Are We Really Prepared for the Genetic Revolution?
Genetic data could lead to more personalized, meaningful education, but only if parents, teachers and policymakers understand genetics well enough to correctly use the information

Are We Really Prepared for the Genetic Revolution?
Credit: Sebastian Kaulitzki Getty Images
The following essay is reprinted with permission from The Conversation, an online publication covering the latest research.

When humans’ genetic information (known as the genome) was mapped 15 years ago, it promised to change the world. Optimists anticipated an era in which all genetic diseases would be eradicated. Pessimists feared widespread genetic discrimination. Neither of these hopes and fears have been realised.

The reason for this is simple: our genome is complex. Being able to locate specific differences in the genome is only a very small part of understanding how these genetic variants actually work to produce the traits we see. Unfortunately, few people understand just how complex genetics really is. And as more and more products and services start to use genetic data, there’s a danger that this lack of understanding could lead people to make some very bad decisions.

At school we are taught that there is a dominant gene for brown eyes and a recessive one for blue. In reality, there are almost no human traits that are passed from generation to generation in such a straightforward way. Most traits, eye colour included, develop under the influence of several genes, each with its own small effect.

What’s more, each gene contributes to many different traits, a concept called pleiotropy. For example, genetic variants associated with autism have also been linked with schizophrenia. When a gene relates to one trait in a positive way (producing a healthy heart, say) but another in a negative way (perhaps increasing the risk of macular degeneration in the eye), it is known as antagonistic pleiotropy.

As computing power has increased, scientists have been able to link many individual molecular differences in DNA with specific human characteristics, including behavioural traits such as educational attainment and psychopathy. Each of these genetic variants only explains a tiny amount of variation in a population. But when all these variants are summed together (giving what’s known as a characteristic’s polygenic score) they begin to explain more and more of the differences we see in the people around us. And with a lack of genetic knowledge, that’s where things start to be misunderstood.

For example, we could sequence the DNA of a newborn child, calculate their polygenic score for academic achievement and use it to predict, with some degree of accuracy, how well they will do in school. Genetic information may be the strongest and most precise predictor of a child’s strengths and weaknesses. Using genetic data could allow us to more effectively personalise education and target resources to those children most in need.

But this would only work if parents, teachers and policymakers have enough understanding of genetics to correctly use the information. Genetic effects can be prevented or enhanced by changing a person’s environment, including by providing educational opportunity and choice. The misplaced view that genetic influences are fixed could lead to a system in which children are permanently separated into grades based on their DNA and not given the right support for their actual abilities.

In a medical context, people are likely to be given advice and guidance about genetics by a doctor or other professional. But even with such help, people who have better genetic knowledge will benefit more and will be able to make more informed decisions about their own health, family planning, and health of their relatives. People are already confronted with offers to undergo costly genetic testing and gene-based treatments for cancer. Understanding genetics could help them avoid pursuing treatments that aren’t actually suitable in their case.

It is now possible to edit the human genome directly using a technique called CRISPR. Even though such genetic modification techniques are regulated, the relative simplicity of CRISPR means that biohackers are already using it to edit their own genomes, for example, to enhance muscle tissue or treat HIV.

Such biohacking services are very likely to be made available to buy (even if illegally). But as we know from our explanation of pleiotropy, changing one gene in a positive way could also have catastrophic unintended consequences. Even a broad understanding of this could save would-be biohackers from making a very costly and even potentially fatal mistake.

When we don’t have medical professionals to guide us, we become even more vulnerable to potential genetic misinformation. For example, Marmite recently ran an ad campaign offering a genetic test to see if you either love or hate Marmite, at a cost of £89.99. While witty and whimsical, this campaign also has several problems.

First, Marmite preference, just like any complex trait, is influenced by complex interactions between genes and environments and is far from determined at birth. At best, a test like this can only say that you are more likely to like Marmite, and it will have a great deal of error in that prediction.

Second, the ad campaign shows a young man seemingly “coming out” to his father as a Marmite lover. This apparent analogy to sexual orientation could arguably perpetuate the outdated and dangerous notion of “the gay gene”, or indeed the idea that there is any single gene for complex traits. Having a good level of genetic knowledge will enable people to better question advertising and media campaigns, and potentially save them from wasting their money.

My own research has shown that even the well-educated amongst us have poor genetic knowledge. People are not empowered to make informed decisions or to engage in fair and productive public discussions and to make their voices heard. Accurate information about genetics needs to be widely available and more routinely taught. In particular, it needs to be incorporated into the training of teachers, lawyers and health care professionals who will very soon be faced with genetic information in their day-to-day work.

This article was originally published on The Conversation. Read the original article.

ABOUT THE AUTHOR(S)
Robert Chapman
PhD Candidate, Goldsmiths, University of London.

Tesla Model 3 travels 606 miles on a single charge in new hypermiling record

Hypermiling is the practice of driving vehicles as efficiently as possible in order to achieve the longest distance possible on one charge/fuel tank.

It’s not a useful way to determine the range of a vehicle for normal driving, but it’s an interesting way to see how the way someone drives can impact fuel efficiency.

Tesla owners have now established a new hypermiling record in a Model 3 by traveling 606 miles on a single charge.

This weekend, Tesla owners Erik Strait and Sean Mitchel set out to achieve the record on a public road circuit.

Their goal was 600 miles (965 km) and they narrowly beat it for what could very well be the Guinness World Record for the longest distance driven in a production electric car on a single charge.

The attempt basically consists of driving at extremely low-speed in order to get the most efficient driving speed for the vehicle while also not using power consuming onboard features like climate control.

In the case of the Model 3, Strait and Mitchel found that maintaining the speed under 25 mph (40 km/h) was ideal.

32 hours later, they had the record.

They streamed the entire hypermiling run on Youtube, which you can watch below, but a fair warning: hypermiling might very well be the most boring motorsport to watch by a long shot:

But the results were quite interesting. Mitchell reported a very efficient 110 Wh per mile for a total 66 kWh used during the run:

View image on Twitter

Sean M Mitchell@seanmmitchell

Final #Model3 hypermile numbers from @teslainventory and I: 606.2 miles (975 km), 66 kWh, and 110 wh/mi, and 32 hours of driving. At its peak it was 108F in the cabin with no a/c running. Thank you @Tesla and @elonmusk for making such an incredible piece of machinery!

11:16 PM – May 26, 2018

• 216

• 71 people are talking about this

Twitter Ads info and privacy

As we previously reported in our feature on the Model 3 battery pack architecture, the Long Range Model 3 battery pack has a capacity of about 74 kWh, but they surprisingly got much less usable energy in their run and it’s not clear why.

There’s always some capacity left as a buffer, but it seems higher than usual in this case.

Electrek’s Take

It’s a very impressive performance – though I wouldn’t be surprised if it eventually gets surpassed with a route that results in fewer stops.

But it’s still a nice achievement and the newest hypermiling record for a Tesla vehicle – beating the previous Tesla Model S hypermiling record of just over 900 km (560 miles) on a single charge in a Model S P100D.

Interestingly, when talking about hypermiling, Tesla CEO Elon Musk said in 2015 that he would expect people to reach 600 miles (965 km) on a single charge in a Tesla vehicle in 2017.

The comment resulted in a lot of misinformation as media reported it as if Tesla plans to release a vehicle with a real-world range of 600 miles.

Of course, it’s not the case at all since hypermiling is in no way representative of the actual normal range of a vehicle, electric or not.

It’s a fun way to see how much efficiency you can get out of a car.

NanoPC-T4: A powerful Raspberry Pi alternative without the bottleneck issues

Scientists Just Found an Unexpected Link Between Tuberculosis And Parkinson’s Disease

What could they possibly have in common?

MIKE MCRAE

23 MAY 2018

At first glance, tuberculosis and Parkinson’s disease are about as different as diseases get, but a new study has found an important link between the two.

This connection is down to a protein called leucine-rich repeat kinase 2 (LRRK2), and not only could it help develop new treatments for both diseases, but it also demonstrates a key connection between the brain and our immune system.

Parkinson’s disease is a neurodegenerative disorder that develops as nerve cells in the brain die, depriving the tissue of a key chemical messenger called dopamine.

Exactly what causes these cells to die in some people is a mystery, though an increasing number of signs point to a confused immune system.

Mutations in LRRK2 have also been implicated in the development of Parkinson’s, a find that is already helping scientists who are developing a new class of treatments.

And research led by a team from the Francis Crick Institute and Newcastle University in the UK has now explained how LRRK2 interferes with one of the processes white blood cells use to kill bacteria.

This is where tuberculosis (TB) comes in, because it’s an infection caused by the bacterium Mycobacterium tuberculosis, usually within lung tissue.

In most cases, our bodies do a fairly good job of dealing with the infection by sending in white blood cells called macrophages – they swallow the microbes and pack them inside bubbles called phagosomes.

Once the germs are safely trapped inside these compartments, packets of enzymes called lysosomes click into place and empty their bacteria-dissolving contents, killing the infection.

Broad studies of the human genome have hinted at some kind of relationship between inflammation caused by Mycobacterium diseases – including TB and leprosy – and the LRRK2 gene.

What’s been missing are the details; just how does a gene connected to Parkinson’s disease mess with the way white blood cells deal with mycobacteria?

To get a better idea of what was going on at a cellular level, the team developed several experiments that exposed the chemical’s functions.

It turns out that LRRK2 regulates a process that connects those bacterial jail cells with their horror-show bubbles of death, effectively preventing them from joining. Meanwhile, macrophages that were engineered to have LRRK2 missing had no problem digesting their TB captives.

Not only does this discovery shed light on how TB and leprosy infections might get a foothold, but it could also explain why certain proteins accumulate inside nerves.

“We think that this mechanism might also be at play in Parkinson’s disease, where abnormal masses of protein called ‘Lewy bodies’ build up in neurons in the brain and cause damage,” says one of report’s first authors, Susanne Herbst from the Francis Crick Institute.

This makes the find a two-for-the-price-of-one deal, and the findings could potentially lead to new ways of dealing with Parkinson’s – since researchers don’t normally think about it in immunology terms.

“The dogma in the Parkinson’s field has been to focus almost exclusively on what is happening to neurons in the brain to make them degenerate,” says biochemist Patrick Lewis from the University of Reading.

“This study reinforces why we should think more broadly about the events that cause neurodegeneration, and that some of the answers to Parkinson’s disease might come from immunology.”

Our global society is an aging one, and with that comes an increasing number of neurodegenerative conditions such as Parkinson’s. We’re going to need all the help we can get in keeping those numbers low.

As for tuberculosis, the timing also couldn’t be better. A lengthy course of antibiotics is usually enough to clear up an infection, but the disease still manages to kill more than a million people each year.

In recent years, strains of TB Mycobacterium have emerged that show resistance to one or more of the medications commonly used to treat it. That means the writing’s on the wall for a possible resurgence of this deadly disease, one that could prove difficult to control without new classes of drugs.

Knowing more about potential weak points in our own immune system is looking critical, which makes research drawing links between such disparate diseases all the more valuable.

This research was published in The EMBO Journal.

Learn More

1. Link between tuberculosis and Parkinson’s disease discoveredThe Francis Crick Institute, ScienceDaily
2. New Drug Target Identified For Fighting Parkinson’s DiseaseJohns Hopkins Medical Institutions, ScienceDaily
3. A defence mechanism that can trap and kill TB bacteriaThe Francis Crick Institute, ScienceDaily

1. Microbe Profile: Mycobacterium tuberculosis: Humanity’s deadly microbial foeStephen V. Gordon et al., Microbiology
2. Blood Assay Can Predict Latent TB That May Become Active in Children, Study Finds360Dx
3. International Team Developing Reagent Test That Could Broaden Access to TB Screening360Dx

Cannabis May Protect the Brain Against Stress and Injury, and Here’s Why

Each year, around 2 million Americans experience a sport-related traumatic brain injury (TBI). Soldiers are also at elevated risk for TBI; 17% of deployed soldiers to Iraq experienced a TBI, and among them, 59% experienced multiple TBIs. On a less overt level, our stress levels are on the rise. And to make matters worse, there’s a direct link between stress and increased risk for cardiovascular effects like heart attack and stroke. Both brain injury and cardiovascular events elevate risk for age-related brain disease like dementia.

RELATED STORY

Can Cannabis Prevent and Treat Traumatic Brain Injury?

Do we have tools at our disposal to mitigate these risks? Sure. Proper nutrition, maintaining healthy body weight, and regular exercise all help. Helmets do, too. But a growing body of research over the last couple decades suggests that there’s another potential strategy to making the brain more resilient to the damaging effects of injury, the changes associated with stress, and the effects of age. It involves cannabis.

What Happens When the Brain Is Injured?

It seems intuitive that the greatest amount of brain damage occurs at the time of physical trauma.  But for most closed head injuries and cardiovascular events, the majority of damage occurs during the recovery period—minutes to days after the injury. It’s this delayed response that inflicts long-term havoc on the brain.

RELATED STORY

How Does Cannabis Consumption Affect the Brain?

Many current strategies to protect the brain after injury act to reduce this secondary response to injury, but by the time these interventions are initiated, it may be too late. A better strategy would be to intervene before the trauma in at-risk individuals to weaken the brain’s own damaging response should one occur. Some elements in cannabis, like THC and especially cannabidiol (CBD), seem ideal for such a task.

There are three general mechanisms that damage the brain in the period after the trauma, and it’s thought that THC and CBD can protect against each:

• Increase in excitatory brain chemicals. Injury causes the massive release of the excitatory brain chemical, glutamate. Glutamate plays an important role in an uninjured brain, but its levels need to be tightly regulated. Too much glutamate can kill brain cells, which is what can happen following injury.
• Increase in free radicals. Injury releases harmful chemicals called free radicals that cause damage to brain cells by damaging DNA, impairing the cell’s machinery, and even causing cell death. Free radicals are a byproduct of normal cell function and we have mechanisms of neutralizing them to limit damage. But after injury, their levels become so high that only potent anti-oxidants can limit their damaging effects.
• Increase in brain inflammation. Injury activates the brain’s inflammatory response to repair the damage. Unfortunately, this repair process can cause permeant changes in the way brain cells communicate with one another. It’s becoming increasingly appreciated that brain inflammation contributes to the development of age-related diseases like Alzheimer’s and dementia. Therefore, the tools used to protect the brain from secondary injury may also prevent or reduce the severity of cognitive decline with age.’

How Cannabis Can Help Prevent Damage in the Brain 

The endocannabinoid system provides a framework for many of cannabis’ protective benefits. The cannabinoid type I and II receptors (CB1 and CB2) are powerful regulators of glutamate release, can be anti-inflammatory, and facilitate anti-oxidant effects.

RELATED STORY

What Is the Endocannabinoid System and What Is Its Role?

In support of THC’s protective benefits, TBI patients with THC in their blood were more likely to survive their injury than those without.

This important role for CB receptors supports the benefits of THC, which directly activates CB1 and CB2 receptors, and CBD, which indirectly activates them. CB1 receptors are found on brain cells and their activation by endogenous cannabinoids or THC dampens their communication.

Particularly, CB1 receptors have a profound ability to reduce glutamate release, highlighting the potential for prominent cannabinoids to suppress the harmful effects of glutamate following brain trauma. Since excessive glutamate signaling is a main contributor to early stage damage after brain injury, this is an important place to start to limit the risk of severe brain damage and even death.

RELATED STORY

CTE in Professional Football Players, and the Potential of CBD to Address the Crisis

In support of THC’s protective benefits, TBI patients with THC in their blood were more likely to survive their injury than those without (only 2% of those with THC in their blood did not survive their injury, compared to 12% without THC).

Low doses of THC can be anti-inflammatory, but high-doses may increase inflammation, which highlights the importance of proper dosing.

THC’s protection against brain damage has also been observed in controlled pre-clinical studies with lab animals. Mice who underwent a simulated stroke had fewer signs of brain damage if they were given either THC or CBD prior to stroke, but only CBD was effective at reducing signs of damage if given afterwards. Importantly, mice given THC for two weeks prior to a stroke developed tolerance to its brain-protecting abilities. This tolerance isn’t observed with repeated CBD treatment, suggesting that CBD may be a better long-term protective strategy because its strength doesn’t decrease with repeated use, and its protective abilities continue after the damaging event.

How were THC and CBD protective? Reduced glutamate signaling protects brain cells from dying after an injury and cardiovascular event. But the potential for behavioral recovery also depends on the levels of free radicals and brain inflammation. Low doses of THC can be anti-inflammatory, but high-doses may increase inflammation, which highlights the importance of proper dosing.

RELATED STORY

A Physician’s Perspective on Optimal Cannabis Dosing

Cannabis Protects Against Subtle Brain Changes, Too

Cannabis may also make the brain more resilient to the harmful effects of chronic stress and the aging process. Both chronic stress and aging are associated with a reduction in new brain cell production in a brain region called the hippocampus, one of two known brain areas where new brain cells are produced in adulthood. These new brain cells are important for many brain functions including learning and memory, reducing anxiety and depression, and keeping the body’s stress response in check.

RELATED STORY

What Are the Best Cannabis Strains for Anxiety?

Activating CB1 receptors can facilitate the growth of new brain cells. In part through this mechanism, low doses of THC can preserve cognitive abilities in old mice by protect the brain from age-related changes (covered previously by Leafly). CBD can indirectly activate CB1 receptors by increasing levels of the endogenous cannabinoid, anandamide. It’s in part through this increase in anandamide levels that CBD is thought to protect against the damaging effects of chronic stress on the brain.

More studies are needed to identify dose and duration of cannabis use to achieve maximum protective benefits, and whether there are some conditions in which cannabis could exacerbate the damage to the brain. But in the meantime, many may needlessly suffer the long-term consequences of brain trauma.

Sleeping in on weekends can help you live longer: Study

Physical fitness could protect against too much sedentary time

Results from a UK study have added to the growing body of research that an active lifestyle can help offset the negative health effects of too much time spent sitting, suggesting that those who are fitter and stronger are less likely to be impacted by sedentary time.

Carried out by researchers at Glasgow University, the study analyzed data on 391,089 participants taken from the UK Biobank, a large, long-term study that includes data on all-cause mortality, cardiovascular disease (CVD) and cancer incidence, along with television viewing, computer screen time, grip strength, fitness and physical activity.

The team found that both types of screen time — leisure time spent watching a television or time in front of a computer screen — were significantly associated with all health outcomes, with higher levels of screen time associated with a higher risk of all-cause mortality, cancer, and CVD.

However, screen time had almost double the impact on the risk of death, cancer, and CVD in those who had low grip strength or low fitness levels compared to those who had the highest levels of fitness and grip strength.

A similar association was also observed between physical activity and all-cause mortality and cancer incidence.

The team noted that the use of self-reported screen time and physical activity data may have impacted the accuracy of the findings, and as an observational study no conclusions can be made about cause and effect.

However, they added that the results suggest that increasing strength and fitness may provide some protection against the negative health effects of too much time spent sitting down in front of a screen.

“Our study shows that the risks associated with sedentary behavior are not the same for everyone; individuals with low physical activity experience the greatest adverse effects,” commented corresponding author Dr. Carlos Celis-Morales.

“This has potential implications for public health guidance as it suggests that specifically targeting people with low fitness and strength for interventions to reduce the time they spend sitting down may be an effective approach.”

“While fitness testing can be difficult in healthcare and community settings, grip strength is a quick, simple and cheap measure, therefore it would be easy to implement as a screening tool in a variety of settings,” Dr. Celis-Morales added.

The results can be found published online in the journal BMC Medicine.