Scientists argue that addiction is not a disease
Addiction is not a disease
A neuroscientist argues that it’s time to change our minds on the roots of substance abuse, 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.)
“The Biology of Desire” is grouped around several case studies, each one illustrating a unique path to dependency. A striving Australian entrepreneur becomes caught up in the “clarity, power and potential” he feels after smoking meth, along with his ability to work long hours while on the drug. A social worker who behaves selflessly in her job and marriage constructs a defiant, selfish, secret life around stealing and swallowing prescription opiates. A shy Irishman who started drinking as a way to relax in social situations slowly comes to see social situations as an occasion to drink and then drinking as a reason to hole up in his apartment for days on end.
Each of these people, Lewis argues, had a particular “emotional wound” the substance helped them handle, but once they started using it, the habit itself eventually became self-perpetuating and in most cases ultimately served to deepen the wound.
Each case study focuses on a different part of the brain involved in addiction and illustrates how the function of each part — desire, emotion, impulse, automatic behavior — becomes shackled to a single goal: consuming the addictive substance. The brain is built to learn and change, Lewis points out, but it’s also built to form pathways for repetitive behavior, everything from brushing your teeth to stomping on the brake pedal, so that you don’t have to think about everything you do consciously. The brain is self-organizing. Those are all good properties, but addiction shanghais them for a bad cause.
As Lewis sees it, addiction really is habit; we just don’t appreciate how deeply habit can be engraved on the brain itself. “Repeated (motivating) experience” — i.e., the sensation of having one’s worries wafted away by the bliss of heroin — “produce brain changes that define future experiences… So getting drunk a lot will sculpt the synapses that determine future drinking patterns.”
More and more experiences and activities get looped into the addiction experience and trigger cravings and expectations like the bells that made Pavlov’s dogs salivate, from the walk home past a favorite bar to the rituals of shooting up. The world becomes a host of signs all pointing you in the same direction and activating powerful unconscious urges to follow them. At a certain point, the addictive behavior becomes compulsive, seemingly as irresistibly automatic as a reflex. You may not even want the drug anymore, but you’ve forgotten how to do anything else besides seek it out and take it.
Yet all of the addicts Lewis interviewed for “The Biology of Desire” are sober now, some through tried-and-true 12-Step programs, others through self-designed regimens, like the heroin addict who taught herself how to meditate in prison. Perhaps it’s no surprise that a psychologist would argue for some form of talk therapy addressing the underlying emotional motivations for turning to drugs. But Lewis is far from the only expert to voice this opinion, or to recommend cognitive behavioral therapy as a way to reshape the brain and redirect its systems into less self-destructive patterns.
Without a doubt, AA and similar programs have helped a lot of people. But they’ve also failed others. One size does not fit all, and there’s a growing body of evidence that empowering addicts, rather than insisting that they embrace their powerlessness and the impossibility of ever fully shedding their addiction, can be a road to health as well.
If addiction is a form of learning gone tragically wrong, it is also possible that it can be unlearned, that the brain’s native changeability can be set back on track. “Addicts aren’t diseased,” Lewis writes, “and they don’t need medical intervention in order to change their lives. What they need is sensitive, intelligent social scaffolding to hold the pieces of their imagined future in place — while they reach toward it.”
Further reading
The Irrationality of Alcoholics Anonymous
Its faith-based 12-step program dominates treatment in the United States. But researchers have debunked central tenets of AA doctrine and found dozens of other treatments more effective. By Gabrielle Glaser, The Atlantic 4/2015 The Irrationality of Alcoholics Anonymous, The Atlantic
The Surprising Failures of 12 Steps
How a pseudoscientific, religious organization birthed the most trusted method of addiction treatment. By Jake Flanagan 3/25/2014
https://www.theatlantic.com/health/archive/2014/03/the-surprising-failures-of-12-steps/284616/
Why the Disease Definition of Addiction Does Far More Harm Than Good.
Among other problems, it has obstructed other channels of investigation, including the social, psychological and societal roots of addiction. By Marc Lewis on February 9, 2018
…Viewing addiction as pathology has other, more direct detriments. If you feel that your addiction results from an underlying pathology, as implied by the brain disease model, and if that pathology is chronic, as highlighted by both NIDA and the 12-step movement, then you are less likely to believe that you will ever be free of it or that recovery can result from your own efforts. This characterization of addiction flies in the face of research indicating that a great majority of those addicted to any substance or behavior do in fact recover, and most of those who recover do so without professional care.
Why the Disease Definition of Addiction Does Far More Harm Than Good. Scientific American.
Addiction and the Brain: Development, Not Disease
By Mark Lewis, Neuroethics, April 2017, Volume 10, Issue 1, pp 7–18
I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement. This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, behavioral addictions, normative compulsive behaviors, and falling in love. I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation.
Addiction and the Brain: Development, Not Disease. Neuroethics (journal)
The chronic disease concept of addiction: Helpful or harmful?
Thomas K. Wiens & Lawrence J. Walker. Addiction Research & Theory, Volume 23, 2015 – Issue 4
This study provides empirical support to the notion that framing addiction within a biological conceptualisation, as opposed to a psychological and social framework, weakens perceptions of agency in relation to drinking. Likewise, no evidence was found to support the common assertion that the disease model reduces feelings of stigma and shame.
The chronic disease concept of addiction: Helpful or harmful?
Probability and predictors of remission from lifetime nicotine, alcohol, cannabis, or cocaine dependence
Results from the National Epidemiologic Survey on Alcohol and Related Conditions
By Catalina Lopez-Quintero, M.D., M.P.H., Deborah S. Hasin, Ph.D., […], and Carlos Blanco, M.D., Ph.D. Addiction. 2011 Mar; 106(3): 657–669.
Most People With Addiction Simply Grow Out of It: Why Is This Widely Denied?
By Maia Szalavitz, Addictionblog.org 6/22/2015
The idea that addiction is typically a chronic, progressive disease that requires treatment is false, the evidence shows. Yet the “aging out” experience of the majority is ignored by treatment providers and journalists.
Most People With Addiction Simply Grow Out of It: Why Is This Widely Denied?
Most of Us Still Don’t Get It: Addiction Is a Learning Disorder
By Maia Szalavitz
Addiction is not about our brains being “hijacked” by drugs or experiences—it’s about learned patterns of behavior. Our inability to understand this leads to no end of absurdities.
Most of Us Still Don’t Get It: Addiction Is a Learning Disorder
5 Addiction Myths. A book review of Unbroken Brain: A Revolutionary New Way of Understanding Addiction. Laurel Sindewald, Handshake Media, 6/20/2016
Learned behavior model also explains wide array human behaviors, including political anger
Author David Brin writes
“For years I’ve followed advances that investigate reinforcement processes in the human brain, especially those involving dopamine and other messenger chemicals that are active in mediating pleasure response. One might call this topic chemically-mediated states of arousal that self-reinforce patterns of behavior.
Of course, what this boils down to — at one level — is addiction. But not only in the sense of illegal drug abuse. In very general terms, “addiction” may include desirable things, like bonding with our children and “getting high on life.” These good patterns share with drug addiction the property of being reinforced by repeated chemical stimulus, inside the brain…
Consider studies of gambling. Researchers led by Dr. Hans Breiter of Massachusetts General Hospital examined with functional magnetic resonance imaging (fMRI) which brain regions activate when volunteers won games of chance — regions that overlapped with those responding to cocaine!…
Moving along the spectrum toward activity that we consider more “normal” — neuroscientists at Harvard have found a striking similarity between the brain-states of people trying to predict financial rewards (e.g., via the stock market) and the brains of cocaine and morphine users.
… researchers at Emory University monitored brain activity while asking staunch party members, from both left and right, to evaluate information that threatened their preferred candidate prior to the 2004 Presidential election. “We did not see any increased activation of the parts of the brain normally engaged during reasoning,” said Drew Westen, Emory’s director of clinical psychology. “Instead, a network of emotion circuits lit up… reaching biased conclusions by ignoring information that could not rationally be discounted. Significantly, activity spiked in circuits involved in reward, similar to what addicts experience when they get a fix,” Westen explained.
Addicted to Self-Righteousness? An Open Letter to Researchers In the Fields of Addiction, Brain Chemistry, and Social Psychology
Indignation, addiction and hope — does it help to be “mad as hell?”: David Brin at TEDxUCSD
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Newfound Wormhole Allows Info to Escape Black Holes
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.

“Figure 13: Sketch of 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.” – Maldacena and Susskind
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?’”
Newfound Wormhole Allows Information to Escape Black Holes 10
Arxiv paper: Cool horizons for entangled black holes Juan Maldacena and Leonard Susskind
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Teaching about evolution
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:
Abiogenesis & spontaneous generation
Abiogenesis – modern discoveries
Charles Darwin’s Voyage of Discovery and Darwin’s notebook
Fossils: Evidence of evolution over time and Dating of fossils
Convergent evolution and Homologous and analogous structures
clades rotate = equivalent phylogenies
Gradualism vs. Punctuated Equilibrium
Examples of evolution
Where did the idea of evolution develop? How has the idea of evolution changed over time?
Advanced topics
Evolution of the first animals
Ontogeny and Phylogeny: Addressing misconceptions
Horizontal Gene Transfer and Kleptoplasty
Teaching about cells
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:
Characteristics of Life
Organelles, an introduction
Organelles: In more depth
What is the role of enzymes in cells?
Then we move on to types of cells
Now the nitty-gritty: Cell reproduction
For those teaching Honors Biology
Active transport across cell membranes
Psychopathy
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.
| Subtype | Features |
|---|---|
| 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.
Conduct disorder
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….
https://www.quora.com/Is-Conduct-disorder-compulsory-in-Psychopathy
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
- impulsivity
- irresponsibility
- 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.
Results
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
Psychiatry is a medical field devoted to the diagnosis, study, and treatment of mental disorders.
The following intro has been 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. Examples include:
Diagnostic and Statistical Manual of Mental Disorders (DSM),
by the American Psychiatric Association (APA),
and the International Classification of Diseases (ICD),
by the World Health Organization (WHO).
Psychopharmacology became important starting with Otto Loewi‘s discovery of the neuromodulatory properties of acetylcholine. This is 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.
Another major discovery (1948) was the chemical lithium carbonate. This molecule can stabilize mood highs and lows in bipolar disorder.
Biopsychiatric research – This has shown us how biology is related to psychiatry.
We have discovered that there are relationships between certain mental illnesses, and certain abnormalities of brain structure. This includes schizophrenia.
We have also discovered that some genetic mutations are related to psychiatric disorders. This includes schizophrenia, bipolar disorder, and autism.
In general, though, science has not progressed to the stage that we can identify clear biomarkers of these disorders.
In other words, we don’t have specific biochemical tests for mental disorders.
Mental disorders don’t exist on their own
From The hidden links between mental disorders
Psychiatrists have a dizzying array of diagnoses and not enough treatments.
Hunting for the hidden biology underlying mental disorders could help.
Michael Marshall, Nature 581, 19-21 (2020). doi: 10.1038/d41586-020-00922-8
In 2018, psychiatrist Oleguer Plana-Ripoll was wrestling with a puzzling fact about mental disorders. He knew that many individuals have multiple conditions — anxiety and depression, say, or schizophrenia and bipolar disorder. He wanted to know how common it was to have more than one diagnosis, so he got his hands on a database containing the medical details of around 5.9 million Danish citizens.
He was taken aback by what he found. Every single mental disorder predisposed the patient to every other mental disorder — no matter how distinct the symptoms. “We knew that comorbidity was important, but we didn’t expect to find associations for all pairs,” says Plana-Ripoll, who is based at Aarhus University in Denmark.
The study tackles a fundamental question that has bothered researchers for more than a century. What are the roots of mental illness? In the hope of finding an answer, scientists have piled up an enormous amount of data over the past decade, through studies of genes, brain activity and neuroanatomy. They have found evidence that many of the same genes underlie seemingly distinct disorders, such as schizophrenia and autism, and that changes in the brain’s decision-making systems could be involved in many conditions.
They have a few theories. Perhaps there are several dimensions of mental illness — so, depending on how a person scores on each dimension, they might be more prone to some disorders than to others. An alternative, more radical idea is that there is a single factor that makes people prone to mental illness in general: which disorder they develop is then determined by other factors. Both ideas are being taken seriously, although the concept of multiple dimensions is more widely accepted by researchers.
The details are still fuzzy, but most psychiatrists agree that one thing is clear: the old system of categorizing mental disorders into neat boxes does not work. They are also hopeful that, in the long run, replacing this framework with one that is grounded in biology will lead to new drugs and treatments. Researchers aim to reveal, for instance, the key genes, brain regions and neurological processes involved in psychopathology, and target them with therapies. Although it might take a while to get there, says Steven Hyman of the Broad Institute of MIT and Harvard in Cambridge, Massachusetts, “I am long-term optimistic if the field really does its work.”
Related articles
Neuroscientist argues that addiction is not a disease
Is a ‘Spectrum’ the Best Way to Talk About Autism?
Learning styles and multiple intelligences
Psychopathy
Psychopaths Don’t Care If They Hurt You. This Is Why. New research shows why the psychopathic are so likely to harm others.
Detecting genetic disorders with 3d face scans
Link between marijuana and pyschosis, and depression, hyperactivity, and inattention in children.
Mysterious link between immune system and mental illness – He Got Schizophrenia. He Got Cancer. And Then He Got Cured.
Article on mental health disorders
NIMH Disruptive Mood Dysregulation Disorder
Learning Standards
Massachusetts Comprehensive Health Curriculum Framework
PreK–12 STANDARD 5: Mental Health. Students will acquire knowledge about emotions and physical health, the management of emotions, personality and character development, and social awareness; and will learn skills to promote self-acceptance, make decisions, and cope with stress, including suicide prevention.
Benchmarks: American Association for the Advancement of Science
Stresses are especially difficult for children to deal with and may have long-lasting effects. 6F/H1
Biological abnormalities, such as brain injuries or chemical imbalances, can cause or increase susceptability to psychological disturbances. 6F/H2
Reactions of other people to an individual’s emotional disturbance may increase its effects. 6F/H3
Human beings differ greatly in how they cope with emotions and may therefore puzzle one another. 6F/H4
Ideas about what constitutes good mental health and proper treatment for abnormal mental states vary from one culture to another and from one time period to another. 6F/H5
Psychological distress may also affect an individual’s vulnerability to biological disease. 6F/H6** (SFAA)
According to some theories of mental disturbance, anger, fear, or depression may result from exceptionally upsetting thoughts or memories that are blocked from becoming conscious. 6F/H7** (SFAA)
When can correlation equal causation?
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.
Causality is the actual relationship between causes and effects.
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”).

- Smoking and lung/bronchial cancer rates (data via the CDC). P < 0.0001
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.
Conclusion
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.
Organelles in depth
Cell membrane
Made of 2 layers of lipids (fats); aka lipid bilayer.
We sometimes see simplified 2D drawings of this.
This drawing shows a small section of the lipid bilayer: 2 layers of lipids and some proteins floating in these lipids.

Cell membrane lipid bilayer Regents diagram http://www.hobart.k12.in.us/jkousen/Biology/cell.htm#plcell_dia_ans
A more accurate visualization would be to show this in three dimensions:

We sometimes see simplified 2D drawings of this. This drawing shows a small section of the lipid bilayer: 2 layers of lipids and some proteins floating in these lipids.

Cell membrane lipid bilayer Regents diagram http://www.hobart.k12.in.us/jkousen/Biology/cell.htm#plcell_dia_ans
Cytoplasm
A thick viscous liquid filling the cell.
All the organelles float in it.
Filled with millions of enzymes, dissolved salt ions, and other chemicals.

Here is a (false color) visualization of proteins floating in a cell’s cytoplasm. Densely packed!

Nucleus
The command-and-control center of the cell.
Chromosomes (made of DNA) are stored in here. In this animation we see DNA in the nucleus, and a copy of it (RNA) leaving the nucleus and going out into the rest of the cell.

Here we see a more realistic image of the nucleus (lower left); we see mRNA copies of DNA coming out of the nucleus through nuclear pores.

Nucleus to ribosomes to ER GIF from NPR: Protein synthesis
Chromosomes
If we magnify a cell we see chunks floating in the nucleus called chromosomes. They are made of a chemical called DNA.

Here we see a cell nucleus being lysed (broken open) and all the chromosomes are spilling out on the right.
The color was added by hand to make it easier to tell them apart. We cut-and-paste each of the chromosomes, number them, and line them up (lower left.)
In humans we find 23 pairs of chromosomes in every cell.
These X shaped chromosomes are not solid; they are like objects made of wound-up yarn.
A chromosome could be unwound into a long, thing string.
This string is made of DNA molecules.

Each section of the chromosome has difference sequences of DNA.
A complete sequence of DNA is called a gene; it is an instruction on how to build a protein.
Mitochondrion
Plural is mitochondria.
Converts energy from food molecules into a form usable by the cell.

Jay Swan http://www.slideshare.net/jayswan http://www.slideshare.net/jayswan/honors-biology-cellular-respiration
and

Jay Swan http://www.slideshare.net/jayswan http://www.slideshare.net/jayswan/honors-biology-cellular-respiration
Ribosomes
Little organic machines that take in amino acids (from our food) and turn them into proteins.
They are very tiny compared to the size of a cell – often seen as mere dots.

Here we see the ribosomes picking up RNA, and using that instruction to build a protein.

Nucleus to ribosomes to ER GIF from NPR: Protein synthesis
Ribosomes struck on an organelle
On the right we can just barely see the ribosomes as small dots stuck to the ER (endoplasmic reticulum.)
On the left we see the ER magnified.
The ribosomes are a bit clearer here (although we still don’t see their details.)
When the ER is covered with ribosomes we call it the “rough ER.”

Darryl Leja, NHGRI Rough endoplasmic reticulum and ribosomes
Other ribosomes float freely in the cytoplasm.
Here we see mRNA copies of DNA coming out of a cell nucleus, and moving to a ribosome floating nearby.
Here’s how we remember this:
ER (endoplasmic reticulum)
This manufactures lipids and proteins.
Like an assembly line which makes our products.

Next, molecules from the ER are packaged into vesicles, and transported to the Golgi apparatus.

Golgi body
This organelle packages proteins into vesicles, tags them with an “address” and send them to their destination.

another image will be here:
Details of Golgi bodies function and organization

From The Cell: A Molecular Approach, 5th ed. Cooper & Hausman. 2009
The Endomembrane system
Here we see the while system, from products leaving the nucleus, going to the ER, then to the Golgi, and then secreted as a vesicle.
In this case the products are going out to the cell membrane (“plasma membrane.)

From Biotech Review YouTube channel.
More details: The endomembrane system is composed of the different membranes that are suspended in the cytoplasm within a eukaryotic cell.

Endomembrane system by Mariana Ruiz Villarreal, LadyofHats
Cytoskeleton
These thin protein tubes give the cell its shape and mechanical resistance to deformation.
With the right stains, one can take a beautiful photo of the cytoskeleton.
Lysosome
Contain enzymes that can break down virtually all kinds of biomolecules. Garbage disposal.

Vacuoles
A lipid bag that can store organic molecules.

Chloroplasts
In this movie of plant cells, we some small, green discs moving around: these are chloroplasts.

They contain a light-absorbing pigment (colored molecule), chlorophyll.
This molecules captures the energy from some wavelengths of light.
The plant cell stores this energy in chemical bonds. The plant builds ATP and sugar molecules which store this energy.
In this image we see some chloroplasts floating within a plant cell.
Here we see a single chloroplast, vastly magnified with a TEM (transmission electron microscope.)
We see that there is quite a bit of detail within them.

Cell wall
Note that animal cells don’t have this organelle. Only plants and bacteria have it.
Made of cellulose – a special sugar used to provide structure, and not used for energy.
If the cell membrane is like a balloon, then the cell wall is like a cardboard box around the balloon, protecting it.
Gives strength and support. Allows plants like bamboo and trees to grow tall.

Here we see a typical boxy shaped plant cell, clearly showing the cell wall (green) and the lipid bilayer (yellow, aka plasma membrane.)

Plant cell has a wall adapaproject
Large central vacuole
A membrane that stores watery bags of food or waste molecules.
How do we know what these organelles really look like?
Visualizing cells and organelles in 3D
Sample questions
Feb 2016 MCAS: Which of the following types of organisms have cell walls composed of cellulose?
A. amoebas B. birds C. grasses D. worms
==========
Feb 2016 MCAS. Antibiotics are medicines used to treat bacterial infections in humans. Some antibiotics work by interfering with the bacteria’s ribosomes. Other antibiotics work by interfering with the bacteria’s plasma membrane.
a. Describe the function of the ribosomes and explain why interfering with the ribosomes would kill the bacteria.
b. Describe the function of the plasma membrane and explain why interfering with the plasma membrane [lipid bilayer] would kill the bacteria.
Medicines called antifungals are used to treat infections caused by fungi. One way antifungals work is by targeting cell parts that are present in fungal cells but not in human cells.
c. Identify one cell part other than a ribosome or a plasma membrane that human cells and fungal cells have in common.
d. Describe what would happen to a human cell if the cell part you identified in part (c) were affected by an antifungal. Explain your answer based on the function of the cell part.
==========
External resources
Biology MCAS exams
Previous MCAS exams from the Massachusetts Department of Elementary and Secondary Education
Below you will find each released short-response question, open-response question, and writing prompt that was included on High School Biology MCAS tests; the scoring guide for each question; and a sample of student work at each score point for that question. Taken together, these provide a picture of the expectations for student performance on the MCAS tests.
Special Education accommodations
February 2018 MCAS Biology Test Administration Resources
MCAS Accessibility and Accommodations
SAMPLE MCAS High School Biology Reference Sheet For Students with Accommodation 20
]MCAS Access & Accommodations Manual Spring 2018
MCAS TEST ACCOMMODATIONS FOR STUDENTS WITH DISABILITIES (PDF document)
MCAS Standard Accommodations
Frequent Breaks: The test is administered in short periods with frequent breaks
Time of Day: The test is administered at a time of day that takes into account the student’s medical or learning needs (IEP or 504 plan must specify time of day)
Small Group: The test is administered in a small group setting (no more than 10 students)
Separate Setting: The test is administered in a room other than the one used by the rest of the class
Individual: The test is administered to the student individually
Specified Area: The test is administered with the student seated at the front or other specified area of the room, in a study carrel, or in another enclosed area (IEP or 504 plan must specify where)
Familiar Test Administrator: The test is administered by a test administrator familiar to the student
Noise Buffers: The student wears noise buffers, after test administration instructions have been read (headphones with music playing are not allowed)
Magnification or Overlays: The student uses magnifying equipment, enlargement devices, colored visual overlays, or specially tinted lenses (IEP or 504 plan must specify which)
Test Directions: The test administrator clarifies general administration instructions No portion of the test items themselves (eg, the introduction to a reading selection) may be read or signed
Large-Print: The student uses a large-print version of the test
Braille: The student uses a Braille version of the test
Place Marker: The student uses a place marker
Track Test Items: The test administrator assists the student in tracking test items (eg, moving from one test question to the next) or by redirecting the student’s attention to the test
Amplification: The student uses sound amplification equipment
Test Administrator Reads Test Aloud (except ELA Reading Comprehension test): Test Administrator reads entire test session word-for-word exactly as written
Test Administrator Reads Test Aloud (except ELA Reading Comprehension test): Test administrator reads selected words, phrases, and/or sentences as directed by the student. The student points to the word, phrase, or sentence that he or she needs read aloud.
Test Administrator Signs Test (except ELA Reading Comprehension test): The test administrator signs the ELA Composition writing prompt or the Mathematics, Science and Technology/Engineering, and/or History and Social Science passages and test items to a student who is deaf or hard of hearing
Electronic Text Reader (except ELA Reading Comprehension test): The student uses an electronic text reader for the ELA Composition writing prompt or the Mathematics and Science and Technology/Engineering tests
Scribe Test (except ELA Composition): For open-response test items (and multiple-choice items if needed), the student dictates responses to a scribe or uses a speech-to-text conversion device to record responses
Organizer, Checklist, Reference Sheet, or Abacus: The student uses a graphic organizer, checklist, individualized mathematics reference sheet, or abacus
Student Signs or Reads Test Aloud: The student reads the test aloud to himself or herself, or student reads the test and records answers on audiotape, then writes responses to test items while playing back the tape; a student who is deaf or hard of hearing signs test items/responses onto video, then writes answers while playing back the tape
Monitor Placement of Responses: The test administrator monitors placement of student responses in the student’s answer booklet
Word Processor: The student uses a word processor, Alpha-Smart, or similar electronic keyboard to type the ELA Composition and/or answers to open-response questions
Answers Recorded in Test Booklet: The student records answers directly in the test booklet
Other Standard Accommodation: Other standard accommodation that is identified by the IEP Team or team, documented in the student’s IEP, and not on this list
Alternate Assessment (Portfolio)
MCAS Nonstandard
Test Administrator Reads Aloud ELA Reading Comprehension Test: The test administrator reads the ELA Reading Comprehension test to a student
Test Administrator Signs ELA Reading Comprehension Test for a Student Who Is Deaf or Hard of Hearing
Electronic Text Reader for the ELA Reading Comprehension Test: The student uses an electronic text reader for the ELA Reading Comprehension test
Scribe ELA Composition: The student dictates the ELA Composition to a scribe or uses a speech-to-text conversion device to record the ELA Composition
Calculation Devices: The student uses a calculator, arithmetic table (including multiplication and division charts), or manipulatives on all sections of the Mathematics or Science and Technology/Engineering test
Spell- or Grammar-Checking Function on Word Processor, Spell-Checking Device, or Word Prediction Software for the ELA Composition: The student uses a spell- or grammar-checking function, spelling device (including hand-held electronic spellers), or word prediction software (IEP must specify which device) for the ELA Composition
Other Nonstandard Accommodation: Other nonstandard accommodation that is identified by the IEP Team or team, documented on the student’s IEP, and not on this list
.
How do point particles create atoms with size?
This article is archived for use with my students from Ask Ethan: If Matter Is Made Of Point Particles, Why Does Everything Have A Size?
Forbes, Stars With a Bang, by Ethan Siegel 9/16/17

Proton Structure Brookhaven National Laboratory
The big idea of atomic theory is that, at some smallest, fundamental level, the matter that makes up everything can be divided no further. Those ultimate building blocks would be literally ἄ-τομος, or un-cuttable.
As we’ve gone down to progressively smaller scales, we’ve found that molecules are made of atoms, which are made of protons, neutrons, and electrons, and that protons and neutrons can be further split into quark and gluons. Yet even though quarks, gluons, electrons, and more appear to be truly point-like, all the matter made out of them has a real, finite size. Why is that? That’s what Brian Cobb wants to know:
Many sources state that quarks are point particles… so one would think that objects composed of them — in this instance, neutrons — would also be points. Is my logic flawed? Or would they be bound to each other in such a way that they would cause the resulting neutron to have angular size?
Let’s take a journey down to the smallest scales, and find out what’s truly going on.

Magdalena Kowalska / CERN / ISOLDE team
If we take a look at matter, things behave similar to how we expect they should, in the macroscopic world, down to about the size of molecules: nanometer (10-9meter) scales. On smaller scales than that, the quantum rules that govern individual particles start to become important.
Single atoms, with electrons orbiting a nucleus, come in at about the size of an Angstrom: 10-10 meters. The atomic nucleus itself, made up of protons and neutrons, is 100,000 times smaller than the atoms in which they are found: a scale of 10-15 meters. Within each individual proton or neutron, quarks and gluons reside.
While molecules, atoms, and nuclei all have sizes associated with them, the fundamental particles they’re made out of — quarks, gluons, and electrons — are truly point-like.

E. Siegel / Beyond The Galaxy
The way we determine whether something is point-like or not is simply to collide whatever we can with it at the highest possible energies, and to look for evidence that there’s a composite structure inside.
In the quantum world, particles don’t just have a physical size, they also have a wavelength associated with them, determined by their energy. Higher energy means smaller wavelength, which means we can probe smaller and more intricate structures. X-rays are high-enough in energy to probe the structure of atoms, with images from X-ray diffraction and crystallography shedding light on what molecules look like and how individual bonds look.

Imperial College London
At even higher energies, we can get even better resolution. Particle accelerators could not only blast atomic nuclei apart, but deep inelastic scattering revealed the internal structure of the proton and neutron: the quarks and gluons lying within.
It’s possible that, at some point down the road, we’ll find that some of the particles we presently think are fundamental are actually made of smaller entities themselves. At the present point, however, thanks to the energies reached by the LHC, we know that if quarks, gluons, or electrons aren’t fundamental, their structures must be smaller than 10-18 to 10-19 meters. To the best of our knowledge, they’re truly points.

Brookhaven National Laboratory
So how, then, are the things made out of them larger than points? It’s the interplay of (up to) three things: Forces, Particle properties, and Energy.
The quarks that we know don’t just have an electric charge, but also (like the gluons) have a color charge. While the electric charge can be positive or negative, and while like charges repel while opposites attract, the force arising from the color charges — the strong nuclear force — is always attractive. And it works, believe it or not, much like a spring does.
Warning: Analogy ahead!

Here we go:

How did the Proton Get Its Spin? Brookhaven National Laboratory
Above: The internal structure of a proton, with quarks, gluons, and quark spin shown. The nuclear force acts like a spring, with negligible force when unstretched but large, attractive forces when stretched to large distances
When two color-charged objects are close together, the force between them drops away to zero, like a coiled spring that isn’t stretched at all.
When quarks are close together, the electrical force takes over, which often leads to a mutual repulsion.
But when the color-charged objects are far apart, the strong force gets stronger. Like a stretched spring, it works to pull the quarks back together.
Based on the magnitude of the color charges and the strength of the strong force, along with the electric charges of each of the quarks, that’s how we arrive at the size of the proton and the neutron: where the strong and electromagnetic forces roughly balance.

APS/Alan Stonebraker
The three valence quarks of a proton contribute to its spin, but so do the gluons, sea quarks and antiquarks, and orbital angular momentum as well. The electrostatic repulsion and the attractive strong nuclear force, in tandem, are what give the proton its size.
On slightly larger scales, the strong force holds protons and neutrons together in an atomic nucleus, overcoming the electrostatic repulsion between the individual protons. This nuclear force is a residual effect of the strong nuclear force, which only works over very short distances.
Because individual protons and neutrons themselves are color-neutral, the exchange is mediated by virtual, unstable particles known as pions, which explains why nuclei beyond a certain size become unstable; it’s too difficult for pions to be exchanged across larger distances. Only in the case of neutron stars does the addition of gravitational binding energy suppress the nucleus’ tendency to rearrange itself into a more stable configuration.

Wikimedia Commons user Manishearth
And on the scale of the atom itself, the key is that the lowest-energy configuration of any electron bound to a nucleus isn’t a zero-energy state, but is actually a relatively high-energy one compared to the electron’s rest mass.
This quantum configuration means that the electron itself needs to zip around at very high speeds inside the atom; even though the nucleus and the electron are oppositely charged, the electron won’t simply hit the nucleus and remain at the center.
Instead, the electron exists in a cloud-like configuration, zipping and swirling around the nucleus (and passing through it) at a distance that’s almost a million times as great as the size of the nucleus itself.

The energy levels and electron wavefunctions that correspond to different states within a hydrogen atom, although the configurations are extremely similar for all atoms. The energy levels are quantized in multiples of Planck’s constant, but the sizes of the orbitals and atoms are determined by the ground-state energy and the electron’s mass.
There are some fun caveats that allow us to explore how these sizes change in extreme conditions. In extremely massive planets, the atoms themselves begin to get compressed due to large gravitational forces, meaning you can pack more of them into a small space.
Jupiter, for example, has three times the mass of Saturn, but is only about 20% larger in size. If you replace an electron in a hydrogen atom with a muon, an unstable electron-like particle that has the same charge but 206 times the mass, the muonic hydrogen atom will be only 1/206th the size of normal hydrogen.
And a Uranium atom is actually larger in size than the individual protons-and-neutrons would be if you packed them together, due to the long-range nature of the electrostatic repulsion of the protons, compared to the short-range nature of the strong force.

Image credit: Calvin Hamilton.
The planets of the Solar System, shown to the scale of their physical sizes, show a Saturn that’s almost as large as Jupiter. However, Jupiter is 3 times as massive, indicating that its atoms are substantially compressed due to gravitational pressure.
By having different forces at play of different strengths, you can build a proton, neutron, or other hadron of finite size out of point-like quarks. By combining protons and neutrons, you can build nuclei of larger sizes than their individual components, bound together, would give you. And by binding electrons to the nucleus, you can build a much larger structure, all owing to the fact that the zero-point energy of an electron bound to an atom is much greater than zero.
In order to get a Universe filled with structures that take up a finite amount of space and have a non-zero size, you don’t need anything more than zero-dimensional, point-like building blocks. Forces, energy, and the quantum properties inherent to particles themselves are more than enough to do the job.
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Ethan Siegel is the founder and primary writer of Starts With A Bang!
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