Friday Links: eat your egg yolks, avoid antimicrobial soap

Most of this post will be about egg yolks, but I'll start with the following PSA: if a soap is labeled "antimicrobial," don't use it. Just don't use it.

http://cebulka26.wordpress.com/2012/08/16/triclosan-its-in-everything-but-is-it-warranted/

If I see antimicrobial soap at a restaurant, I don't use it. I just wash with hot water. This concise and informative blog post from Ania (fellow MD/PhD) reminded me of why I do this. The active ingredient is triclosan, but I doubt it's very active anymore because it's in a bazillion products. Many of the microbes that we would theoretically want to kill are probably already immune to it. Continued use will just give microbes more and more chances to evolve resistance to not just it but also all related antibiotics, resulting in antibiotic-resistant bacteria that could kill a lot of people. The Black Death wasn't much fun, so I hear.

The fact is, there's currently zero evidence that antimicrobial soap helps prevent infection compared to regular soap. And given the potential health risks that Ania outlines (triclosan could affect your hormones, muscles, cancer…), why the hell would you use it? You're better off not using soap at all.

Egg yolks OMG!!

http://www.dailymail.co.uk/health/article-2188265/Eating-egg-yolks-bad-smoking-speeding-coronary-artery-disease.html?ito=feeds-newsxml

For some reason, the least-significant studies seem to get the most publicity, and the media likes to create outrageous headlines like "eating eggs yolks as bad as smoking." Incredibly misleading and not at all implied by the paper- especially when you consider that the audience is the public-at-large. For some people cutting back on egg yolks is prudent (but not at all proven to be beneficial), but should average 25 year olds avoid egg yolks as they should avoid smoking? Absolutely not, and the lack of context in this article is irresponsible.

First, some conceptual background: when you drink a lot of water, do you get water intoxication? No, you pee it out. Guess what? You excrete cholesterol through your liver into your digestive tract, and you can simply make less cholesterol. Your body reacts to greater cholesterol intake by decreasing cholesterol synthesis, and you end up with the same amount in your blood. The cholesterol that your body makes on a daily basis is significantly greater (about 3-5 fold) than what is recommended in your diet. Thus, your body can easily handle twice as much cholesterol consumption as normal, and eating more cholesterol per se does not increase your blood cholesterol. Your body needs cholesterol, and it will handle it as needed.

If you don't eat this, your body will probably make it instead and you'll end up with the same blood cholesterol either way. OK, maybe not for this many egg yolks, but you get the idea.

Of course, if you drink TONS of water (>12L), you can get water intoxication (this happens to ill-informed marathon runners). So there's a point at which cholesterol intake will start adversely affecting your blood cholesterol, and yes high blood cholesterol is a huge risk factor for heart disease. Furthermore, individuals with kidney disease will not be able to deal with water overload. Similarly, if you already have cholesterol imbalances (due to genetics, age, obesity, microbiome perturbation, whatever) then you should start watching your cholesterol intake, because the mechanisms to keep your blood cholesterol in check have already been overwhelmed.

Getting to the study, I have many objections:

1. Glaring source of recall bias. Egg yolk intake is self-reported in a questionnaire. But how many people actually keep track of their egg yolks? I'm guessing extremely few- and any variable that people do not consciously track is subject to huge memory bias. Furthermore, egg yolk intake is really hard to estimate, because eggs are used in all sorts of foods (bakery items, etc). I certainly would not trust my own estimation. And there is a huge source of memory bias in this study: people with the worst heart disease (regardless of the cause) are far more likely to "remember" that they ate a lot of egg yolks. We know that people's memories are heavily biased by their situation, and there is a pre-conceived notion out there that egg yolks are "supposed" to clog your arteries. People naturally look for an explanation for their disease, and if they find an easy explanation (eg egg yolks), then they will sub-consciously alter their memories to believe that they ate more egg-yolks. The memory effect should get stronger with greater severity of disease, and so all of the results of this paper could be explained by recall bias. Furthermore, the study itself can influence people's memories. You're going around a clinic full of worried people asking them how many eggs they eat. At least subconsciously, people are going to start blaming eggs for their health, even if they ate the same # of eggs as the next person.
2. The study population is heavily biased. The patients are already attending a vascular clinic! As I mentioned, there are likely sub-populations for whom cholesterol intake will increase their blood cholesterol (morbidly obese individuals, patients with familial hypercholesterolemia who are genetically unable to regulate their own cholesterol, etc). Those are the sub-populations whose cholesterol homeostasis mechanisms are already out of whack, and they are the ones most likely to be attending the clinic.
3. The data is nothing but correlative. Eating egg yolks (self-reported, again) is shown to be correlated with artery blockage. Sure, they use some statistical analysis to show that the effect is still present after you adjust for "coronary risk factors" but many risk factors are still unknown (yay science!), so you can't adjust for everything. The problem is that there are thousands of variables out there, and they are all correlated with each other to different degrees. People who live in a certain part of the country might eat foods rich in cholesterol, but guess what- that might also be the most polluted part of the country. Or there is a virus circulating in warm climates that increases your risk. Or people in that part of the country might be older, etc. If you look at 1000 variables, eventually you'll find one that fits simply by chance.
4. Simplistic clinical endpoint. Small point, but they just looked at neck artery blockage. Artery blockage, even if systemic, does not translate to disease. It's a risk factor like any other, and like all risk factors it doesn't affect all individuals in the same way.

Plant Zen

http://www.disneyresearch.com/research/projects/hci_botanicus_drp.htm

http://www.benchfly.com/blog/forget-wireless-keyboards-and-touch-your-plant-instead/

Finally, I have no idea what to make of this. You can hook up a plant (any plant, like a potted plant) to your computer, and somehow an electrode in the soil can tell what part of the plant you're holding. So you can control your computer by touching a plant. Is this a hoax?

I predict that eventually we'll be able to hook up anything to computers. But I think it will take a little more than just sticking an electrode into the soil.

wtf?

Alzheimer's: commentary on treatment strategies

My goal is that any reader can take something away from this Alzheimer's post, regardless of their experience in medicine or science. It's Friday Links-driven, but with far more of my own commentary/explanation than normal.

First up: an article about a clinical trial for Alzheimer's treatment that appears to have failed. While I don't research Alzheimer's, I'm going to argue in this blog post that 1) single "magic bullet" treatments are unlikely to ever work for a chronic complex disease that develops over many decades like Alzheimer's (once the disease has actually manifested symptomatically), but 2) single "magic bullet" prevention methods might work for specific patient sub-populations. In this case, different prevention methods would work for different sub-populations. Meanwhile 3) Broad, non-specific treatments that target multiple biological processes are better for stabilizing Alzheimer's after it's been diagnosed (discussed in the second link). Note that this is NOT the same as combination therapy.

http://www.technologyreview.com/view/428592/pfizer-disappointed-with-first-results-for/?ref=rss

Bapineuzamab is an antibody that recognizes and binds to beta-amyloid, one of the molecules involved in the pathogenesis of Alzheimer's (note that I don't say it's the cause or even a significant cause). For my non-biomedical readers, this is a common treatment strategy nowadays. Say protein X causing disease Y is floating around in the space between cells in your body. Specific antibodies can be made to bind specifically to protein X which physically blocks protein X from damaging other things ("neutralization"). Furthermore immune cells are then able to recognize the antibody bound to protein X, and clear protein X from the body. This strategy is used in treatment of diseases like rheumatoid arthritis and lymphoma, and it works wonders.

But Bapineuzamab failed to have any effect on Alzheimer's progression in this Pfizer trial. Why? I'm going to use my extraordinary powers of hindsight (dig deep- you probably have this ability too!) and say that it probably has far more to do with the fact that beta-amyloid is just a tiny piece of the puzzle for Alzheimer's than any problem with the drug. Bapineuzamab probably recognizes beta-amyloid just fine, and it might even clear beta-amyloid from the body. But I doubt that clearance of beta-amyloid would have any effect on Alzheimer's. Why? Because it's too late.

The trial looked at treatment of early-to-moderate Alzheimer's, but Alzheimer's develops over decades. For a while, it's just Mild Cognitive Impairment (MCI), but lots of people get MCI and never progress to Alzheimer's. So figuring out a way to predict Alzheimer's progression through things like blood tests and brain imaging is all the rage now (see third link). And that's why the trial focused on Alzheimer's rather than pre-Alzheimer's. But in the patients that do progress, what's going on?

The length of time that it takes for Alzheimer's to develop means that, even if beta-amyloid were to be the ultimate cause, then beta-amyloid can trigger numerous other biological processes that are themselves damaging to the brain. By the time someone has Alzheimer's symptoms, these "secondary processes" are already robust so more damage is occurring independent of beta-amyloid, and a lot of neurons are already malfunctioning or dead. This fundamentally alters the biology of the brain so that treatments are unlikely to reverse anything, and multiple causes of degeneration make it unlikely that single treatment would slow the progression of the disease. I won't review the ginormous body of literature implicating all sorts of things in Alzheimer's pathogenesis, but I'll take a couple as an example.

One way to abstract Alzheimer's (see picture below) is that everything causes everything else. It's a complicated feedback loop (or feedback web) where a bunch of biological processes all cause and worsen each other over a period of many years. For example (highlighting a tiny portion of the feedback web), extracellular amyloid or intracellular tau (hallmarks of protein misfolding) acting on one subset of neurons might interfere with normal breakdown of neurotransmitters, as well as directly causing neurons to fire inappropriately. Too much excitation of nearby neurons results in excitotoxicity (killing those cells) or in inappropriate activation. The brain might remodel in reaction, forming new synapses that result in electrical feedback loops that reinforce each other. The resultant clinical and subclinical seizures might interfere with brain function long after the damage is done. As neurotransmitters start to diffuse inappropriately due to synaptic dysfunction, they start affecting other cells indiscriminately, and damage may occur to brain's extensive blood system. This allows in immune cells that further alter the blood vessels to essentially break down the blood-brain barrier.  This lets in various molecules that again might cause excitotoxicity or protein misfolding, and maybe it even lets in bacteria. So damage leads to biological response that causes more damage, leading to further responses etc.

All of these processes cause each other, and all of them cause disease. Targeting a single initiating factor (which varies from patient to patient) might work for prevention, but not for treatment.

Importantly, many of the damaging processes are variations of normal brain biology. For example, microglia (kind of like the brain's immune system) see damaged neurons and eat them up. If you remove the source of damage, it is perfectly possible they continue eating up neurons instead of letting the neurons recover after the damage. There are medical examples where a disease has manifested for so long that cells that normally act to ameliorate a disease are "locked in" to their action even when it's no longer necessary, and they end up causing damage themselves (for example tertiary hyperparathyroidism). I think of this as part of the more general inflammatory response that occurs whenever there is damage- all sorts of immune cells react to initial damage and can end up causing more damage than the original insult (if you think that makes no evolutionary sense, it actually does. I might expand on that in a future post).

What about prevention? Note that things like excitotoxicity, brain remodeling, and breakdown of the blood-brain barrier can in turn cause beta-amyloid buildup. So there's no reason why beta-amyloid had to be the initial insult- in many (most?) patients beta-amyloid is probably secondary to another biological process. In these cases, drugs targeting beta-amyloid production and degradation probably would not have any preventative effect, because beta-amyloid was not the initial cause. However, there are subsets of patients where beta-amyloid is implicated as a major genetic cause (mutations that affect beta-amyloid production like in Down's syndrome, ApoE4, and presenilin). Prevention using Bapineuzamab is conceivable in those patients, as it would stop the secondary processes from occurring in the first place. However, if we found in another sub-population that inappropriate inflammation due to immune system malfunction (kind of like an autoimmune disease), then prevention would involve anti-inflammatory drugs (Aspirin? IVIg? Prednisone?). Thus, preventative measures for Alzheimer's would be specific to the patient's initial cause(s) of degeneration, which can vary widely depending on the patient.

http://www.technologyreview.com/news/428546/study-suggests-alzheimers-disease-can-be/?ref=rss

On the bright side, a very small trial showed stabilization of Alzheimer's with treatment with IVIg (intravenous immunoglobulin). IVIg is simply the mix of the collection of antibodies isolated from multiple human volunteers. There are antibodies against everything- bacteria, toxins, some human proteins, etc. The authors here speculate that there is an antibody targeting amyloid-beta, tau, or some other molecule. While this might be part of the picture, I worry that researchers might go after specific antibodies (which is just like the above Bapineuzamab trial). I challenge the notion that IVIg's broad and non-specific effects are a disadvantage. While one might think it's not 'optimized' for Alzheimer's treatment, the very fact that Alzheimer's involve a complicated web of numerous biological processes means that we need to target them all at the same time. Thus, a non-specific treatment with numerous antibodies doing many different things might in fact be the key to IVIg's efficacy.

For example, IVIg is used in the treatment of autoimmune disease, dampening down immune responses. How it accomplishes that is unclear (and is a bit counter-intuitivee since antibodies MEDIATE the immune response), but it is believed that it both interferes with the specific endogenous antibody that causes disease, as well as flooding the system with so many antibodies that it diverts the immune system from inflammation. Perhaps IVIg is dealing with the inflammatory component of Alzheimer's? Perhaps it interferes with the endogenous cells/antibodies that are damaging the brain? Thus, trying to narrow down the treatment to a single antibody or a few antibodies would eliminate some of the broad effects of IVIg that would be critical for influencing the numerous biological processes. This is different from combination therapy because we're looking for one or two treatments to influence many things (100+) things at once, rather than multiple (3-5) treatments for multiple (3-5) things.

Also note that IVIg only stabilized the disease, it didn't reverse anything. That's because the damage is done- the neurons are dead and the brain has remodeled itself. At this point, Alzheimer's could only be reversed by making new neurons by stem cell therapy. Because many of those dead neuronal circuits likely encoded specific memories and personality traits, we would need to find a way to program those back into the new neurons. Those would be Sci-Fi technologies that haven't even been imagined yet.

http://www.technologyreview.com/news/428480/an-alzheimers-warning-25-years-before-symptoms/?ref=rss

More on prevention: you need to be able to predict who is going to get the disease in order for a prevention to fulfill a cost-benefit analysis (since preventative treatments might have their own side effects, and you don't want to expose people who will never get the disease to unnecessary risk). This brain imaging study suggests that this is possible, at least in one inherited subtype of the disease.

http://www.newscientist.com/article/dn22128-alzheimers-villain-cures-multiple-sclerosis-in-mice.html

I'll just leave with you an interesting tidbit- they used beta-amyloid injected into the body cavity of mice to reverse multiple sclerosis (MS). What? Isn't beta-amyloid bad? But this sort of goes with my idea that injecting IVIg "distracts" the immune system from attacking brain cells, just like beta-amyloid might "distract" the immune system from attacking myelin sheaths in MS. I think the lesson here is: We need to think outside of the box and consider counter-intuitive treatments to deal with these complex diseases.

Friday Links: Online education, crime algorithm, health care

I was looking at my Blogger stats and discovered that someone found my site by googling "help i'm addicted to wasting time on the internet." I googled it and asked an acquaintance to do the same (since Google results are personalized), and it turns out my article on Internet time-wasting is hit #3-#5, depending on who searches for it. Nice. Interestingly, it goes down with "i'm addicted to wasting time to the Internet," and doesn't come up if you just google "addicted to wasting time on the internet."

http://www.nytimes.com/2012/07/20/opinion/the-trouble-with-online-education.html?_r=1&smid=fb-share

Those who started reading my blog from the beginning know that I started off by explaining an interesting example from an online course on Coursera. To me, online courses are one way of exposing my mind to new ideas that break my preconceptions and defy conventional wisdom. Letting go of long-held ideas is critical to getting anywhere in science. But while I currently treat online education as a fun side project, there is a good debate going on as to what the role of online education will be in general for K-12 and college. Since it's the new thing, everyone wants to know to what extent it will replace traditional classroom learning. In this NY Times article Mark Edmundson, a professor at University of Virginia appears to argue against the widespread use of online education, saying there's nothing you can get from an online course that you can't get from a good book. I largely disagree.

I agree only with his thesis, "But can online education ever be education of the very best sort?" Well sure, it can't be the BEST by itself, but it sure beats the average educational experience in the US. In my opinion, education isn't about learning facts, it's about learning how to make arguments and how to understand and solve problems. And yes (agreeing with Edmundson), this can't be accomplished in a one-way didactic lecture. It needs dialogue and requires students to get to the answer themselves, with proper cultivation from the professor. However, I disagree that this says anything about the value of online education in the grand scheme of things. I don't think online education is meant to completely replace classroom learning, and certainly won't replace the best professors at the best universities. Learning how to solve problems requires some starting facts (and in science, LOTS of starting facts), and those facts should be communicated in the most efficient and organized manner. When done properly, one-way didactic lectures synergize with books (rather than being redundant). And no, I don't find it likely that every teacher individually optimizes the communication of those facts. Furthermore, in many school systems this is so inefficient that they spend all their time lecturing facts and no time on critical thinking. Only a few lucky students get real dialogue learning, since you inherently need small classroom sizes for that. Thus online education, taught by THE best educators (like, the best in the world), would go a long way to improving K-12 education. Then teachers can focus on problem solving sessions rather than lecturing facts.

I envision two parts to future education (both K-12 and college): 1) one-way lectures taught by the very best people who have developed the best ways to explain something. These can be online and available for everyone in the world. 2) actual teachers or TAs that focus entirely on face-to-face dialogue. They don't provide any actual information- they present a problem and work with the students to reason through the problem, using information that they learned in the lectures. They are more like older colleagues than anything else. In college, I often learned way more in small discussion sections than in lecture. Lectures are necessary but not sufficient for education.

In fact, when I served as a TA, there was one module that I didn't know anything about. So what did I do? I studied it just enough to get an intuitive feel for it, and then I just pummeled my students with questions while working through problems. I didn't provide a single answer for them (because I didn't know how to solve the problem), and if they asked a question I just asked a question back. The result? In my student evaluations, they specifically mentioned how well I taught that module. Real teachers don't need to know the answer.

http://www.technologyreview.com/news/428354/la-cops-embrace-crime-predicting-algorithm/

A crime-prediction algorithm takes crime data and balances information on the day, week, month, year, and decade scale to figure out where crime is statistically most likely to strike next in the city. Maybe a certain part of the city sees more crime frequently around the holidays, for example. Humans can't physically process and balance all of the data, so let a computer do it. This leaves more time for humans to do what they do best- interact with other humans. They show up, talk to people, and just by having a presence decrease crime.

http://ayoungmomsmusings.blogspot.com/2012/07/how-i-lost-my-fear-of-universal-health.html

Blog of a die-hard conservative Republican who moves to Canada and of course fears Universal Health Care. However, she soon discovers it's great and that more government control = more freedom for individuals to choose. A far more complicated issue than I'd want to address in a Friday Links entry.

Other random links:

http://www.newscientist.com/article/dn22088-heart-muscle-helps-cyborg-jellyfish-come-alive.html?DCMP=OTC-rss&nsref=online-news

http://www.huffingtonpost.com/2012/07/07/pacu-testicle-eating-fish-illinois-lake_n_1656015.html?utm_hp_ref=mostpopular

Friday Links: DNA + dark matter, E.O. Wilson, skeleton racing

More Friday Links! 

http://www.technologyreview.com/view/428391/revolutionary-dna-tracking-chamber-could-detect/

A really cool research venture: using DNA to detect dark matter. Deep sequencing technologies require you to compactly array DNA molecules (all of different sequences) on a solid surface, and biologists have standard techniques (PCR + sequencing) to uniquely identify a DNA molecule from any given spot in the array. Guess what? That's a great setup for detecting dark matter. The hypothesis is that the Earth should be plowing through dark matter as it revolves and/or rotates, assuming that dark matter is diffusely distributed.

Essentially, here's how the DNA dark matter detector works:

1) Earth rotates, brushing through dark matter in a predictable rhythm that varies directionally throughout the day

2) DNA molecules are arrayed on a gold sheet. Dark matter can knock gold nuclei out of the sheet and into the array of DNA molecules.

3) The gold nucleus cuts a swath through the forest of DNA molecules, severing them

4) severed DNA molecules fall from the array and are collected, then amplified by PCR and sequenced so the biologists can figure out exactly which DNA molecules were severed

5) since they know where each DNA molecule was anchored, they can put together the path that the gold nucleus took

6) Match the path with the direction from which you'd expect the dark matter to be coming from at the given time of day.

One word: awesome.

http://www.ted.com/talks/e_o_wilson_advice_to_young_scientists.html

E.O. Wilson, the famed evolutionary biologist who studies eusocial organisms, advocates the kind of cross-pollination exemplified by the above DNA-dark matter example. His message to scientists-in-training: learn broadly and collaborate broadly. Too many PhDs spend all their time doing experiments in a narrow field and never venture into other areas. But they are missing out: new discoveries are found in non-intuitive connections between different fields.

One idea I had relevant to MD/PhDs was inspired by E.O. Wilson's two strategies for doing good science:

1) Medicine shows the problems. Seek to learn all the problems (literally, ALL) then look for scientific phenomena that can explain the problems and provide a means to intervene

2) Science observes phenomena without necessarily knowing if they have consequences relevant to human well-being. Seek to learn all (literally, ALL) the phenomena then look for problems that might be linked to the phenomena and apply your knowledge to the problem

http://www.freakonomics.com/2012/06/29/how-to-make-a-better-athlete/

Every sport is a unique combination of agents (players + equipment) and rules that those agents follow (official rules + rules of physics). Fortunately, that's all you need to create a model of something, with the purpose of identifying the most important factors, and to predict and explain emergent properties.

Here, Freakonomics spotlights the Australian team in the skeleton, an Olympic sledding sport. They don't have career skeleton athletes (except one) and they don't have a chance to practice because, well, they're in Australia. You might think that the skill and practice time of the athlete are the two most important factors. In fact, that might be true in most sports. But if you carefully examine the rules of the game, you'll realize that there are two components to a race: the actual sledding, and the 30-meter sprint beforehand to get the sled going. Guess what? Australia has plenty of good sprinters. And as it turns out, using a little bit of modeling, you can show that the actual sledding is of minimal importance in terms of time. Skill might prevent you from wiping out, but as long as you stay on course you're not going to shave much time off with good sledding. So instead, they focused their efforts on finding really good sprinters and training them.

The result? An Australian qualified for the Olympics within 18 months, getting in about 1/10 as much practice time as a "career skeleton athlete." Very often, working smarter is 10x than working harder. Science knows best, and conventional wisdom fails miserably.

http://www.npr.org/blogs/thetwo-way/2012/07/05/156280450/kaboom-san-diegos-entire-fireworks-show-ignites-at-once

Haha all of San Deigo's July 4 fireworks goes off all at once:

Friday Links: Nigerian scammers, Cue, Texas GOP

Inauguration of Friday Links! I've decided to start weekly or bi-weekly short comments on links. This will be in addition to 1.5 posts per week that I've been averaging. After all, I spend a lot of time reading things like this on the Internet, so this really doesn't take extra time out of my day. Writing about these links just helps me solidify the information in my head.

http://www.npr.org/blogs/money/2012/06/22/155581764/those-nigerian-email-scams-are-ridiculous-for-a-reason

So I used to think that Nigerian e-mail scammers either don't care that their e-mails are ridiculous or don't realize that their e-mails are ridiculous, because they had been receiving money from the extremely gullible either way. However, as the Microsoft research paper cited by NPR shows, ridiculousness is a huge advantage. Nigerian scammers deliberately make their e-mails ridiculous in order to filter out the non-gullible, which represent a far larger portion of the population. Essentially, if the Nigerians tried to make the e-mails reasonable (and hide the fact that they want bank account information up front), then a decent number of non-gullible people would respond expressing interest, but none of them would give up their sensitive information. That would waste all the Nigerians' time and they wouldn't get any money because they can't pick out the gullible ones.

I think this actually points to a possible solution: anytime Google detects a Nigerian scam via people's spam boxes, perhaps they should simply respond to the scammers using automated accounts, in order to flood the Nigerians' inboxes with false responses and fake bank account information. Then the Nigerians would no longer be able to pick out the ones from real gullible people. It would be easier than trying to track them down.

http://www.technologyreview.com/news/428321/a-personal-assistant-mines-your-life-to-help-out/?ref=rss

Cue is trying to do what would actually make Siri useful: the ability to scan, read and understand all the information across all your accounts (e-mail, flight info, Facebook, the cloud, your calendar). Rather than searching the web like Siri does, it searches your information and makes it personal. That way you don't need to manually juggle all the information in your accounts.

I don't think Cue would require any loss of privacy, given that Apple and Google already have all of your personal information.

http://s3.amazonaws.com/texasgop_pre/assets/original/2012Platform_Final.pdf

Finally, I'm not even going to comment on this, just let it speak for itself:

From the Texas GOP 2012 official platform:

"We oppose the teaching of Higher Order Thinking Skills (HOTS) (values clarification), critical thinking skills and similar programs that are simply a relabeling of Outcome-Based Education (OBE) (mastery learning) which focus on behavior modification and have the purpose of challenging the student’s fixed beliefs and undermining parental authority."

Also, word of the day: gheegle (Filipino): the urge to pinch or squeeze something that is irresistibly cute.