Addiction is not a disease: A neuroscientist argues that it’s time to change our minds on the roots of substance abuse
By Laura Miller, for Salon. 6/27/15
A psychologist and former addict insists that the illness model for addiction is wrong, and dangerously so.
The mystery of addiction — what it is, what causes it and how to end it — threads through most of our lives. Experts estimate that one in 10 Americans is dependent on alcohol and other drugs, and if we concede that behaviors like gambling, overeating and playing video games can be addictive in similar ways, it’s likely that everyone has a relative or friend who’s hooked on some form of fun to a destructive degree. But what exactly is wrong with them? For several decades now, it’s been a commonplace to say that addicts have a disease. However, the very same scientists who once seemed to back up that claim have begun tearing it down.
Once, addictions were viewed as failures of character and morals, and society responded to drunks and junkies with shaming, scolding and calls for more “will power.” This proved spectacularly ineffective, although, truth be told, most addicts do quit without any form of treatment. Nevertheless, many do not, and in the mid-20th century, the recovery movement, centered around the 12-Step method developed by the founders of Alcoholics Anonymous, became a godsend for those unable to quit drinking or drugging on their own. The approach spread to so-called “behavioral addictions,” like gambling or sex, activities that don’t even involve the ingestion of any kind of mind-altering substance.
Much of the potency of AA comes from its acknowledgement that willpower isn’t enough to beat this devil and that blame, rather than whipping the blamed person into shape, is counterproductive. The first Step requires admitting one’s helplessness in the face of addiction….
…. Another factor promoting the disease model is that it has ushered addiction under the aegis of the healthcare industry, whether in the form of an illness whose treatment can be charged to an insurance company or as the focus of profit-making rehab centers.
….The recovery movement and rehab industry (two separate things, although the latter often employs the techniques of the former) have always had their critics, but lately some of the most vocal have been the neuroscientists whose findings once lent them credibility.
One of those neuroscientists is Marc Lewis, a psychologist and former addict himself, also the author of a new book “The Biology of Desire: Why Addiction is Not a Disease.”
Lewis’s argument is actually fairly simple: The disease theory, and the science sometimes used to support it, fail to take into account the plasticity of the human brain.
Of course, “the brain changes with addiction,” he writes. “But the way it changes has to do with learning and development — not disease.” All significant and repeated experiences change the brain; adaptability and habit are the brain’s secret weapons. The changes wrought by addiction are not, however, permanent, and while they are dangerous, they’re not abnormal.
Through a combination of a difficult emotional history, bad luck and the ordinary operations of the brain itself, an addict is someone whose brain has been transformed, but also someone who can be pushed further along the road toward healthy development. (Lewis doesn’t like the term “recovery” because it implies a return to the addict’s state before the addiction took hold.)
By Natalie Wolchover, Senior Writer, Quanta Magazine
October 23, 2017
In 1985, when Carl Sagan was writing the novel Contact, he needed to quickly transport his protagonist Dr. Ellie Arroway from Earth to the star Vega. He had her enter a black hole and exit light-years away, but he didn’t know if this made any sense. The Cornell University astrophysicist and television star consulted his friend Kip Thorne, a black hole expert at the California Institute of Technology (who won a Nobel Prize earlier this month). Thorne knew that Arroway couldn’t get to Vega via a black hole, which is thought to trap and destroy anything that falls in. But it occurred to him that she might make use of another kind of hole consistent with Albert Einstein’s general theory of relativity: a tunnel or “wormhole” connecting distant locations in space-time.
While the simplest theoretical wormholes immediately collapse and disappear before anything can get through, Thorne wondered whether it might be possible for an “infinitely advanced” sci-fi civilization to stabilize a wormhole long enough for something or someone to traverse it.
He figured out that such a civilization could in fact line the throat of a wormhole with “exotic material” that counteracts its tendency to collapse. The material would possess negative energy, which would deflect radiation and repulse space-time apart from itself. Sagan used the trick in Contact, attributing the invention of the exotic material to an earlier, lost civilization to avoid getting into particulars. Meanwhile, those particulars enthralled Thorne, his students and many other physicists, who spent years exploring traversable wormholes and their theoretical implications. They discovered that these wormholes can serve as time machines, invoking time-travel paradoxes — evidence that exotic material is forbidden in nature.
Now, decades later, a new species of traversable wormhole has emerged, free of exotic material and full of potential for helping physicists resolve a baffling paradox about black holes. This paradox is the very problem that plagued the early draft of Contact and led Thorne to contemplate traversable wormholes in the first place; namely, that things that fall into black holes seem to vanish without a trace. This total erasure of information breaks the rules of quantum mechanics, and it so puzzles experts that in recent years, some have argued that black hole interiors don’t really exist — that space and time strangely end at their horizons.
The flurry of findings started last year with a paper that reported the first traversable wormhole that doesn’t require the insertion of exotic material to stay open. Instead, according to Ping Gao and Daniel Jafferis of Harvard University and Aron Wall of Stanford University, the repulsive negative energy in the wormhole’s throat can be generated from the outside by a special quantum connection between the pair of black holes that form the wormhole’s two mouths. When the black holes are connected in the right way, something tossed into one will shimmy along the wormhole and, following certain events in the outside universe, exit the second.
Remarkably, Gao, Jafferis and Wall noticed that their scenario is mathematically equivalent to a process called quantum teleportation, which is key to quantum cryptography and can be demonstrated in laboratory experiments.
John Preskill, a black hole and quantum gravity expert at Caltech, says the new traversable wormhole comes as a surprise, with implications for the black hole information paradox and black hole interiors. “What I really like,” he said, “is that an observer can enter the black hole and then escape to tell about what she saw.” This suggests that black hole interiors really exist, he explained, and that what goes in must come out.
The new wormhole work began in 2013, when Jafferis attended an intriguing talk at the Strings conference in South Korea. The speaker, Juan Maldacena, a professor of physics at the Institute for Advanced Study in Princeton, New Jersey, had recently concluded, based on various hints and arguments, that “ER = EPR.” That is, wormholes between distant points in space-time, the simplest of which are called Einstein-Rosen or “ER” bridges, are equivalent (albeit in some ill-defined way) to entangled quantum particles, also known as Einstein-Podolsky-Rosen or “EPR” pairs. The ER = EPR conjecture, posed by Maldacena and Leonard Susskind of Stanford, was an attempt to solve the modern incarnation of the infamous black hole information paradox by tying space-time geometry, governed by general relativity, to the instantaneous quantum connections between far-apart particles that Einstein called “spooky action at a distance.”
The paradox has loomed since 1974, when the British physicist Stephen Hawking determined that black holes evaporate — slowly giving off heat in the form of particles now known as “Hawking radiation.” Hawking calculated that this heat is completely random; it contains no information about the black hole’s contents. As the black hole blinks out of existence, so does the universe’s record of everything that went inside. This violates a principle called “unitarity,” the backbone of quantum theory, which holds that as particles interact, information about them is never lost, only scrambled, so that if you reversed the arrow of time in the universe’s quantum evolution, you’d see things unscramble into an exact re-creation of the past.
Almost everyone believes in unitarity, which means information must escape black holes — but how? In the last five years, some theorists, most notably Joseph Polchinski of the University of California, Santa Barbara, have argued that black holes are empty shells with no interiors at all — that Ellie Arroway, upon hitting a black hole’s event horizon, would fizzle on a “firewall” and radiate out again.
Many theorists believe in black hole interiors (and gentler transitions across their horizons), but in order to understand them, they must discover the fate of information that falls inside. This is critical to building a working quantum theory of gravity, the long-sought union of the quantum and space-time descriptions of nature that comes into sharpest relief in black hole interiors, where extreme gravity acts on a quantum scale.
The quantum gravity connection is what drew Maldacena, and later Jafferis, to the ER = EPR idea, and to wormholes. The implied relationship between tunnels in space-time and quantum entanglement posed by ER = EPR resonated with a popular recent belief that space is essentially stitched into existence by quantum entanglement. It seemed that wormholes had a role to play in stitching together space-time and in letting black hole information worm its way out of black holes — but how might this work? When Jafferis heard Maldacena talk about his cryptic equation and the evidence for it, he was aware that a standard ER wormhole is unstable and non-traversable. But he wondered what Maldacena’s duality would mean for a traversable wormhole like the ones Thorne and others played around with decades ago. Three years after the South Korea talk, Jafferis and his collaborators Gao and Wall presented their answer. The work extends the ER = EPR idea by equating, not a standard wormhole and a pair of entangled particles, but a traversable wormhole and quantum teleportation: a protocol discovered in 1993 that allows a quantum system to disappear and reappear unscathed somewhere else.
When Maldacena read Gao, Jafferis and Wall’s paper, “I viewed it as a really nice idea, one of these ideas that after someone tells you, it’s obvious,” he said. Maldacena and two collaborators, Douglas Stanford and Zhenbin Yang, immediately began exploring the new wormhole’s ramifications for the black hole information paradox; their paper appeared in April. Susskind and Ying Zhao of Stanford followed this with a paper about wormhole teleportation in July. The wormhole “gives an interesting geometric picture for how teleportation happens,” Maldacena said. “The message actually goes through the wormhole.”
In their paper, “Diving Into Traversable Wormholes,” published in Fortschritte der Physik, Maldacena, Stanford and Yang consider a wormhole of the new kind that connects two black holes: a parent black hole and a daughter one formed from half of the Hawking radiation given off by the parent as it evaporates. The two systems are as entangled as they can be. Here, the fate of the older black hole’s information is clear: It worms its way out of the daughter black hole.
During an interview this month in his tranquil office at the IAS, Maldacena, a reserved Argentinian-American with a track record of influential insights, described his radical musings. On the right side of a chalk-dusty blackboard, Maldacena drew a faint picture of two black holes connected by the new traversable wormhole.
On the left, he sketched a quantum teleportation experiment, performed by the famous fictional experimenters Alice and Bob, who are in possession of entangled quantum particles a and b, respectively.
Say Alice wants to teleport a qubit q to Bob. She prepares a combined state of q and a, measures that combined state (reducing it to a pair of classical bits, 1 or 0), and sends the result of this measurement to Bob. He can then use this as a key for operating on b in a way that re-creates the state q. Voila, a unit of quantum information has teleported from one place to the other.
Maldacena turned to the right side of the blackboard. “You can do operations with a pair of black holes that are morally equivalent to what I discussed [about quantum teleportation]. And in that picture, this message really goes through the wormhole.”
Say Alice throws qubit q into black hole A. She then measures a particle of its Hawking radiation, a, and transmits the result of the measurement through the external universe to Bob, who can use this knowledge to operate on b, a Hawking particle coming out of black hole B. Bob’s operation reconstructs q, which appears to pop out of B, a perfect match for the particle that fell into A. This is why some physicists are excited: Gao, Jafferis and Wall’s wormhole allows information to be recovered from black holes. In their paper, they set up their wormhole in a negatively curved space-time geometry that often serves as a useful, if unrealistic, playground for quantum gravity theorists. However, their wormhole idea seems to extend to the real world as long as two black holes are coupled in the right way: “They have to be causally connected and then the nature of the interaction that we took is the simplest thing you can imagine,” Jafferis explained. If you allow the Hawking radiation from one of the black holes to fall into the other, the two black holes become entangled, and the quantum information that falls into one can exit the other.
The quantum-teleportation format precludes using these traversable wormholes as time machines. Anything that goes through the wormhole has to wait for Alice’s message to travel to Bob in the outside universe before it can exit Bob’s black hole, so the wormhole doesn’t offer any superluminal boost that could be exploited for time travel. It seems traversable wormholes might be permitted in nature as long as they offer no speed advantage. “Traversable wormholes are like getting a bank loan,” Gao, Jafferis and Wall wrote in their paper: “You can only get one if you are rich enough not to need it.”
A Naive Octopus
While traversable wormholes won’t revolutionize space travel, according to Preskill the new wormhole discovery provides “a promising resolution” to the black hole firewall question by suggesting that there is no firewall at black hole horizons. Preskill said the discovery rescues “what we call ‘black hole complementarity,’ which means that the interior and exterior of the black hole are not really two different systems but rather two very different, complementary ways of looking at the same system.” If complementarity holds, as is widely assumed, then in passing across a black hole horizon from one realm to the other, Contact’s Ellie Arroway wouldn’t notice anything strange. This seems more likely if, under certain conditions, she could even slide all the way through a Gao-Jafferis-Wall wormhole.
The wormhole also safeguards unitarity — the principle that information is never lost — at least for the entangled black holes being studied. Whatever falls into one black hole eventually exits the other as Hawking radiation, Preskill said, which “can be thought of as in some sense a very scrambled copy of the black hole interior.”
Taking the findings to their logical conclusion, Preskill thinks it ought to be possible (at least for an infinitely advanced civilization) to influence the interior of one of these black holes by manipulating its radiation. This “sounds crazy,” he wrote in an email, but it “might make sense if we can think of the radiation, which is entangled with the black hole — EPR — as being connected to the black hole interior by wormholes — ER. Then tickling the radiation can send a message which can be read from inside the black hole!” He added, “We still have a ways to go, though, before we can flesh out this picture in more detail.”
Indeed, obstacles remain in the quest to generalize the new wormhole findings to a statement about the fate of all quantum information, or the meaning of ER = EPR.
In Maldacena and Susskind’s paper proposing ER = EPR, they included a sketch that’s become known as the “octopus”: a black hole with tentacle-like wormholes leading to distant Hawking particles that have evaporated out of it.
The authors explained that the sketch illustrates “the entanglement pattern between the black hole and the Hawking radiation. We expect that this entanglement leads to the interior geometry of the black hole.”
But according to Matt Visser, a mathematician and general-relativity expert at Victoria University of Wellington in New Zealand who has studied wormholes since the 1990s, the most literal reading of the octopus picture doesn’t work. The throats of wormholes formed from single Hawking particles would be so thin that qubits could never fit through. “A traversable wormhole throat is ‘transparent’ only to wave packets with size smaller than the throat radius,” Visser explained. “Big wave packets will simply bounce off any small wormhole throat without crossing to the other side.”
Stanford, who co-wrote the recent paper with Maldacena and Yang, acknowledged that this is a problem with the simplest interpretation of the ER = EPR idea, in which each particle of Hawking radiation has its own tentacle-like wormhole.
However, a more speculative interpretation of ER = EPR that he and others have in mind does not suffer from this failing. “The idea is that in order to recover the information from the Hawking radiation using this traversable wormhole,” Stanford said, one has to “gather the Hawking radiation together and act on it in a complicated way.”
This complicated collective measurement reveals information about the particles that fell in; it has the effect, he said, of “creating a large, traversable wormhole out of the small and unhelpful octopus tentacles. The information would then propagate through this large wormhole.” Maldacena added that, simply put, the theory of quantum gravity might have a new, generalized notion of geometry for which ER equals EPR. “We think quantum gravity should obey this principle,” he said. “We view it more as a guide to the theory.”
In his 1994 popular science book, Black Holes and Time Warps, Kip Thorne celebrated the style of reasoning involved in wormhole research. “No type of thought experiment pushes the laws of physics harder than the type triggered by Carl Sagan’s phone call to me,” he wrote; “thought experiments that ask, ‘What things do the laws of physics permit an infinitely advanced civilization to do, and what things do the laws forbid?’”
So, we’re supposed to teach our students about evolution – but where to start? What topics to cover? And in what order should we cover them? And for each topic, what are the relevant learning standards? This sequence works for me:
Examples of evolution
So, we’re supposed to teach our students biology – but where to start? What topics to cover? And in what order should we cover them? And for each topic, what are the relevant learning standards? This sequence works for me:
Then we move on to types of cells
Now the bitty-gritty: Cell reproduction
For those teaching Honors Biology
Psychopathy, sometimes considered synonymous with sociopathy, is a personality disorder characterized by persistent antisocial behavior, impaired empathy and remorse, and bold, disinhibited, egotistical traits.
The Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Diseases (ICD) introduced the diagnoses of antisocial personality disorder (ASPD) and dissocial personality disorder respectively, stating that these diagnoses have been referred to as psychopathy or sociopathy. (Antisocial personality disorder#Psychopathy)
Psychopathy has been proposed as a specifier under an alternative model for ASPD. In the DSM-5, under “Alternative DSM-5 Model for Personality Disorders”, ASPD with psychopathic features is described as characterized by “a lack of anxiety or fear and by a bold interpersonal style that may mask maladaptive behaviors (e.g., fraudulence).” Low levels of withdrawal and high levels of attention-seeking combined with low anxiety are associated with “social potency” and “stress immunity” in psychopathy.
Theodore Millon suggested 5 subtypes of ASPD.
|Nomadic antisocial (including schizoid and avoidant features)||Drifters; roamers, vagrants; adventurer, itinerant vagabonds, tramps, wanderers; they typically easy to adapt in difficult situations, shrewd and impulsive. Mood centers in doom and invincibility.|
|Malevolent antisocial (including sadistic and paranoid features)||Belligerent, mordant, rancorous, vicious, sadistic, malignant, brutal, resentful; anticipates betrayal and punishment; desires revenge; truculent, callous, fearless; guiltless; many dangerous criminal fits this criteria.|
|Covetous antisocial (including negativistic features)||Rapacious, begrudging, discontentedly yearning; an angle was seen as assertively hostile as to dominate; was envious, seek more profit, and avariciously greedy; pleasures more in taking than in having.|
|Risk-taking antisocial(including histrionic features)||Dauntless, venturesome, intrepid, bold, audacious, daring; reckless, foolhardy, heedless; unfazed by hazard; pursues perilous ventures.|
|Reputation-defending antisocial (including narcissisticfeatures)||Needs to be thought of as infallible, unbreakable, indomitable, formidable, inviolable; intransigent when status is questioned; overreactive to slights.|
The study of psychopathy is an active field of research.
Unfortunately the term is used by the general public, popular press, and in fictional portrayals in a variety of contradictory and non-scientific ways, and occasionally as an ad homenim remark.
A prolonged pattern of antisocial behavior in childhood and/or adolescence, and may be seen as a precursor to Antisocial personality disorder (ASPD), also known as sociopathy. The DSM allows differentiating between childhood onset before age 10, and adolescent onset at age 10 and later. Childhood onset is argued to be more due to a personality disorder caused by neurological deficits interacting with an adverse environment.
The DSM-5 includes a specifier for those with conduct disorder who also display a callous, unemotional interpersonal style across multiple settings and relationships. The specifier is based on research which suggests that those with conduct disorder who also meet criteria for the specifier tend to have a more severe form of the disorder with an earlier onset as well as a different response to treatment. – Wikipedia
Is Conduct disorder compulsory in Psychopathy?
Cherie Valeithian, I am a licensed psychologist
In a word, yes, at least when using The Diagnostic and Statistical Manual of Mental and Emotional Disorders, published by the American Psychiatric Association, and currently in it’s 5th edition. The official name for psychopathy/sociopathy is Antisocial Personality Disorder, which is diagnosed only in individuals age 18 or older. One of the criteria required for that diagnosis is that the person met criteria for Conduct Disorder prior to the age of 18, whether or not the person was ever officially diagnosed as such….
Hare Psychopathy Checklist
The Hare PCL-R contains two parts, a semi-structured interview and a review of the subject’s file records and history. During the evaluation, the clinician scores 20 items that measure central elements of the psychopathic character. The items cover the nature of the subject’s interpersonal relationships; his or her affective or emotional involvement; responses to other people and to situations; evidence of social deviance; and lifestyle. The material thus covers two key aspects that help define the psychopath: selfish and unfeeling victimization of other people, and an unstable and antisocial lifestyle.
The twenty traits assessed by the PCL-R score are:
- glib and superficial charm
- grandiose (exaggeratedly high) estimation of self
- need for stimulation
- pathological lying
- cunning and manipulativeness
- lack of remorse or guilt
- shallow affect (superficial emotional responsiveness)
- callousness and lack of empathy
- parasitic lifestyle
- poor behavioral controls
- sexual promiscuity
- early behavior problems
- lack of realistic long-term goals
- failure to accept responsibility for own actions
- many short-term marital relationships
- juvenile delinquency
- revocation of conditional release
- criminal versatility
The interview portion of the evaluation covers the subject’s background, including such items as work and educational history; marital and family status; and criminal background. Because psychopaths lie frequently and easily, the information they provide must be confirmed by a review of the documents in the subject’s case history.
When properly completed by a qualified professional, the PCL-R provides a total score that indicates how closely the test subject matches the “perfect” score that a classic or prototypical psychopath would rate. Each of the twenty items is given a score of 0, 1, or 2 based on how well it applies to the subject being tested.
A prototypical psychopath would receive a maximum score of 40.
One with absolutely no psychopathic traits would receive a score of zero.
A score of 30 or above qualifies a person for a diagnosis of psychopathy.
People with no criminal backgrounds normally score around 5.
Many non-psychopathic criminal offenders score around 22.
Psychiatry is a medical field devoted to the diagnosis, study, and treatment of mental disorders. The following intro has been excerpted/adapted from Wikipedia:
Psychiatric assessment of a person typically begins with a case history and mental status examination. Physical examinations and psychological tests may be conducted. On occasion, neuroimaging or other neurophysiological techniques are used.
Mental disorders are often diagnosed in accordance with criteria listed in diagnostic manuals such as the widely used Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association (APA), and the International Classification of Diseases (ICD), edited and used by the World Health Organization (WHO).
Psychopharmacology became an integral part of psychiatry starting with Otto Loewi‘s discovery of the neuromodulatory properties of acetylcholine; thus identifying it as the first-known neurotransmitter. Neuroimaging was first utilized as a tool for psychiatry in the 1980s.
The discovery of chlorpromazine‘s effectiveness in treating schizophrenia in 1952 revolutionized treatment of the disorder, as did lithium carbonate‘s ability to stabilize mood highs and lows in bipolar disorder in 1948.
Biopsychiatric research has shown reproducible abnormalities of brain structure and function, and a strong genetic component for a number of psychiatric disorders. It has elucidated some of the mechanisms of action of medications that are effective in treating some of these disorders.
Still, this research has not progressed to the stage that they can identify clear biomarkers of these disorders.
Research has shown that serious neurobiological disorders such as schizophrenia reveal reproducible abnormalities of brain structure (such as ventricular enlargement) and function. Compelling evidence exists that disorders including schizophrenia, bipolar disorder, and autism to name a few have a strong genetic component. Still, brain science has not advanced to the point where scientists or clinicians can point to readily discernible pathologic lesions or genetic abnormalities that in and of themselves serve as reliable or predictive biomarkers of a given mental disorder or mental disorders as a group.
Ultimately, no gross anatomical lesion such as a tumor may ever be found; rather, mental disorders will likely be proven to represent disorders of intercellular communication; or of disrupted neural circuitry. Research already has elucidated some of the mechanisms of action of medications that are effective for depression, schizophrenia, anxiety, attention deficit, and cognitive disorders such as Alzheimer’s disease. These medications clearly exert influence on specific neurotransmitters, naturally occurring brain chemicals that effect, or regulate, communication between neurons in regions of the brain that control mood, complex reasoning, anxiety, and cognition. In 1970, The Nobel Prize was awarded to Julius Axelrod, Ph.D., of the National Institute of Mental Health, for his discovery of how anti-depressant medications regulate the availability of neurotransmitters such as norepinephrine in the synapses, or gaps, between nerve cells.
Lesson excerpted from The Logic of Science blog
“Correlation does not equal causation.” … although useful, the phrase can be misleading because it often leads to the misconception that correlation can never equal causation, when in reality there are situations in which you can use correlation to infer causation.
Why correlation doesn’t always equal causation
When X and Y are correlated, why can’t we automatically assume that the change in X is causing the change in Y?
There are four possible explanations for why X and Y would change together:
- X is causing Y to change
- Y is causing X to change
- A third variable (Z) is causing both of them to change
- The relationship isn’t real and is being caused by chance
[So we] can’t jump to the conclusion that X is causing Y. Further, in most cases, these four possibilities can’t be disentangled. For more details see Why correlation doesn’t have to mean causation
One of my personal favorites is the correlation between ice cream sales and drowning. As ice cream sales increase, so do drowning accidents. Does that mean that eating ice cream is causing people to drown? Of course not. [Clearly] a third variable (time of the year/temperature) is driving both the drowning accidents and the ice cream sales (i.e., people both swim more often and eat more ice cream when it is hot, resulting in a correlation between drowning and eating ice cream that is not at all causal).
Additionally, sometimes two things really do correlate tightly just by chance. The website tylervigen.com has collected a bunch of these, such as the comical correlation between the number of films that Nicholas Cage stars in and the number of drowning accidents in a given year (everything correlates with drowning for some reason)….
Correlation can equal causation
All scientific tests rely on correlation – there is a way to go from correlation to causation: controlled experiments.
If, for example, a scientist does a large, double-blind, randomized controlled trial of a new drug (X) and finds that people who take it have increased levels of Y, we could then say that taking X is correlated with increased levels of Y, but we could also say that taking X causes increased levels of Y.
The key difference is that in this case, we controlled all of the other possibilities such that only X and Y changed. In other words, we eliminated the possibilities other than causation.
[Consider the misleading] correlation between autism rates and organic food sales, but this time let’s say that someone was actually testing the notion that organic food causes autism (obviously it doesn’t, but just go with it for the example).
Therefore, they select a large group of young children of similar age, sex, ethnicity, medication use, etc. They randomly assign half of them to a treatment group that will eat only organic food, and they randomly assign the other half to a control group that will eat only non-organic food.
Further, they blind the study so that none of the doctors, parents, or children know what group they are in. Then, they record whether or not the children develop autism.
Now, for the sake of example, let’s say that at the end, they find that the children who ate only organic food have significantly higher autism rates than those who ate non-organic food. As with the drug example earlier, it would be accurate to say that autism and organic food are correlated, but it would also be fair to say that organic food causes autism (again, it doesn’t, it’s just an example).
So, how is this different than the previous example where we simply showed that, over time, organic food sales and autism rates are correlated? Quite simply, the key difference is that this time, we controlled the confounding factors so that the only differences between the groups were the food (X). Therefore, we have good reason to think that the food (X) was actually causing the autism (Y), because nothing else changed.
Let’s walk through this step by step, starting with the general correlation between organic food sales (X) and autism rates (Y) and looking at each of the four possibilities I talked about earlier.
- Could organic food be causing autism? Yes
- Could autism be causing people to buy more organic food? Yes (perhaps families with an autistic family member become more concerned about health and, therefore, buy organic food [note: organic food isn’t actually healthier])
- Could a third variable be causing both of them? Maybe, though I have difficulty coming up with a plausible mechanism in this particular case.
- Could the relationship be from chance? Absolutely. Indeed, this is the most likely answer.
Now, let’s do the same thing, but with the controlled experiment.
- Could the organic diet be causing autism? Yes
- Could autism be causing the diet? No, because diet was the experimental variable (i.e., the thing we were manipulating), thus changes in it preceded changes in the response variable (autism).
- Could it be caused by a third variable? No, because we randomized and controlled for confounding variables. This is critically important. To assign causation, you must ensure that the X and Y variables are the only things that are changing/differ among your groups.
- Could the relationship be from chance? Technically yes, but statistically unlikely.
Is the difference clear now? In the controlled experiment, we could assign causation because changes in X preceded changes in Y (thus Y couldn’t be causing X) and nothing other than X and Y changed. Therefore, X was most likely causing the changes in Y.
That “most likely” clause is an important one that I want to spend a few moments on. Science does not deal in proof, nor does it provide conclusions that we are 100% certain of. Rather, it tells us what is most likely true given the current evidence… The fact that science does not give us absolute certainty does not mean that it is unreliable. Science clearly works, and the ability to assign probabilities is a vast improvement over the utter guesswork that we have without it.
Assigning specific causation when general causation has already been established
Next, I want to talk about causes where you can use a correlation between X and Y as evidence of causation based on an existing knowledge of causal relationships between X and Y.
In other words, if it is already known that X causes Y, then you can look at specific instances where X and Y are increasing together (if it is a positive relationship) and say, “X is causing at least part of that change in Y” (or, more accurately, “probably causing”).
Let me use an example that I have used before to illustrate this. Look at the data to the right on smoking rates and lung cancer in the US. There is a clear correlation (lung cancer decreases as smoking rates decrease), and I don’t think that anyone would take issue with me saying that the decrease in smoking was probably at least partially the cause for the decrease in lung cancer rates.
Now, why can I make that claim? After all, if we run this through our previous four possibilities, surely we can come up with other explanations.
So, why can I say, with a high degree of confidence, that the smoking rate is probably contributing to the decrease? Quite simply, because a causal relationship between smoking and lung cancer has already been established.
In other words, we already know from previous studies that smoking (X) causes lung cancer (Y). Therefore, we already know that an increase in smoking will cause an increase in lung cancer and a decrease in smoking will cause a decrease in lung cancer.
Therefore, when we look at situations like this, we can conclude that the decrease in smoking is contributing to the decrease in cancer rates because causation has already been established.
To be clear, other factors might be at play as well, and, ideally, we would measure those and determine how much each one is contributing, but even with those other factors, our prior knowledge tells us that smoking should be a causal factor.
This same line of reasoning is what lets us look at things like the correlation between climate change and CO2 and conclude that the CO2 is causing the change. We already know from other studies that CO2 traps heat and drives the earth’s climate. Indeed, we already know that increases in CO2 cause the climate to warm. Therefore, just like in our smoking example, we can conclude that CO2 is a causal factor in the current warming.
Further, in this case, we have also measured all of the other potential contributors and determined that CO2 is the primary one (I explained the evidence in detail with citations to the relevant studies here, here, and here, so please read those before arguing with me in the comments).
The same thing applies to the correlation between vaccines and the decline in childhood diseases. Multiple studies have already established a causal relationship (i.e., vaccines reduce diseases), therefore we know that vaccines were a major contributor to the reduction in childhood diseases (more details and sources here).
Argument from ignorance fallacies
Finally, I want to talk about a common, and invalid, argument that people often use when presenting a correlation as evidence of causation (here I am talking about examples like in the first section where the results aren’t from controlled studies and causation has not previously been established).
I often find that people defend their assertions of causation with arguments like, “well what else could it be?” or “prove that it was something else.” For example, one who is claiming that vaccines cause autism might defend their argument by insisting that unless a skeptic can prove that something else is causing the supposed increase in autism rates, then it is valid to conclude that vaccines are the cause.
There are two closely related logical problems occurring here. The first is known as shifting the burden of proof. The person who is making a claim is always responsible for providing evidence to back up their claim, and shifting the burden happens when, rather than providing evidence in support of their position, the person making the claim simply insists that their opponent has to disprove the claim.
That’s not how logic works. You have to back up your own position, and your opponent is not obligated to refute your position until you have provided actual evidence in support of it.
The second problem is the argument from ignorance fallacy. This happens when you use a gap in our knowledge as evidence of the thing that you are arguing for.
A good example of this would be someone who says, “well you can’t prove that aliens aren’t visiting earth, therefore, they are” or, at the very least, “therefore my belief that they are is justified.”
Do you see how that works? An absence of evidence is just that: a lack of knowledge. You can’t use that lack of knowledge as evidence of something else.
If you can control for all of those other factors and ensure that the changes in X precede the changes in Y and only X and Y are changing, then you can establish causation within the confidence limits of your statistics.