I took a look at Shell's first ever 1.5C scenario and found that it is... remarkably similar to its “well-below 2C” scenario.

Oil, gas, coal, solar.... all basically unchanged.

The key difference: A new forest the size of Brazil to suck up the extra CO2.

Including "nature-based solutions" in the outlook brings forward the date for net-zero emissions to 2058.

Without them their pathway for CO2 emissions is the same as the previous one.

(It's also towards the higher end of 1.5C emissions pathways.)
The "Brazil-sized" forest idea isn't actually new, it has been kicking around for a couple of years.

It was referenced in the "well-below 2C" scenario although not formally included in it, and Shell's CEO has been framing it as the only viable way of getting to 1.5C.
Fine, but who is going to plant all those trees? Well... Shell says it will plant some of them.

Only yesterday Shell said forests were a key part of its net-zero strategy.

Not everyone is convinced though

https://t.co/RaJm7tOHxb
Given that Shell's 1.5C scenario also sees a big scaling up of bioenergy, the question remains: where are all those trees and bioenergy crops going to go?
Shell's scenario sits towards the higher end of 1.5C scenarios that scientists have come up with for energy use, oil, coal and solar

For emissions removed using carbon capture technology, it actually sits at the lower end. 1.5C scenarios rely _a lot_ on (largely untested) CCS
So getting to 1.5C is hard and most estimates say it will rely on lots of carbon removal.

Of course, the more fossil fuels are burned, the harder it gets.

Shell says oil and gas, “will remain significant for decades” and “there needs to be continued investment in…supply”.
Finally, Shell says it makes these scenarios not as forecasts or to reflect a business plan, but rather as “a useful tool for exploring future possibilities”.

A legal disclaimer adds:

“Ultimately, whether society meets its goals to decarbonise is not within Shell’s control.”
For more details on all of this, check out my analysis of Shells "Sky 1.5 scenario" in this piece >>>>

https://t.co/Ngj6MRMMTk

More from Science

JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz


2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.

3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.


4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.


5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.
Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).

Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.


You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.

The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.

In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.

The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.
"The new answer to a 77-year-old problem"

😭


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https://t.co/8fKDiKjSWc


https://t.co/jkaicC1F2x


https://t.co/PpxWT4Jef4
All modern research questions frame your mindset and self-frame research paradigm. Broad thinking: how little of everything can a citizen survive on; how cheap can your upkeep be? /1


When an American patient lands in an Austrian hospital for a back problem, a doctor tells him to perform a set of exercises.

- How many?
- Do you have anything else to do? /2

This interchange illustrates two mindsets colliding at bedside. How little can I get away with vs there is no limit to effort when it comes to your wellness. /3

When you were robbed of movement, somebody started selling you exercise. To understand that digging a ditch, to build a house, or to carry a child around, or waking to your grandparents for an hour is not the same as jogging on a treadmill... will reveal what research hides.
/4

When I talk about doing a purposeful activity outdoors, I look at complexity of movement, purpose, meaning, sun, and air, even an opportunity to meet a neighbor... that is now reduced to a calcium pill, vitamin D, an antidepressant, an osteoporosis shot, and an oxygen tank. /5

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