🟢3 ways to measure your adaptability and how to improve it

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🟢3 ways to measure your adaptability and how to improve it

I met 273 start-up founders last year. And each one was looking for money. As a tech investor, my goal was to sort through everyone that I met and make a quick determination about which ones had the potential to make something really big.
But what makes a great founder? This is a question I ask myself daily. Some venture capitalists place bets based on a founder's previous background. Did they go to an Ivy League school? Have they worked at a blue-chip company? Have they built out a big vision before? Effectively, how smart is this person?
Other VCs asses a founder's emotional quotient, or EQ. How well will this person build teams and build rapport across customers and clients?
I have a different methodology to assess start-up founders, though, and it's not complicated. I look for signs of one specific trait. Not IQ, not EQ. It's adaptability: how well a person reacts to the inevitability of change, and lots of it. That's the single most important determinant for me. I subscribe to the belief that adaptability itself is a form of intelligence, and our adaptability quotient, or AQ, is something that can be measured, tested and improved.
AQ isn't just useful for start-up founders, however. I think it's increasingly important for all of us. Because the world is speeding up. We know that the rate of technological change is accelerating, which is forcing our brains to react. Whether you're navigating changing job conditions brought on by automation, shifting geopolitics in a more globalized world, or simply changing family dynamics and personal relationships. Each of us, as individuals, groups, corporations and even governments are being forced to grapple with more change than ever before in human history.
So, how do we assess our adaptability? I use three tricks when meeting with founders. Here's the first. Think back to your most recent job interview. What kind of questions were you asked? Probably some variation of, "Tell me about a time when," right? Instead, to interview for adaptability, I like to ask "what if" questions. What if your main revenue stream were to dry up overnight? What if a heat wave prevented every single customer from being able to visit your store? Asking "what if," instead of asking about the past, forces the brain to simulate. To picture multiple possible versions of the future. The strength of that vision, as well as how many distinct scenarios someone can conjure, tells me a lot.
Practicing simulations is a sort of safe testing ground for improving adaptability. Instead of testing how you take in and retain information, like an IQ test might, it tests how you manipulate information, given a constraint, in order to achieve a specific goal.
The second trick that I use to assess adaptability in founders is to look for signs of unlearning. Active unlearners seek to challenge what they presume to already know, and instead, override that data with new information. Kind of like a computer running a disk cleanup. Take the example of Destin Sandlin, who programed his bicycle to turn left when he steered it right and vice versa. He called this his Backwards Brain Bike, and it took him nearly eight months just to learn how to ride it kind of, sort of normally. The fact that Destin was able to unlearn his regular bike in favor of a new one, though, signals something awesome about our adaptability. It's not fixed. Instead, each of us has the capacity to improve it, through dedication and hard work.
On the last page of Gandhi's autobiography, he wrote, "I must reduce myself to zero." At many points in his very full life, he was still seeking to return to a beginner's mindset, to zero. To unlearn. In this way, I think it's pretty safe to say Gandhi had a high AQ score.

The third and final trick that I use to assess a founder's adaptability is to look for people who infuse exploration into their life and their business. There's a sort of natural tension between exploration and exploitation. And collectively, all of us tend to overvalue exploitation. Here's what I mean. In the year 2000, a man finagled his way into a meeting with John Antioco, the CEO of Blockbuster, and proposed a partnership to manage Blockbuster's fledgling online business. The CEO John laughed him out of the room, saying, "I have millions of existing customers and thousands of successful retail stores. I really need to focus on the money."
The other man in the meeting, however, turned out to be Reed Hastings, the CEO of Netflix. In 2018, Netflix brought in 15.8 billion dollars, while Blockbuster filed for bankruptcy in 2010, directly 10 years after that meeting. The Blockbuster CEO was too focused on exploiting his already successful business model, so much so that he couldn't see around the next corner. In that way, his previous success became the enemy of his adaptability potential.
For the founders that I work with, I frame exploration as a state of constant seeking. To never fall too far in love with your wins but rather continue to proactively seek out what might kill you next. When I first started exploring adaptability, the thing I found most exciting is that we can improve it. Each of us has the capacity to become more adaptable. But think of it like a muscle: it's got to be exercised. And don't get discouraged if it takes a while. Remember Destin Sandlin? It took him eight months just to learn how to ride a bike.
Over time, using the tricks that I use on founders -- asking "what if" questions, actively unlearning and prioritizing exploration over exploitation can put you in the driver's seat -- so that the next time something big changes, you're already prepared.
We're entering a future where IQ and EQ both matter way less than how fast you're able to adapt. So I hope that these tools help you to raise your own AQ.
Thank you.

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🟢How close are we to uploading our minds?

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🟢How close are we to uploading our minds?

Imagine a future where nobody dies— instead, our minds are uploaded to a digital world. They might live on in a realistic, simulated environment with avatar bodies, and could still call in and contribute to the biological world.
Mind uploading has powerful appeal— but what would it actually take to scan a person’s brain and upload their mind? The main challenges are scanning a brain in enough detail to capture the mind and perfectly recreating that detail artificially.
But first, we have to know what to scan. The human brain contains about 86 billion neurons, connected by at least a hundred trillion synapses. The pattern of connectivity among the brain’s neurons, that is, all of the neurons and all their connections to each other, is called the connectome. We haven’t yet mapped the connectome, and there’s also a lot more to neural signaling. There are hundreds, possibly thousands of different kinds of connections, or synapses. Each functions in a slightly different way. Some work faster, some slower. Some grow or shrink rapidly in the process of learning; some are more stable over time. And beyond the trillions of precise, 1-to-1 connections between neurons, some neurons also spray out neurotransmitters that affect many other neurons at once. All of these different kinds of interactions would need to be mapped in order to copy a person’s mind. There are also a lot of influences on neural signaling that are poorly understood or undiscovered. To name just one example, patterns of activity between neurons are likely influenced by a type of cell called glia. Glia surround neurons and, according to some scientists, may even outnumber them by as many as ten to one. Glia were once thought to be purely for structural support, and their functions are still poorly understood, but at least some of them can generate their own signals that influence information processing.
Our understanding of the brain isn’t good enough to determine what we’d need to scan in order to replicate the mind, but assuming our knowledge does advance to that point, how would we scan it? Currently, we can accurately scan a living human brain with resolutions of about half a millimeter using our best non-invasive scanning method, MRI. To detect a synapse, we’ll need to scan at a resolution of about a micron— a thousandth of a millimeter. To distinguish the kind of synapse and precisely how strong each synapse is, we’ll need even better resolution. MRI depends on powerful magnetic fields. Scanning at the resolution required to determine the details of individual synapses would requires a field strength high enough to cook a person’s tissues. So this kind of leap in resolution would require fundamentally new scanning technology. It would be more feasible to scan a dead brain using an electron microscope, but even that technology is nowhere near good enough– and requires killing the subject first.
Assuming we eventually understand the brain well enough to know what to scan and develop the technology to safely scan at that resolution, the next challenge would be to recreate that information digitally. The main obstacles to doing so are computing power and storage space, both of which are improving every year. We’re actually much closer to attaining this technological capacity than we are to understanding or scanning our own minds. Artificial neural networks already run our internet search engines, digital assistants, self-driving cars, Wall Street trading algorithms, and smart phones. Nobody has yet built an artificial network with 86 billion neurons, but as computing technology improves, it may be possible to keep track of such massive data sets.
At every step in the scanning and uploading process, we’d have to be certain we were capturing all the necessary information accurately— or there’s no telling what ruined version of a mind might emerge.

While mind uploading is theoretically possible, we’re likely hundreds of years away from the technology and scientific understanding that would make it a reality. And that reality would come with ethical and philosophical considerations: who would have access to mind uploading? What rights would be accorded to uploaded minds? How could this technology be abused? Even if we can eventually upload our minds, whether we should remains an open question.

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🟢Is it possible to lose weight fast?

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🟢Is it possible to lose weight fast?

In the wealthiest circles of Victorian England, bizarre fads ran rampant. But perhaps none was as strange as the tapeworm diet, in which dieters swallowed an unhatched tapeworm and let it grow inside them by consuming undigested meals. Obviously, this is an exceptionally dangerous and unhealthy way to manage your weight. However, while modern fad diets aren't usually this extreme, they do promise similar results; specifically, losing weight fast. So, are there any fast diets that do work? And are any of them actually healthy for you?
To answer these questions, let’s consider a thought experiment. Sam and Felix are identical twins both planning to go on a diet. They share the same height, weight, fat and muscle mass. But Sam is hoping to lose weight slowly, while Felix wants to go fast.
Sam's plan is to gradually decrease his calorie intake and increase his regular exercise. With less energy coming in and more being expended, he’s creating an energy deficit inside his body. To compensate, Sam’s body begins breaking down his emergency glucose supply, stored in the liver in the form of glycogen. Then, after 4 to 6 hours, his body starts burning fat cells as a major energy source. This process releases lipid droplets which are broken down into compounds that float through the bloodstream and provide energy to organs and tissues.
Felix aims to create a similar energy deficit by dramatically cutting his calorie intake. Unlike Sam, who’s still eating smaller meals, Felix is eating almost nothing. And his body responds by going into a starvation response. Felix’s body breaks down his entire store of emergency glucose in just 18 hours. And while Sam steadily replenishes glycogen with every healthy meal, Felix’s low-calorie diet does not. Desperate for energy, his body starts breaking down other materials, including his muscles. Meanwhile, Sam’s regular exercise is maintaining his muscle mass. This means he’ll use more energy both during exercise and at rest, making it easier for him to lose weight. Felix, on the other hand, is losing muscle mass and burning fewer calories than ever for his body's basic functions, making weight loss even more difficult.
Despite all this, there’s one element of Felix’s fast diet that might make him think he's on the right track. Every gram of glycogen is bound to several grams of water. This can add up to two kilograms of water weight, all of which is lost when the glycogen is depleted. For Felix, this might seem like he’s losing weight fast. But as soon as he stops starving himself, his body will replenish its glycogen store and regain that weight.
Clearly, Felix’s plan does more harm than good, but extreme calorie reduction diets aren’t the only regimens promising to shed weight fast. Plans called “detoxification diets” either promote or restrict certain foods to provide specific nutrients in high quantities. These can be useful for addressing some nutritional problems, but they’re far too specific to be used as general cure-alls. For example, for a person with low vitamin A, a juice diet might be helpful. But for someone high in vitamin A, juicing could be disastrous. And regardless of personal nutrition, maintaining a juice diet over multiple weeks is likely to compromise the immune system due to a lack of essential fats and proteins.

Therein lies the problem with all these fast-moving diets— whether you’re cutting calories or food groups, extreme diets are a shock to your system. There are well-established rates of healthy weight loss motivated by both diet and exercise that account for genetic and medical differences. And staying on those timelines requires a dietary lifestyle that’s sustainable. In fact, some of the worst side effects of extreme diets are rarely discussed since so few people stick with them, it also bears mentioning that many societies have unhealthy relationships with weight, and people are often pressured to diet for reasons other than health or happiness. So rather than trying to lose weight fast, we should all be taking our time to figure out what the healthiest lifestyle is for ourselves.

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🟢What is schizophrenia?

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🟢What is schizophrenia?

Schizophrenia was first identified more than a century ago, but we still don’t know its exact causes. It remains one of the most misunderstood and stigmatized illnesses today. So, let’s walk through what we do know— from symptoms to causes and treatments.
Schizophrenia is considered a syndrome, which means it may encompass a number of related disorders that have similar symptoms but varying causes. Every person with schizophrenia has slightly different symptoms, and the first signs can be easy to miss— subtle personality changes, irritability, or a gradual encroachment of unusual thoughts. Patients are usually diagnosed after the onset of psychosis, which typically occurs in the late teens or early twenties for men and the late twenties or early thirties for women. A first psychotic episode can feature delusions, hallucinations, and disordered speech and behavior. These are called positive symptoms, meaning they occur in people with schizophrenia but not in the general population. It’s a common misperception that people with schizophrenia have multiple personalities, but these symptoms indicate a disruption of thought processes, rather than the manifestation of another personality. Schizophrenia also has negative symptoms, these are qualities that are reduced in people with schizophrenia, such as motivation, expression of emotion, or speech. There are cognitive symptoms as well, like difficulty concentrating, remembering information, and making decisions.
So what causes the onset of psychosis? There likely isn’t one single cause, but a combination of genetic and environmental risk factors that contribute. Schizophrenia has some of the strongest genetic links of any psychiatric illness. Though about 1% of people have schizophrenia, children or siblings of people with schizophrenia are ten times likelier to develop the disease, and an identical twin of someone with schizophrenia has a 40% chance of being affected. Often, immediate relatives of people with schizophrenia exhibit milder versions of traits associated with the disorder— but not to an extent that requires treatment. Multiple genes almost certainly play a role, but we don’t know how many, or which ones.
Environmental factors like exposure to certain viruses in early infancy might increase the chance that someone will develop schizophrenia, and use of some drugs, including marijuana, may trigger the onset of psychosis in highly susceptible individuals. These factors don’t affect everyone the same way. For those with very low genetic risk, no amount of exposure to environmental risk factors will lead them to develop schizophrenia; for those with very high risk, moderate additional risk might tip the balance.
The antipsychotic drugs used to treat schizophrenia have helped researchers work backwards to trace signatures of the disorder in the brain. Traditional antipsychotics block dopamine receptors. They can be very effective in reducing positive symptoms, which are linked to an excess of dopamine in particular brain pathways. But the same drugs can make negative symptoms worse, and we’ve found that negative symptoms of schizophrenia may be tied to too little dopamine in other brain areas. Some people with schizophrenia show a loss of neural tissue, and it’s unclear whether this atrophy is a result of the disease itself or drug-induced suppression of signaling. Fortunately, newer generations of antipsychotics aim to address some of these issues by targeting multiple neurotransmitters, like serotonin in addition to dopamine. It’s clear that no one transmitter system is responsible for all symptoms, and because these drugs affect signaling throughout the brain and body, they can have other side effects like weight gain.

In spite of these complications, antipsychotics can be very effective, especially when combined with other interventions like cognitive-behavioral therapy. Electroconvulsive therapy, though it provides relatively short-lived relief, is also re-emerging as an effective treatment, especially when other options have failed. Early intervention is also extremely important. After months or years of untreated psychosis, certain psychoses can become embedded in someone’s personality. And yet, the dehumanizing stigma attached to this diagnosis can prevent people from seeking help. People with schizophrenia are often perceived as dangerous, but are actually much more likely to be the victims of violence than the perpetrators. And proper treatment may help reduce the likelihood of violence associated with schizophrenia.
That’s why education— for patients, their families, and their communities— helps erode the stigma and improves access to treatment.

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🟢Why haven't we cured arthritis?

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🟢Why haven't we cured arthritis?

While regaling you with daring stories from her youth, it might be hard to believe your grandmother used to be a trapeze artist. However, the bad backs, elbow pain, and creaky knees so common in older people is more than just “old age." In fact, the source of this stiffness plagues many young people as well. The culprit is arthritis: a condition that causes inflammation and pain in the joints of over 90 million people in the U.S. alone. But are stiff, creaky joints really inevitable? What makes arthritis so pervasive, and why haven’t we found a cure for this widespread condition?
The first hurdle is that arthritis is actually a spectrum of over 100 different arthritic conditions. All these conditions share symptoms of joint pain and inflammation, but the origin and severity of those symptoms vary widely.
Even the most common type, osteoarthritis, is trickier to prevent than one might think. It’s a general misconception that arthritis is confined to old age. The origins of osteoarthritis can often be traced to a patient’s early life, from any seemingly ordinary joint injury. Following impact, immune cells rush in to help clean and repair the damaged site and begin pumping out enzymes, including matrix metalloproteinases and aggrecanases. These enzymes clear out the damaged tissue and contribute to inflammation. But while this rapid swelling helps protect the joint during recovery, inadequately healed tissue can cause these immune cells to overstay their welcome. The continuing flood of enzymes starts to degrade the cartilage, weakening the joint and leading to arthritis later on.
Not all forms of arthritis can simply be traced to an old sports injury. Take rheumatoid arthritis, which affects 1.3 million U.S. adults. This condition is actually an autoimmune disease in which autoantibodies target natively produced proteins, some of which are secreted by cartilage cells. We still don’t know what causes this behavior, but the result is that the body treats joint tissue like a foreign invader. Immune cells infiltrate the joint despite there being no tissue damage to repair. This response leads to chronic inflammation, which destroys bone and cartilage.

Yet another condition, spondyloarthritis, has similarities to both of the conditions we’ve covered. Patients experience continuous inflammation in the joints and at the sites where ligaments and tendons attach to bones, even without any initial injury. This leads to the flood of enzymes and degradation seen in osteoarthritis, but is driven by different inflammatory proteins called cytokines. As the enzymes eat away at cartilage, the body attempts to stabilize smaller joints by fusing them together. This process sometimes leads to outgrowths called bone spurs, which also cause intense stiffness and joint pain.
With so many factors causing arthritis, our current treatments are tailored to tackle specific symptoms rather than underlying causes. These range from promising MACI techniques, which harvest cells from small pieces of cartilage to grow replacement tissue. To a technique called microfracture, where surgeons create small holes in the bone, allowing bone marrow stem cells to leak out and form new cartilage. As a last resort, people with withered cartilage can even undergo full joint replacements.
But outside these drastic measures, the underlying drivers of autoimmune arthritis still present a unique treatment challenge. Scientists are making progress with therapies that block TNF-alpha, one of the primary proteins causing inflammation in rheumatoid arthritis. But even this approach only treats the symptoms of the condition, not the cause.
In the meantime, some of our best defenses against arthritis are lifestyle choices: maintaining a healthy weight to take pressure off joints, low-impact exercises like yoga or cycling, and avoiding smoking. These arthritis-fighting behaviors can help us lead longer lives as we continue to research cures and treatments for the huge diversity of arthritic conditions.

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🟢How policewomen make communities safer?

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🟢How policewomen make communities safer?

I've been a police officer in an urban city for nearly 25 years. That's crazy, right? And in that time, I've served in every rank, from police officer to police chief. A few years ago, I noticed something alarming.
Starting in 2014, I started monitoring recruits as they cycled through police academies in the state of New Jersey, and I found that women were failing at rates between 65 and 80 percent, due to varying aspects of the physical fitness test. I learned that a change in policy now required recruits to pass the fitness exam within 10 short workout sessions. This had the greatest impact on women. The change meant that recruits had about three weeks out of a five-month-long academy to pass the fitness exam. This just didn't make sense, though.
Police agencies and police recruits had made huge investments to get those recruits into the academy. Police recruits had passed lengthy background checks, they had passed medical and psychological exams, they had quit their jobs. And many had spent more than 2,000 dollars in fees and equipment just to get kicked out within the first three weeks?
The dire situation in New Jersey led me to examine the status of women in policing across the United States.
I found that women make up less than 13 percent of police officers. A number that hasn't changed much in the past 20 years. And they make up just three percent of police chiefs as of 2013, the last time the data was collected. We know that we can improve those rates. Other countries like Canada, Australia and the UK have nearly twice the amount of policewomen. And New Zealand is steadily marching towards their goal of recruit gender parity by 2021. Other countries are actively working to increase the number of women in policing, because they know of a vast body of research evidence, spanning more than 50 years, detailing the advantages to women in policing.
From that research, we know that policewomen are less likely to use force or to be accused of excessive force. We know that policewomen are less likely to be named in a lawsuit or a citizen complaint. We know that the mere presence of a policewoman reduces the use of force among other officers. And we know that policewomen are met with the same rates of force as their male counterparts, and sometimes more, and yet they're more successful in defusing violent or aggressive behavior overall. So there are vast advantages to women in policing, and we're losing them to arbitrary fitness standards.
The problem is, the United States has nearly 18,000 police agencies -- 18,000 agencies with wildly varying fitness standards. We know that a majority of academies rely on a masculine ideal of policing that works to decrease the number of women in policing. These types of academies overemphasize physical strength, with much less attention spent to subjects like community policing, problem-solving and interpersonal communication skills. This results in training that does not mirror the realities of policing. Physical agility is but a small component of police work. Much of an officer's day is spent mediating interpersonal conflicts. That's the reality of policing.
These are my babies. And we can reduce the disparity in policing by changing exams that produce disparate outcomes. The federal courts have stated that men and women simply are not physiologically the same for the purposes of physical fitness programs. And that's based on science.
Respected institutions that law enforcement deeply respects, like the FBI, the US Marshals Service, the DEA and even the US military -- they rigorously test fitness programs to ensure they measure fitness without gender-disparate outcomes. Why is that? Because recruiting is expensive. They want to recruit and retain qualified candidates. You know what else the research finds? Well-trained women are as capable as their male counterparts in overall fitness, but more importantly, in how they police.

The law-enforcement community is admittedly experiencing a recruitment crisis. Yet, if they truly want to increase the number of applicants, they can. We can easily recruit more women and reap all those research benefits by training well-qualified candidates to pass validated, work-related, physiologically-based fitness exams, as required by Title VII of the Civil Rights Act.
We can increase the number of women, we can reduce that gender disparity, by simply changing exams that produce disparate outcomes. We have the tools. We have the research, we have the science, we have the law. This, my friends, should be a very easy fix.
Thank you.

#Social_Change #Women #Justice_System #Work #Feminism #United_States #Diversity #TED_Fellows #Gender

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🟢The Chemistry Of Cookies

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🟢The Chemistry Of Cookies

In a time-lapse video, it looks like a monster coming alive. For a moment, it sits there innocuously. Then, ripples move across its surface. It bulges outwards, bursting with weird boils. It triples in volume. Its color darkens ominously, and its surface hardens into an alien topography of peaks and craters. Then, the kitchen timer dings. Your cookie is ready. What happened inside that oven? Don't let the apron deceive you! Bakers are mad scientists. When you slide the pan into the oven, you're setting off a series of chemical reactions that transform one substance, dough, into another, cookies. When the dough reaches 92 degrees Fahrenheit, the butter inside melts, causing the dough to start spreading out. Butter is an emulsion, or mixture of two substances that don't want to stay together, in this case, water and fat, along with some dairy solids that help hold them together. As the butter melts, its trapped water is released. And as the cookie gets hotter, the water expands into steam. It pushes against the dough from the inside, trying to escape through the cookie walls like Ridley Scott's chest-bursting alien. Your eggs may have been home to squirming salmonella bacteria. An estimated 142,000 Americans are infected this way each year. Though salmonella can live for weeks outside a living body and even survive freezing, 136 degrees is too hot for them. When your dough reaches that temperature, they die off. You'll live to test your fate with a bite of raw dough you sneak from your next batch. At 144 degrees, changes begin in the proteins, which come mostly from the eggs in your dough. Eggs are composed of dozens of different kinds of proteins, each sensitive to a different temperature. In an egg fresh from the hen, these proteins look like coiled up balls of string. When they're exposed to heat energy, the protein strings unfold and get tangled up with their neighbors. This linked structure makes the runny egg nearly solid, giving substance to squishy dough. Water boils away at 212 degrees, so like mud baking in the sun, your cookie gets dried out and it stiffens. Cracks spread across its surface. The steam that was bubbling inside evaporates, leaving behind airy pockets that make the cookie light and flaky. Helping this along is your leavening agent, sodium bicarbonate, or baking soda. The sodium bicarbonate reacts with acids in the dough to create carbon dioxide gas, which makes airy pockets in your cookie. Now, it's nearly ready for a refreshing dunk in a cool glass of milk. One of science's tastiest reactions occurs at 310 degrees. This is the temperature for Maillard reactions. Maillard reactions result when proteins and sugars break down and rearrange themselves, forming ring-like structures, which reflect light in a way that gives foods like Thanksgiving turkey and hamburgers their distinctive, rich brown color. As this reaction occurs, it produces a range of flavor and aroma compounds, which also react with each other, forming even more complex tastes and smells. Caramelization is the last reaction to take place inside your cookie. Caramelization is what happens when sugar molecules break down under high heat, forming the sweet, nutty, and slightly bitter flavor compounds that define, well, caramel. And, in fact, if your recipe calls for a 350 degree oven, it'll never happen, since caramelization starts at 356 degrees. If your ideal cookie is barely browned, like a Northeasterner on a beach vacation, you could have set your oven to 310 degrees. If you like your cookies to have a nice tan, crank up the heat. Caramelization continues up to 390 degrees. And here's another trick: you don't need that kitchen timer; your nose is a sensitive scientific instrument. When you smell the nutty, toasty aromas of the Maillard reaction and caramelization, your cookies are ready. Grab your glass of milk, put your feet up, and reflect that science can be pretty sweet.

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🟢Kids are speaking up for the environment. Let's listen

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