You Want to Climb Mount Everest? Here’s What It Takes

You Want to Climb Mount Everest? Here’s What It Takes

Q: How high is Mount Everest?

At 29,029 feet (8,848 meters), Everest is the world’s tallest mountain. It straddles Nepal and Tibet.

Q: How do you get there?

Most climb Everest from the Nepal side. From Kathmandu, Nepal’s bustling capital, mountaineers take a short flight to Lukla, then trek about 10 days to Everest Base Camp (17,500 feet). Most will spend weeks there in the spring, acclimating to the altitude with rest and day hikes, waiting for the route to Everest’s summit to open in May.

Q: How many try to climb it every year? How many succeed? How many die?

Everest’s popularity continues to surge. In a typical year now, more than 600 people reach the summit of Everest, which is about half of the number who attempt it (or, at least, pay for permits). About two-thirds of those who summit do it from the south side, in Nepal, while the rest approach from Tibet, on the north. Almost all do it during Everest’s short climbing season, usually a few weeks in May, between the winter and the region’s summer monsoons.

In 2017, six people died, a typical number, including a cook in Base Camp and an Indian man near the summit. A seventh, famous mountaineer Ueli Steck, died in a fall on a nearby mountain while waiting for Everest’s route to open.

Q: How many bodies are on Everest?

Nearly 300 people are known to have died on Everest. Nepal’s government estimates that most of them, perhaps 200, remain there.

Q: How do people die, and what are the primary dangers?

Most famously, as depicted in popular culture, climbers die from exposure to the elements — the subfreezing temperatures and the high altitude, especially after running out of supplemental oxygen and getting caught in sudden storms. But many climbers die from falls and avalanches, and others from health problems like heart attacks. Increasingly, climbers worry about the role of the crowds on Everest, where routes can be jammed with people desperate to reach the summit. More than 20 years after it was published, Jon Krakauer’s “Into Thin Air” remains the cautionary tale.

Q: What does extreme altitude do to the body?

The area above 8,000 meters (about 26,000 feet), from Camp 4 to the summit, is called the “death zone,” because of its thin air and brutal weather. With gains in altitude, each breath draws less oxygen for the lungs and bloodstream, which is why most climbers, including guides, use supplemental oxygen.

Typical effects of altitude include headaches, nausea and exhaustion. But in the death zone, high-altitude cerebral edema can create a lack of muscle control, impaired speech, confusion and hallucinations. High-altitude pulmonary edema results in coughing and breathing problems. Frostbite, snow blindness and hypothermia are major threats.

Q: I want to climb Everest someday. Can anyone do it?

The primary barriers are money and fitness. While Nepal’s government has placed restrictions on foreigners — expensive permits, the necessity of hiring an outfitter with guides, and an age requirement of 18, for example — it is only now considering ways to restrict attempts to highly experienced mountaineers.

Q: How much does it cost?

The range is wide — from nearly $30,000 to $100,000 or more. Foreigners must buy an $11,000 permit from the Nepalese government, plus pay other fees, but the variance has to do with the outfitters hired. Some offer Western guides for Western clients, which can be more expensive than local ones, or some hybrid in the ratio between climbers and guides. (For example, 1 local guide per climber, plus one Western guide for every four climbers.) Other substantial costs include travel, gear, oxygen and weeks of food and camping while acclimatizing at Base Camp (17,600 feet).

Q: Who are the sherpas?

Guides in the Himalayas are often called “sherpas,” though not all are part of the ethnic group of Sherpa, from which many take their surname. Most are young men, living anywhere from small villages to the chaotic city of Kathmandu, who find they can make more money as a guide than in other lines of work. The Nepal government said that most guides earn about $6,000 per expedition, but the range is broad, from camp cooks (perhaps $2,500) to lead guides ($10,000). They are not immune to the dangers; nearly half the people who have died on Everest have been sherpa guides.

How to control your worrying (according to neuroscience)

How to control your worrying (according to neuroscience)

People try lots of things to mitigate the suffering that comes with waiting for exam scores, hospital test results, or the outcome of a job interview. They try to distract themselves. They try to stay positive. They brace for the worst.

Past research by UC Riverside “worry and waiting” expert Kate Sweeny has studied the effectiveness of those techniques. None of it works, her research has found. Those tactics not only fail to reduce distress — they can even backfire and make it worse.

But now, Sweeny’s research finds something that can help: supplementing those ineffective strategies with “mindfulness” meditation. That is, focusing on the present using meditation.

Stopping painful “mental time-travel”

In the journal Personality and Social Psychology Bulletin, research funded by the National Science Foundation asserts that mindfulness is a sort of antidote to the “curse” of waiting. That curse is a focus on the past or future, represented by questions such as “Why did I say that?” and “What if things don’t go my way?”

“We try to predict our fate and regain a sense of certainty and control over our life,” said Sweeny, who is an associate professor of psychology at UC Riverside. “We know from lots of research that rumination (repetitive thoughts about the past) and worry (repetitive thoughts about the future) are quite unpleasant and even harmful to our health and well-being, so it’s important to seek solutions to this painful form of mental time-travel.”

Better to focus on the present, Sweeny said, and accept your thoughts and feelings as they arise rather than engage in tactics to avoid them. It means you’ll process your emotions differently and — Sweeny argues — more effectively.

The study was performed using 150 California law students who had taken the bar exam and were awaiting the results, which take four months to post online. The students completed a series of questionnaires in that four-month waiting period.

There are few “waiting” scenarios more stressful than the potentially career-killing bar exam. The magnitude of the distress is represented in several sample statements Sweeny and her team collected. Among them:

  • “I had a nightmare where I couldn’t determine whether I had passed or failed the bar exam and I spent the entire dream trying to find out my results. I have these sort of bar exam nightmares once every couple weeks.”
  • “I got sick, like fever flu sick, and I think it’s because my anxiety levels have slowly been building up to today!! I was constantly thinking and thinking about the results.”

During the four-month waiting period, the students were asked to participate in a 15-minute audio-guided meditation session at least once a week.

Sweeny found the mindfulness meditation served to postpone the phenomenon of “bracing.” Bracing is essentially preparing for the worst. Previous research by Sweeny and others shows bracing can be an effective technique for managing expectations, but its benefits erode when it occurs too early in the waiting process.

“Optimism feels good; it just does a poor job of preparing us for the blow of bad news,” Sweeny said. “That’s where bracing comes in. In a perfect world, we’d be optimistic as long as possible to get all the good feelings we can from assuming the best, and then we’d brace for the worst at the moment of truth to make sure we’re prepared for bad news.”

First study to show meditation helps with waiting

The benefits of mindfulness meditation have long been asserted, but Sweeny said this is the first research to demonstrate its effectiveness coping with waiting.

“We know that meditation is a great way to reduce everyday stress, but our study is the first to see if it also makes it easier to wait for personally significant news. This study is also one of the first to identify any strategy that helps people wait better, and it also shows that even brief and infrequent meditation can be helpful,” Sweeny said.

Best of all, Sweeny said, the mindfulness tactic requires no training, no money, and minimal time and effort.

“Meditation isn’t for everyone, but our study shows that you don’t have to be a master meditator or go to a silent meditation retreat to benefit from mindfulness,” she said. “Even 15 minutes once a week, which was the average amount of meditation practiced by our participants, was enough to ease the stress of waiting.”

 

In terms of bliss, which is defined as a natural direction you can take as a way to maximize your sense of joy, fulfillment, and purpose.  For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide — the so-called bliss molecule and our own natural marijuana — in our brains.  Find out if you have the genetic make-up for blissfulness: https://mightydna.com/shop/partner-compatibility/

How height happens: Hundreds of genetic ‘switches’ that affect height

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How height happens: Hundreds of genetic 'switches' that affect height

Led by Associate Professor of Human Evolutionary Biology Terence D. Capellini, a team of researchers discovered hundreds of genetic “switches” that have an influence on height and performed functional tests that demonstrated precisely how one such switch alters the function of a key gene involved in height differences. The study is described in a December 5 paper published in eLife.

“Large genome-wide association studies on upwards of 250,000 people found about 700 genetic regions associated with height,” Capellini said. “But within each region there could be many single DNA variants linked together, so there are potentially tens of thousands of variants spanning those regions. The question is how do you whittle that number down to those specific variants that influence height?”

The first step, Capellini said, was to filter the list of more than 60,000 genetic variants to those that are likely functional in the cartilage growth plates of bones. To do this they identified in the femurs of developing mice regions of the DNA that act as regulatory “switches” — that is, sequences of DNA that cause nearby genes to turn on or off. As part of that search, Capellini and colleagues focused on areas where the genome was “open,” or available for transcription using a technique called ATAC-seq.

The problem, however, is that process identifies every switch in the growth plate cartilage cell, many of which may not be involved in bone growth but rather basic cellular processes. To separate those “general” switches from those related to bone growth and thus likely height, the team performed the same test again, but on a different cell type, and identified sequences that were open in both. “If we find a common sequence that’s open in a brain cell and in a cartilage cell, we can say it likely turns on some gene that may be important for cells to live,” Capellini said. “So we filtered those out, but we didn’t ignore them completely, because they may actually be important. While we first concentrated on the bone-specific switches, we know there are a lot of inputs to height — it’s about the length of our bones, but we also know hormones trigger height, malnutrition can impact height, among other inputs so there may be general genetic factors that influence height.”

As part of that work, Capellini said, researchers also performed a number of “quality control” tests to ensure the unique switches they identified were actually involved in bone and cartilage development as well as height.

After performing those tests and filters, Michael Guo, an author on the study, was next able to determine how many of the 60,000 variants associated with height actually reside in on/off switches for bone. This resulted in a list of about 900 genetic variants.

To make sure that this process generated unique height signals, Capellini and colleagues performed additional analyses. “We took genome-wide analyses from other studies that had nothing to do with height and looked to see if we saw the same signal, and we didn’t, which makes sense,” he said. “We also looked at switches from other cell types to see if these genetic variants appeared, and they didn’t. That really suggests to us that the signals we’re seeing are very strong, it’s not just a property of the genome or a property of identifying these switches.”

The team then chose one on/off switch, associated with a gene known as Chondroitin Sulfate Synthase 1, or CHSY1, which plays a key role in how cartilage cells create the extra-cellular matrix that hardens into bone. In turn, the gene influences femur length in mice and humans.

“We did some tests to find out how this switch effects CHSY1 activity, and found that both versions — for taller height and shorter height — act as repressors on the gene,” Capellini said. “But surprisingly the height-increasing variant isn’t as strong.”

To verify that the switch indeed acts in a repressive manner, using CRISPR tools, researchers removed the switch or the variant altogether from human cartilage cells, and saw a very strong increase in the expression of the gene.

Going forward, Capellini and colleagues hope to use high-throughput functional methods to understand the role each variant plays in human height, and to develop other methods to test all 60,000-plus variants in order to study height in a more unbiased manner.

In addition to providing a new understanding of a complex human trait, the study may ultimately demonstrate how genetic tools might be used to understand other conditions — like macular degeneration, diabetes or even heart disease — that are tied to both environmental and genetic factors.

“For any disease or trait, being able to say here is a switch that turns a gene on or off, and here is the mutation in that switch that can effect it dramatically…that’s pretty powerful,” Capellini said. “That will allow us figure out what are the biological pathways that are worth targeting. The future of personalized medicine will rely on knowing what specific pieces of DNA are doing in the body, and this is one way to do that.”

5 Strategies to Demystify the Learning Process for Struggling Students

5 Strategies to Demystify the Learning Process for Struggling Students

 

When students do not understand how their brains learn and retain material, they can develop misconceptions about themselves as learners — such as a faulty assumption that they are bad at a subject or that they suffer from performance anxiety. Oakley shares the common experience of students who reread their notes and think they know the material —  only to enter a test and find that they cannot retrieve the information. “They are horrified and think they must have test anxiety.” More likely, says Oakley, they simply haven’t been taught how to study in a way that allows them to retrieve the information.

Oakley recognizes that “many educators are not at all comfortable with or trained in neuroscience,” so she breaks down a few key principles that teachers can use in the classroom and share with students to help them demystify the learning process.

1. The Hiker Brain vs. The Race Car Brain

Start by teaching students the difference between focused and diffused thinking, says Oakley. When the brain is in focused mode, you can get started on the task at hand. But deep understanding is not fully accomplished in this mode.

Diffused thinking occurs when you allow your mind to wander, to imagine and to daydream. In this mode, the brain is still working —  consolidating information and “making sense of what you are trying to learn,” says Oakley. If a concept is easy for you to grasp right off, the focused mode might be sufficient, but if a new skill or concept “takes consideration, you have to toggle back and forth between these two modes of thinking as you get to true understanding of the material — and this doesn’t happen quickly.”

Because toggling is essential to learning, teachers and students need to build downtime into their day — time when learning can “happen on background” as you play a game, go on a walk or color a picture. It’s also one reason why sleep is so vital to healthy cognitive development.

Since students tend to equate speed with smarts, Oakley suggests sharing this metaphor: “There’s a race car brain and a hiker brain. They both get to the finish line, but not at the same time. The race car brain gets there really fast, but everything goes by in a blur. The hiker brain takes time. It hears birds singing, sees the rabbit trails, feels the leaves. It’s a very different experience and, in some ways, much richer and deeper. You don’t need to be a super swift learner. In fact, sometimes you can learn more deeply by going slowly.”

2. Chains and Chunks

In cognitive psychology, “chunking” refers to the well-practiced mental patterns that are essential to developing expertise in a topic.  Oakley prefers the image of a “chain” when she explains this to students.

Learning is all about developing strong chains. For example, says Oakley, when you are first learning how to back up a car, you have to consciously think about each step, from how to turn the steering wheel to how to use your mirrors. But “once that process is chained, it’s easy” — it becomes automatic. Similarly, once solving certain equations becomes automatic in math, students can apply these equations to more complex problems.

Teachers can help students identify the procedures in a unit of study that they need to master in order to take their learning to the next level —  from the steps of the scientific method to fundamental drawing techniques.

“Any type of mastery involves the development of chains of procedural fluency. Then you can get into more complex areas of fluency,” says Oakley. Here’s another way to think about it. We all have about four slots of working memory that we can use to problem-solve in the moment. One of those slots can be filled with an entire procedural chain —  and then you can put new information in the other slots.

3. The Power of Metaphor

“Metaphor and analogy are extraordinarily powerful teaching tools and very often underused,” says Oakley.  “When you are trying to learn something new, the best way to learn it is to connect it with something you already know.”

The formal term for this is “neural reuse” —  the idea that metaphors use the same neural pathways as the concept a metaphor is describing. So familiar metaphors allow a learner to draw on a concept they have already mastered and apply it to a new situation. Or as Oakley says, metaphors “rapidly on-board” new ideas. For example, says Oakley, comparing the flow of electrons to the flow of water is a way to “jump-start students’ thinking.”

As part of her research, Oakley reached out to thousands of professors who are considered top teachers in their fields. “Many of these professors had a secret that they used in their teaching: metaphor and analogy. It was like a secret shared handshake.” Oakley encourages teachers to not only use metaphor but to challenge students to develop their own metaphors as a study strategy.

4. The Problem of Procrastination

Oakley says that procrastination is the number one challenge facing most learners. To train the brain to systematically focus and relax — to toggle — she  recommends the “Pomodoro Technique.”

Developed by Francesco Cirillo, this strategy uses a timer to help the learner work and break at set intervals. First, choose a task to accomplish. Then, set a timer for 25 minutes and work until the timer goes off.  At that point, take a five-minute break: stand up, walk around, take a drink of water, etc. After three or four 25-minute intervals, take a longer break (15 – 30 minutes) to recharge. This technique “trains your ability to focus and reinforces that relaxing at the end is critical to the process of learning,” says Oakley.  Teachers and administrators can build a similar rhythm into the schoolday, providing brain breaks and movement time to help students toggle between focused and diffused thinking.

5. Expanding Possibilities

When we teach children and teenagers how they learn, we can blow open their sense of possibility, says Oakley. “I would tell students, you don’t just have to be stuck following your passion. You can broaden your passions enormously. And that can have enormous implications for how your life unfolds. We always say ‘follow your passions’ but sometimes that locks people into focusing on what comes easily or what they are already good at. You can get passionate about — and really good at — many things!”

A geneticist take on learning ability involves the study of chromosome 6, using a technique called genome-wide association study (GWAS) that involved over 125,000 individuals. Geneticists and sociologist looked at these individuals’ level of education attained and scores in math and English achievement tests found a link between scholastic achievement and their genetic variants. Find out if you have the genetic make-up to learn with our MightyDNA test: https://mightydna.com/shop/abilities/

How to make our fat’s health rise when most of us would prefer that its quantity decline.

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How to make our fat’s health rise when most of us would prefer that its quantity decline

Most of probably think of our fat tissue as inert and undesirable. But our fat is, in fact, a busy and necessary tissue, producing and sending out multiple biochemical signals that affect biological operations throughout the body.

Fat tissue’s most important responsibility, however, is to securely store fat, and we should hope that it performs this function well. Provocative recent research in both animals and people has found that, if a person’s or animal’s fat tissue is relatively leaky, allowing fatty acids to ooze into the bloodstream, those roving fat blobs can accumulate in other tissues, particularly the muscles and liver. Once there, they contribute to the development of insulin resistance, a serious metabolic condition that often leads to diabetes.

In a study published earlier this year, for instance, scientists from the University of Michigan and elsewhere found that if overweight men and women had low levels of fatty acids in their bloodstream, they also were metabolically healthier than other overweight adults.

Even more interesting, they generally also had healthy fat, the scientists found, with biopsies showing less inflammation and scarring than in the fat from other overweight men and women. (This fat was subcutaneous, meaning it came from just beneath the skin.)

Presumably, the scientists speculated, this robust fat was leaking less than the frailer variety.

But that study did not examine why some people had healthier fat than others and whether the condition of anyone’s fat tissue might be changed.

So for the new study, which was published last month in the Journal of Applied Physiology, the same group of scientists began to consider exercise.

Exercise, of course, is well known to affect the amount of fat we store, since muscles use fatty acids as fuel. Exercise also is believed to prompt small amounts of white fat to transform into brown fat, a particularly desirable form of fat that burns a lot of calories.

But it has not been clear whether exercise directly alters the health of white fat tissue.

To find out, the researchers first gathered 20 men and women who were overweight but did not have insulin resistance. Eight of them exercised regularly. The others had been sedentary.

The researchers tested their volunteers’ body compositions and took fat samples. Then they had each volunteer exercise on a treadmill or stationary bike for an hour at a moderately tiring pace.

An hour later, the scientists repeated the fat biopsies.

Examining the various tissues microscopically afterward, the researchers found several tantalizing differences.

In almost all of the volunteers, the fat tissue after exercise showed greater amounts of a protein that is known to contribute to the development of more blood vessels.

This change could be important over time, says Jeffrey Horowitz, a professor of movement science at the University of Michigan School of Kinesiology who conducted the experiment with Douglas Van Pelt (now a postdoctoral researcher at the University of Kentucky) and others.

“More blood vessels in tissue means greater blood flow,” he says, with augmented delivery of oxygen and nutrients and better overall tissue health.

Interestingly, the fat tissue from those volunteers who regularly exercised also showed a small but meaningful increase in genetic activity related to blood vessel proliferation, suggesting that their tissue was more primed than that from the sedentary volunteers to start creating additional blood flow.

Their fat tissue also showed a slight increase in the gene expression of a substance that helps to reduce inflammation.

These alterations were not enormous, Dr. Horowitz says. They were subtle. But they occurred consistently and after a single session of exercise, he points out, and might, with continued exercise, be expected to improve fat health over time.

This study was small, however, and very short-term and did not look at whether other amounts or types of exercise would have comparable effects within fat. It also did not measure whether exercise actually changed the amounts of fat in the bloodstream and, since the volunteers were overweight, cannot tell us whether the effects would be comparable in people whose weight was normal.

Perhaps most fundamentally, the study concentrated on how to make our fat’s health rise when most of us would prefer that its quantity decline.

Dr. Horowitz understands. “There is no doubt that the best thing for metabolic health is to lose weight.”

But at this time of year, he says, when fat gain is common, a brisk walk or jog might make this added fat healthier and more stable, and the broader effects on our bodies a little less concerning.

In regards to fat tissue, as fat cells become larger, they produce more leptin. This rise in leptin indicates that fat stores are increasing. In the hypothalamus, the binding of leptin to its receptor triggers a series of chemical signals that signals that affect hunger and help produce a feeling of fullness (satiety). LEPR gene variant that cause leptin receptor deficiency prevent the receptor from responding to leptin, leading to the excessive hunger and weight gain associated with this disorder. Do you want to find out if you have the genetic variant in  becoming obese?  Find out with MightyDNA.com:  https://mightydna.com/shop/weight-loss-and-obesity/