking on cardiac arrest, where does this DAG leave us? We only want to know the directed path from smoking to cardiac arrest, but there also exists an indirect, or back-door, path. This is confounding. Judea Pearl, who developed much of the theory of causal graphs, said that confounding is like water in a pipe: it flows freely in open pathways, and we need to block it somewhere along the way. We don’t necessarily need to block the water at multiple points along the same back-door path, although we may have to block more than one path. We often talk about confounders, but really we should talk about confounding, because it is about the pathway more than any particular node along the path.

Chains and forks are open pathways, so in a DAG where nothing is conditioned upon, any back-door paths must be one of the two. In addition to the directed pathway to cardiac arrest, there’s also an open back-door path through the forked path at unhealthy lifestyle and on from there through the chain to cardiac arrest:

We need to account for this back-door path in our analysis. There are many ways to go about that-stratification, including the variable in a regression model, matching, inverse probability weighting-all with pros and cons. But each strategy must include a decision about which variables to account for. Many analysts take the strategy of putting in all possible confounders. This can be bad news, because adjusting for colliders and mediators can introduce bias, as we’ll discuss shortly. Instead, we’ll look at minimally sufficient adjustment sets: sets of covariates that, when adjusted for, block all back-door paths, but include no more or no less than necessary. That means there can be many minimally sufficient sets, and if you remove even one variable from a given set, a back-door path will open. Some DAGs, like the first one in this vignette (x -> y), have no back-door paths to close, so the minimally sufficient adjustment set is empty (sometimes written as “{}”). Others, like the cyclic DAG above, or DAGs with important variables that are unmeasured, can not produce any sets sufficient to close back-door paths.

For the smoking-cardiac arrest question, there is a single set with a single variable: {weight}. Accounting for weight will give us an unbiased estimate of the relationship between smoking and cardiac arrest, assuming our DAG is correct. We do not need to (or want to) control for cholesterol, however, because it’s an intermediate variable between smoking and cardiac arrest; controlling for it blocks the path between the two, which will then bias our estimate (see below for more on mediation).

More complicated DAGs will produce more complicated adjustment sets; assuming your DAG is correct, any given set will theoretically close the back-door path between the outcome and exposure. Still, one set may be better to use than the other, depending on your data. For instance, one set may contain a variable known to have a lot of measurement error or with a lot of missing observations. It may, then, be better to use a set that you think is going to be a better representation of the variables you need to include. Including a variable that doesn’t actually represent the node well will lead to residual confounding.

What about controlling for multiple variables along the back-door path, or a variable that isn’t along any back-door path? Even if those variables are not colliders or mediators, it can still cause a problem, depending on your model. Some estimates, like risk ratios, work fine when non-confounders are included. This is because they are collapsible: risk ratios are constant across the strata of non-confounders. Some common estimates, though, like the odds ratio and hazard ratio, are non-collapsible: they are not necessarily constant across strata of non-confounders and thus can be biased by their inclusion. There are situations, like when the outcome is rare in the population (the so-called rare disease assumption), or when using sophisticated sampling techniques, like incidence-density sampling, when they approximate the risk ratio. Otherwise, including extra variables may be problematic.