Your Daily Tao

One way to circumvent the messiness of open-ended interviews is to turn them into closed-ended, multiple-choice tests. As the critics would predict, children do exhibit less coherence on multiple-choice tests than in open-ended interviews. They select responses consistent with a spherical model of the earth on some questions but select responses consistent with a nonspherical model on others. This finding should not be a surprise, though. Children could easily provide correct answers to multiple-choice questions without understanding why those answers are correct. It’s long been known that multiple-choice questions are easier than fill-in-the-blank questions because the correct answer to a multiple-choice question is provided as part of the question itself; one need only recognize it. And children are surrounded by the correct answers every day. Their classrooms are filled with globes, not hollow spheres, and their textbooks are filled with photographs of a round earth, not an elliptical earth. Multiple-choice tests measure children’s memory for earth-related information but not their understanding of it

Multiple choice questions in our examinations might not help our children in understanding the concepts they are supposed to test. In this excerpt, children who go through the tests select answers that might be contradictory to each other, showing that they did not have a mental model of the shape of the earth.

Multiple choice questions ultimately just serves as a test of pattern recognition and memories and might not really test one’s ability to understand things as much as having to verbalise your thoughts on an open-ended question. While it might be easier to score or mark these tests, open-ended questions can help develop better critical thinking or mental modelling skills which are important for their future.

Several studies have shown that hands-on experiences are no more effective than hands-off experiences (i.e., instruction) at teaching abstract ideas like Newtonian principles. The problem is that abstract ideas need to be abstracted before they can be learned, and hands-on experiences are not suited for that purpose.

This book covers how our intuitions and experiences can tend to betray us when trying to understand scientific theories. That can be one reason why so many of us find its hard to wrap our head around abstract scientific theories.

Imagine the freedom of escaping your genetic inheritance. Envision the possibility of leaving behind any genes that put you at risk for a multitude of cancers. Okay, there’s only one small catch. You would need to have Laron syndrome. Untreated, most people with this condition are typically less than 4 feet 10 inches tall, have a prominent forehead, deep-set eyes, a depressed nasal bridge, a smallish chin, and truncal obesity. We know of around 300 people in the world who have this condition, and about a third of them live in a small number of remote villages in the Andean highlands of Ecuador’s southern Loja Province. And they all appear to be virtually immune from cancer. Why? Well, to understand Laron syndrome, it’s helpful to know a bit about another genetic condition—one that exists on the opposite side of the spectrum, called Gorlin syndrome. People with this disorder are susceptible to a type of skin cancer called basal cell carcinoma.* While basal cell carcinoma is relatively common among adults who have spent a good portion of their lives in the sun, people with Gorlin syndrome can develop this type of skin cancer in their teens and without much sun exposure. About one in 30,000 people are affected by Gorlin syndrome, though many are thought to go undiagnosed. Usually you don’t know you have it until you or someone in your family gets diagnosed with cancer. There are, though, a few visual dysmorphologic clues that are occasionally present and that you could probably easily identify. These include macrocephaly (a large head), hypertelorism (wide eyes), and 2-3 toe syndactyly6 (webbed second and third toes). Other common diagnostic features include small pits on the palms and uniquely shaped ribs that can be seen on a chest radiograph or X-ray. So why are people with Gorlin syndrome so sensitive to getting malignancies, such as skin cancer, without exposure to sun? To answer that question I need to tell you about a gene called PTCH1. Our bodies typically use this gene to makes a protein called Patched-1, which plays a crucial role at keeping cellular growth in check. But when a protein called Sonic Hedgehog* comes along in Gorlin patients, whose Patched-1 is not working properly, it releases the hold on growth that would usually be there and that makes cells free to divide. And divide. And divide. This, of course, is a problem, because as we’ve now seen many times, unrestricted growth is like cellular anarchy. And unfortunately, cancer can result. Okay, so what does Gorlin syndrome teach us about Laron syndrome? Essentially, Gorlin syndrome represents, in a way, the genetic inverse to Laron syndrome. Whereas in one there is a promotion of cellular growth, the other experiences cellular growth restriction. Laron syndrome is caused by mutations in the receptor for growth hormone. This makes people with Laron syndrome insensitive or immune to it—one of the reasons they are often quite short. Rather than the cellular anarchy seen in people with Gorlin syndrome, in those with Laron syndrome there is a stranglehold on growth, a form of extreme cellular totalitarianism. Now, politically you might have some reservations about totalitarianism as an ideology, but from a purely biological perspective it has been incredibly successful. If it weren’t, you wouldn’t be here reading this right now. Neither would I. Neither would any of the other multicellular organisms on this planet. Because, like you and me and all the other multicellular creatures, we are the product of biological totalitarianism that promotes cellular obedience at all costs, an obedience enforced by receptors on the surface of any potentially misbehaving cells that result in cellular seppuku or hara-kiri—a programmed type of cell suicide known as apoptosis. Like samurai warriors who become dishonored, cells that have the impudence to have greater aspirations than just being one in a crowd of many trillion are programmed and occasionally commanded to end their own lives. By this same mechanism, cells that are infected with pathogens can also sacrifice themselves to protect the body from microbial invaders. It’s also the same mechanism we learned about previously that frees our fingers and toes from the webbing that’s there during development. If those cells don’t die—as happens in some genetic conditions—you can end up having mittens for hands. Which is why, as in all things, equilibrium is crucial. Processes that restrict growth need to be constantly balanced with times when growth is needed. Just think about every time you’ve sustained an injury, be it a simple cut or a much more serious accident. Consider the entire repair and remodeling your body did—automatically. All of this is a process of the balance being struck, millions upon millions of times each day, between cellular life and death.

Another heavy (also final) passage but I find this part of the book pretty memorable. Like most things in life, our bodies function at an equilibrium. The same processes controlling the growth of our bodies can also be induced to increase the chance for cancerous growth. Now, whether we are able to eventually split and control these processes to our benefit is a separate issue.

But most of the times, we live in a world where we find the best trade-offs we can get, and try to find the balance between both extremes. It seems our biology is also a reflection of that.

As genetic testing and sequencing becomes more routinely used in different aspects of medical care, from pediatrics to gerontology, we’ll have more information at our disposal to be able to link distinct health risks with our unique genetic inheritance. Obamacare is set to give many Americans better access to health care, but it might also inadvertently set them up for genetic discrimination. Thanks to a glaring loophole intentionally crafted into GINA, insurance companies have free reign to use that genetic information against us when they determine the premiums they will charge us for disability and life insurance. Here’s where things get even more frightening. These days, a potential insurance provider, or anyone else for that matter, doesn’t have to touch a single one of your cells to get a lot of information about your genetic inheritance. Among scientists like myself, it’s common practice to share genetic and sequencing data with other researchers while removing identifying information such as names and social security numbers. But what most of us have always seen as a relatively solid privacy protocol, an astute team of biomedical experts, ethicists, and computer scientists from Harvard, MIT, Baylor, and Tel Aviv University saw as a potential target to be hacked. Plugging short segments of seemingly anonymous information into recreational genealogy websites (the users of which are increasingly including genetic information as a way to track down long-lost family members), the researchers were able to easily identify the anonymous patients’ family groups. And with just a little additional data that’s commonly included in shared samples—age and state of residence, for instance—they were able to triangulate the precise identity of many individuals. This can also work the other way around. Do you have a family member who has survived cancer? Did they keep a blog? Facebook it? Tweet about it? Social media’s not just a great way to keep in touch with our loved ones—it’s also a potentially very deep and rich source of information for genetic cyber sleuths. Already, more than a third of employers say they’ve used information found on social media sites such as Facebook to eliminate job seekers from the applicant pool. With employer-based health-care costs in the United States rising ever skyward, companies might feel justified in making a social media health status sweep a regular, if secretive, part of their hiring practices. Using just your name and the millions of genealogy records publicly available on the Web, an inquisitive and resourceful person—someone considering hiring, dating, or marrying you, perhaps—could come to know more about you than you might even know about yourself. And if you just happen to be that resourceful and inquisitive person and there was a much easier way for you to access someone’s genetic information without them ever knowing, how far would you go? What I’m asking you is this: Would you be willing to hack someone’s genome?

We all might have different reactions to different types of medical care based on our genes. The dangerous thing is, that our genes, something we have no control over, can be used to discriminate and prevent us from getting health insurance as such information can be more easily deduced from our digital footprint. This is the danger of having more information digitised and shared.

But what if our experiences of being bullied did a lot more than just saddle us with some serious psychological baggage? Well, to answer that question, a group of researchers from the UK and Canada decided to study sets of monozygotic “identical” twins from the age of five. Besides having identical DNA, each twin pair in the study, up until that point, had never been bullied. You’ll be glad to know that these researchers were not allowed to traumatize their subjects, unlike how the Swiss mice were handled. Instead, they let other children do their scientific dirty work. After patiently waiting for a few years, the scientists revisited the twins where only one of the pair had been bullied. When they dropped back into their lives, they found the following: present now, at the age of 12, was a striking epigenetic difference that was not there when the children were five years old. The researchers found significant changes only in the twin who was bullied. This means, in no uncertain genetic terms, that bullying isn’t just risky in terms of self-harming tendencies for youth and adolescents; it actually changes how our genes work and how they shape our lives, and likely what we pass along to future generations. What does that change look like genetically? Well, on average, in the bullied twin a gene called SERT that codes for a protein that helps move the neurotransmitter serotonin into neurons had significantly more DNA methylation in its promoter region. This change is thought to dial down the amount of protein that can be made from the SERT gene—meaning the more it’s methylated the more it’s “turned off.” The reason these findings are significant is that these epigenetic changes are thought to be able to persist throughout our lives. This means that even if you can’t remember the details of being bullied, your genes certainly do. But that’s not all these researchers found. They also wanted to see if there were any psychological changes between the twins to go along with the genetic ones that they observed. To test that, they subjected the twins to certain types of situational testing, which included public speaking and mental arithmetic—experiences most of us find stressful and would rather avoid. They discovered that one of the twins, the one with a history of being bullied (with a corresponding epigenetic change), had a much lower cortisol response when exposed to those unpleasant situations. Bullying not only turned those children’s SERT gene to low, it also turned down their levels of cortisol when stressed. At first this may sound counterintuitive. Cortisol is known as the “stress” hormone and is normally elevated in people under stress. Why, then, would it be blunted in the twin who had a history of being bullied? Wouldn’t you think they would be more stressed in a heightened situation? This gets a little complicated, but hang tight: As a response to the persistent bullying trauma, the SERT gene of the bullied twin can alter the hypothalamic-pituitary-adrenal (HPA) axis, which normally helps us cope with the stresses and tumbles of daily living. And according to the scientists’ findings in the bullied twin, the greater the degree of methylation, the more the SERT gene is turned off. The more it’s turned off, the more blunted the cortisol response. To understand the sheer depth of this genetic reaction, this type of blunted cortisol response is also often found in people with post-traumatic stress disorder (PTSD). A spike of cortisol can help us through a tough situation. But having too much cortisol, for too long, can short-circuit our physiology pretty quickly. So, having a blunted cortisol response to stress was the twin’s epigenetic reaction to be being bullied day after day. In other words, the twin’s epigenome changed in response to protect them from too much sustained cortisol. This compromise is a beneficial epigenetic adaptation in these children that helps them survive persistent bullying. The implications of this are nothing short of staggering. Many of our genetic responses to our lives work in such a fashion, favoring the short over the long term. Sure, it’s easier in the short term to dull our response to persistent stress, but in the long run, epigenetic changes that cause long-term blunted cortisol responses can cause serious psychiatric conditions such as depression and alcoholism. And not to scare you too much, but those epigenetic changes are likely heritable from one generation to the next. If we’re finding such changes in individuals like the bullied twin, then what about traumatic events that affect large swaths of the population?

Even if we no longer have memories of being bullied, our genes will remember it. This means that there can be lasting damage to even their descendants.  Imagine the lasting damage this pandemic might have on the number of people and their genes.

Identical genes don’t always behave identically in different people—even people with completely identical DNA. Take Adam and Neil Pearson, for example. Born as monozygotic, or identical, twins, these brothers are thought to carry indistinguishable genomes, including a genetic change that causes neurofibromatosis type 1. But Adam has a face that is bloated and disfigured—so badly that a drunken nightclub patron once tried to rip it off, thinking it was a mask. Neil, on the other hand, could pass for Tom Cruise from a certain angle but suffers from memory loss and occasional seizures. Identical genes, completely different expression. So all of those physical signs I walked you through in chapter 1? They are common expressions and generally indicative of certain genetic conditions, but those traits certainly don’t encompass the spectrum of all expressions of those genetic conditions. All of which prompts us to ask, why the difference in expression? Because our genes do not respond to our lives in a binary fashion. As we will come to learn, and contrary to Mendel’s findings, even if our inherited genes seem set in stone, the way they express themselves can be anything but. Whereas our inheritance may have been initially understood through a black-and-white Mendelian lens, today we’re starting to understand the power of seeing things in full and genetically expressive color. Which is why now, as physicians, we have a new challenge. Patients look to us to have the answers in clean, discrete categories: benign or malignant, treatable or terminal. The hard part of explaining genetics to patients is that everything we thought we knew is not always static or binary. Figuring out the best way to explain that to patients has become much more critical, since they need the best information possible to help them make some of the most important decisions of their lives. Because your behavior can and does dictate your genetic destiny.

A new perspective on how we can view the debate between “nature” and “nurture”. Our nature might set things in stone for us, but our daily environment from the time we are born can impact our lives in deep ways. Our behaviour and the choices we make can also affect our genes.

Even death itself. Until now, most of us have been under the assumption that our life experiences end when our lives end. That’s wrong, too. We are the culmination of our life experience as well as the life experiences of our parents and ancestors. Because our genes don’t easily forget. War, peace, feast, famine, diaspora, disease—if our ancestors went through it and survived, we’ve inherited it. And once we’ve got it, we’re that much more likely to pass it on to the next generation in one way or another. That might mean cancer. It might mean Alzheimer’s disease. It might mean obesity. But it might also mean longevity. It might mean grace under fire. And it might just mean happiness itself. For better or for worse, we are now learning that it is possible to accept and reject our inheritance.

An interesting book that I’ve recently reread as I didn’t absorb too much during the 1st time I read it years ago. One of the key things that stood out was how the way we choose to live our lives can continue to having a lasting impact on our genes and our future descendants.

I’ll be sharing a few more passages (might be highly technical) over the next few days!

When Disney launched Euro Disney in Paris, they learned how much privilege means to the French culture. Originally, the theme park had the same rules as all other Disney parks, barring pets, smoking, and the consumption of alcohol. The French stayed away in droves because they didn’t like such restrictions. Disney broke through to the French market only when they began to offer special “privilege passes” that allowed access (for a premium price) to certain parts of the park where visitors could take their pets, smoke, and drink wine. The idea of islands of privilege in a sea of equality was right on Code for the French.

How culture can affect the expansion of your business. The last passage that I’ll be sharing from this book. I just thought this was an interesting anecdote to share.

Emotions are the keys to learning, the keys to imprinting. The stronger the emotion, the more clearly the experience is learned. Think again of that child and the hot pan. Emotions create a series of mental connections (I call them mental highways) that are reinforced by repetition. These mental highways condition us to see the world in predictable ways. They are the path from our experience with the world (such as touching a hot pan) to a useful approach to the world (avoiding all hot things in the future). We do the overwhelming majority of our learning when we are children. By the time we are seven, most of our mental highways have been constructed. But emotion continues to provide us with new imprints throughout our lives. Most Americans of the Boomer generation can remember where they were and what they were doing when they learned of the assassination of John F. Kennedy. Most Americans alive today can vividly relive the experience of watching the World Trade Center towers fall. This is because these experiences are so emotionally powerful that they are effectively seared onto our brains. We will never forget them, and the simple mention of the topic sends us back to that moment when we imprinted it.

We remember emotions more easily. Experiences that have a strong emotional impact on us stays with us for a long time and we will be easily able to recollect it. It also can be a reason why some advertisers attempt to invoke emotions or meaningful memories in their adverts so their ads can imprinted on us more deeply.

Under these circumstances, Nestlé’s strategy of getting these consumers to switch from tea to coffee could only fail. Coffee could not compete with tea in the Japanese culture if it had such weak emotional resonance. Instead, if Nestlé was going to have any success in this market at all, they needed to start at the beginning. They needed to give the product meaning in this culture. They needed to create an imprint for coffee for the Japanese. Armed with this information, Nestlé devised a new strategy. Rather than selling instant coffee to a country dedicated to tea, they created desserts for children infused with the flavor of coffee but without the caffeine. The younger generation embraced these desserts. Their first imprint of coffee was a very positive one, one they would carry throughout their lives. Through this, Nestlé gained a meaningful foothold in the Japanese market. While no marketer will likely ever be able to convince the Japanese to abandon tea, coffee sales—nearly nonexistent in 1970—now approach half a billion pounds per year in Japan. Understanding the process of imprinting—and how it related directly to Nestlé’s marketing efforts—unlocked a door to the Japanese culture for them and turned around a floundering business venture.

To be honest, this book had a great start for me and then it begin going into “ehhhh….” territory. Nevertheless, there are quite a few anecdotes that were super interesting and stayed with me for quite a while.

The above passage was one of them. It talks about how cultivating the younger generation with coffee based desserts helped Nestle grow their instant coffee sales in the long term for Japan, a culture that was much more dedicated to tea instead.