Survival of the Sickest is one of the most engaging educational books I have come across for a long time. The reason for this is that its scientific content has been woven into narrative by co-writer Jonathan Prince (a Clinton speechwriter who should know a few things about the emotional power of narrative).
First of all, the ingeniously accurate title challenges the simple-mindedness of the phrase "Survival of the Fittest". That notorious trite summary was wrongly attributed to Darwin, then over time misleadingly foisted on the masses through poor teaching and poor journalism, as an explanation of the process of evolution.
The popular misrepresentation of evolution, is that living things progress from generation to generation with randomly created mutations, but only the fittest specimens with the best mutations survive. Even with a cursory understanding of genetics, the mathematics of this made no sense to me. The chance seemed very small that a random mutation could occur in one generation that could KEEP all the best of its ancestor, while ADDING a new superior genetic feature.
For a long time I have only known one example that challenged this view of evolution as a continuous and ever-increasing upward drive toward Genetic Superiority. It was sickle-cell anaemia, where a misshapen red-blood cell that loses a lot of its oxygen-transport capacity, is nonetheless an excellent natural advantage against malaria.
Survival of the Sickest gives new genetic medical examples in Man to show how random mutations often occur causing the LOSS of one useful genetic feature, which accidentally turn out to be an advantage under certain enviromental conditions. Evolution is a constant process of change, and the loss of useful features often comes first and becomes the foundation for further additions and losses.
The first example covers haemochromatosis, a hereditary disorder whose sufferers cannot regulate their blood iron levels, which can build up and damage their organs and can cause death. The preferred treatment is periodic bloodletting (phlebotomy).
One in 200 people of Western European descent have full haemochromatosis, yet as many as one in 3 carry at least one copy of the haemochromatosis gene. How did such a genetic disorder become so widespread in the population?
Iron-locking is usually part of the immune system's acute phase response. It starves invading pathogens of iron. People with haemochromatosis have a form of iron-locking that operates continuously. Particularly their macrophages (one of the types of white blood cell) are so iron-deficient that pathogens engulfed by the macrophages are starved of iron and so prevented from multiplying into the lymphatic system. This probably was a huge advantage when the bubonic plague (yersina pestis) attacked Western Europe.
So haemochromatosis is a superb example of recent human evolution. Initially, normal iron-regulating behaviour would have been lost in a few random individuals. Before Yersina Pestis these individuals would have moaned about aches and pains and died young, while their fellow men lived long and lusty reproductive lives. When Yersina Pestis came along the tables were turned. The ones with the haemochromatosis mutation suddenly became the healthiest and fittest people left alive. They got all the women, or had all the children. Since then continuing evolution has meant that the advantages of haemochromatosis have further varied with other features and been further selected, while the disadvantages have been further dying out. To this extent one third of the population have the genetic advantage of at least one haemochromatosis gene, but only one in two hundred people (not one ninth, as you would expect) actually have it in a combination where it is by itself a disease.
The book also examines the evolutionary roles of Diabetes, high cholesterol, favism (an enzyme deficiency that makes the consumption of fava/broad beans fatal). It looks at how parasites and pathogens continually evolve with their hosts. It explores genetic redundancy and ventures also into epigenetics and has an eloquent indomitable assault on the educators who have ritually ridiculed Lamarck in the teaching of evolution. Finally it explores the evolution of ageing and age-related diseases such as cancer. I will summarize those in a second installment, when time permits.
****
Away from the book, let us revisit the scenario of how Sickle-cell anaemia's evolution may have started and how it might continue to unfold:
Sickle-cell arises randomly in one individual in the sub-Sahara. It is the loss of normal function in haemoglobin and red-blood cells. Without malaria, that individual would be disadvantaged and die out. With malaria, instead of being a disability, the sickle-cell feature actually makes the individual fitter and healthier than his neighbours. He breeds and his offspring have the same advantage. Eventually the incidence of sickle-cell rises to a level in the population where its growth levels off, say at 10%. This is because the advantage of malaria resistance does not sufficiently outweigh the disadvantage of a shorter and attack-filled lifespan, for this population to compete with the non-sickle-cell population.
The sickle-cell presence in the population stabilizes, say, for a thousand years, as being only a disabling condition that confers advantage against malaria. During this time, other random genetic mutations (for other genes, not sickle-cell) in the population continue to occur at each generation, in all sorts of combinations. None of these turn out to be particularly useful, but neither are they a disadvantage, so most changes and mixes of changes survive and are passed on at every generation.
Eventually, some mixture of lost and added genes and mixing within the population spawns a new individual who still has sickle-cell, but who has also at last gotten some genetically working form of compensation for its disadvantage. This individual and its descendants thrives in the population, in malarial conditions, displacing all other people with no sickle-cell feature.
Finally a future scientist comes along to marvel at sickle cell and prononounces these people to be superior with their malarial resistance, ignoring the fact that for a thousand years, the feature was considered a sickness and disability.
So now do you understand how survival of the sickest works in evolution, and how it is more likely than survival of the fittest? The genes of the future fittest lurk amongst those who do not appear today to be the fittest.