The father of the science of evolutionary medicine, Randolph (Randy) Nesse, has a favorite aphorism: “Medicine without evolution is like engineering without physics.” In the same way that it would be impossible to imagine building the Rosetta spacecraft, sending it 300 million miles to rendezvous with Comet 67P, and successfully deploying the Philae lander, chock-full with sampling instruments, without physics and specifically Newtonian mechanics, it proves similarly impossible, for instance, to get to the root of the horrifying scourge of Alzheimer's disease unless we ask deep and fundamental questions, informed by evolution, about what the alleged poisonous plaques of beta-amyloid protein are doing in the brain in the first place. Is amyloid pure pathology or does it have an vital evolved function in the brain? In this sense, Nesse has frequently claimed that the value of evolution to medicine is that it while it may lead directly to changes in medical practice or indeed to new therapies, more fundamentally its value lies in explaining why things are as they are. That is why Nesse argues that evolutionary biology should be the foundation and cornerstone for medicine as it should be for all biology. This book is an attempt to put yet more flesh on the bones of Nesse’s idea that evolution is the “physics” of medicine. I describe the evolutionary background to seven areas of human disease that are causing deep contemporary medical concern to explain why they exist in the first place—why things are how they are - and how evolution might help us to combat them. I hope it will leave readers with a new respect for evolution as the prime mover for the structure and function of human bodies, even if it does, on occasions, cause them to break down and drives us into ER!

Each chapter is built around the sometimes harrowing but always inspiring personal stories of people trapped in the disease process in question. Each chapter provides an evolutionary explanation for why the disease has come about, and each chapter shows how medical researchers, using powerful insights gained from thinking about disease in an evolution-informed way, are charting our way out of it.

How a modern version of the hygiene hypothesis - called the "old friends" hypothesis - explains why the Western world is riddled with allergic and autoimmune diseases, and what we can do about it.
How evolutionary theory explains why the battle between the different selfish genetic interests of mothers, fathers, and fetuses causes low fertility and can lead to diseases of pregnancy like recurrent pregnancy loss, preeclampsia and gestational diabetes.
What is the relationship between the fact that we have evolved to walk upright - our bipedalism - and a range of orthopedic illnesses?
Creationists have always used the example of the "irreducible complexity" of the human eye as the bedrock of their argument that God designed the human body, not evolution. Modern developmental biology, however, not only strongly rebuts creationism but explains the astonishing secret of how the recipe for eyes actually unfolds from within the developing eye itself, not from external influences, and is leading to cures for eye diseases like retinitis pigmentosa and macular degeneration.
How does cancer evolve so remorselessly towards malignancy that it is proving almost impossible to cure? Cancer evolution can be so extreme and drastic it is forcing us to re-write the rules of evolution by resuscitating a heresy from the 1940s.
Why are coronary arteries evolution's answer to feeding our powerful, muscular hearts with the food and oxygen they need and how has this led to the continuing pandemic of coronary heart disease?
Research into curing Alzheimer's disease has become hopelessly bogged down and billions of dollars have been wasted trying to turn the "amyloid hypothesis" into therapy. Can we use evolutionary thought to better explain why dementia comes about in a way that might lead to fresh hope for a cure?


Thursday, 10 September 2015

Protein linked to Alzheimer's could be spread during surgery, say researchers

Tabloid headlines today are screaming "Alzheimer's Bombshell" and, apparently, thousands of health patients are questioning forthcoming surgery for fear they will "catch" Alzheimer's disease from surgical instruments. All because of this, in my opinion, badly-handled release of a very limited piece of scientific work which, and I quote from Ian Sample's piece in the Guardian,  "found that a small number of people who died from Creutzfeldt-Jakob disease (CJD) after being treated with growth hormone taken from cadavers, developed brain changes seen in Alzheimer’s disease.

Doctors examined the brains of eight CJD patients who had received pituitary growth hormone, given predominantly to children with stunted growth until it was stopped in 1985. Six of the brains had an unusual build-up of protein called amyloid beta, which has long been linked to Alzheimer’s disease. The patients were aged 36 to 51 years old, but none carried gene variants that bring about the early onset of dementia.

John Collinge, director of the Medical Research Council Prion Unit at University College London, said the findings suggest that the hormone might have spread tiny pieces, or “seeds”, of amyloid beta, alongside the abnormal proteins, or prions, that gave people CJD."

If you read a little further into this Guardian piece you find that, although there was evidence for amyloid build-up in the deceased brains, none of them had died with any symptoms of Alzheimer's disease. The theory that they had, nevertheless, become "infected" with amyloid comes from the fact that none of the deceased CJD victims had any of the pre-disposing gene variants for Alzheimer's disease that cause early build-up of amyloid in brains. Hence the suggestion that the amyloid was "iatrogenically" introduced in infected batches of pituitary growth hormone.

Two prominent British researchers into Alzheimer's disease and prion disease, John Hardy and John Collinge, are quoted. "Speaking to the journal, John Hardy, a leading Alzheimer’s researcher at UCL, said: “This is the first evidence of real-world transmission of amyloid pathology. It is potentially concerning.” While Collinge said: "his team now suspected people could acquire amyloid beta “seeds” in three different ways: from a spontaneous, unlucky biological event, from a faulty gene or through a medical accident. He said there was no evidence that Alzheimer’s could be transmitted through blood transfusions, but added: “I think it’s not unreasonable to have a look. My concerns would be more to see if there is a risk of seeding from metal surfaces. I think that is something we ought to prioritise.”"

The problem with all this is the very precarious nature of the so-called amyloid theory in Alzheimer's disease research. Despite beta amyloid being heavily implicated as the causative agent in Alzheimer's, ever since the days of the eponymous researcher over a hundred years ago, no treatment of Alzheimer's that relies on preventing the enzymes in the chain to beta amyloid from working, or enhancing the clearance of beta amyloid from the brain, have worked. And it is well known that thousands of people have died with pin-sharp cognition, in old age, yet have been found, on autopsy, to have profound amounts of amyloid in their brains. It may very well be that amyloid is part of the "rubble" left in brains following the disease process, rather than the causative agent. Neither is there any clear collateral evidence that amyloid adhering to surgical instruments during brain operations can survive hospital sterilisation procedures.

It is a classic mis-handled and totally inappropriate scare story and, for their part in promulgating it, John Collinge and John Hardy should probably have their heads banged together.

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