He spent nearly two decades writing and rewriting his two-volume autobiography. He struggled to control his public image, even going so far as asking to have his letters returned to him and then destroying those that he felt might damage his reputation. All the while, English politics were drifting to the left.
Anything that had any scent of government regulation about it, he associated with socialism. Science and philosophy had moved on as well. Still, as remote as Spencer and his ideas seem today, he was a vital figure in his own time, Barton says. Dan Falk is a science journalist based in Toronto.
Herbert Spencer introduced the phrase "survival of the fittest" in his book, Principles of Biology. Herbert Spencer as a young man Engraving by Geo. Perine Born in Derby in central England, Spencer was largely self-taught. Elaine Aron, who has spent years studying introverts, and is one herself. In explaining the idea of different personality traits as part of group selection in evolution, Aron offers this story in an article posted on her website :.
But the non-sensitive ones [extroverts] would be the ones more likely to go out and face the lion. Hence there are more of them than there are of us, since they are willing and even happy to do impulsive, dangerous things that will kill many of us. But also, they are willing to protect us and hunt for us, if we are not as good at killing large animals, because the group needs us. We have been the healers, trackers, shamans, strategists, and of course the first to sense danger.
So together the two types survive better than a group of just one type or the other. The lesson is this: Groups survive better if they have individuals with different strengths to draw on.
The more tools you have, the more likely you can complete a job. The more people you have that are different the more likely you can survive the unexpected.
How then, does one define the group? Who am I willing to help? My immediate little group. But history is full of examples of those who sacrificed significantly for their tribes or sports teams or countries.
That may explain why I will throw myself in front of a speeding car to protect my child, but the beaches of Normandy were stormed by thousands of young, childless men. As technology shrinks our world, our group expands. Technological advancement pushes us into higher degrees of specialization, so that individual survival becomes clearly linked with group survival.
I know that I have a vested interest in doing my part to maintain the health of my group. Many of these individuals may not produce enough antibodies or killer T cells to counter the virus, which allows the virus to multiply unchecked and cause a severe infection.
Normally, there is a wide range of microorganisms, both harmful and benign, that live in harmony in the lungs. However, as the coronavirus spreads, it is likely that the infection and the inflammation that ensues will disrupt this balance, allowing harmful bacteria present in the lungs to dominate. Also, because ACE2 is present throughout the body, the killer T cells from phase 1 can destroy virus-infected cells across multiple organs, causing more widespread destruction.
Thus, patients that produce excessive cytokines and T cells can die from injury not only to the lungs but also to other organs such as the heart and kidneys. Because the majority of people recover from coronavirus infection , it is likely that a vaccine that triggers neutralizing antibodies and T cells to block the virus from getting into the cells and replicate is likely to be successful.
Additionally, in patients who transition to a more severe form such as ARDS and cytokine storm, which is often lethal, there is an urgent need for novel anti-inflammatory drugs.
These drugs can broadly suppress the cytokine storm without causing excessive suppression of immune response, thereby enabling the patients to clear the coronavirus without damage to the lung and other tissues.
There may be only a narrow window of opportunity during which these immunosuppressive agents can be effectively used. Such agents should not be started at an early stage of infection when the patient needs the immune system to fight the infection, but it cannot be delayed too long after ARDS development, when the massive inflammation is uncontrollable.
This window of anti-inflammatory treatment can be determined by monitoring the antibody and cytokine levels in patients. This means a strong immune response in phase 1 to clear the primary coronavirus infection and inhibit its spread in the lungs.
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