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?


Wednesday, 8 July 2015

We all age at a different speeds – and scientists have worked out how to calculate it

Any school or university reunion - when the 'class of '85' all meet up again - will tell you that each of us seems to age differently and at a different rate. The value of extremely large, well-done, longitudinal studies is that they can pick apart this phenomenon and study it properly and infomatively. Avshalom Caspi and Terrie Moffett have been at the heart of this study for decades and have just released their findings on differential aging. As this article says: "The researchers developed a method to determine the pace of ageing in individuals by looking at a range of biomarkers – including blood pressure and gum health. The study participants, all aged 38, varied widely in "biological age" and those ageing more quickly also looked older and reported more health problems."

This companion article in Medical Express adds further detail on how the study was done, according to another of its authors, Dan Belsky:

""We set out to measure aging in these relatively young people," said first author Dan Belsky, an assistant professor of geriatrics in Duke University's Center for Aging. "Most studies of aging look at seniors, but if we want to be able to prevent age-related disease, we're going to have to start studying aging in young people."

Belsky said the progress of aging shows in human organs just as it does in eyes, joints and hair, but sooner. So as part of their regular reassessment of the study population at age 38 in 2011, the team measured the functions of kidneys, liver, lungs, metabolic and immune systems. They also measured HDL cholesterol, cardiorespiratory fitness, lung function and the length of the telomeres—protective caps at the end of chromosomes that have been found to shorten with age. The study also measures dental health and the condition of the tiny blood vessels at the back of the eyes, which are a proxy for the brain's blood vessels. Based on a subset of these biomarkers, the research team set a "biological age" for each participant, which ranged from under 30 to nearly 60 in the 38-year-olds.

The researchers then went back into the archival data for each subject and looked at 18 biomarkers that were measured when the participants were age 26, and again when they were 32 and 38. From this, they drew a slope for each variable, and then the 18 slopes were added for each study subject to determine that individual's pace of aging.

Most participants clustered around an aging rate of one year per year, but others were found to be aging as fast as three years per chronological year. Many were aging at zero years per year, in effect staying younger than their age. As the team expected, those who were biologically older at age 38 also appeared to have been aging at a faster pace. A biological age of 40, for example, meant that person was aging at a rate of 1.2 years per year over the 12 years the study examined."

The source paper for these articles, titled "Quantification of biological aging in young adults" is open access in PNAS at the following link

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