Protecting biodiversity is essential to our health and longevity on this planet. But can we quantify that value? Especially the economic value?

Late last year, researchers from the US and France attempted to put dollar amounts on the importance of biodiversity by correlating it to the prevalence of tropical disease in developing countries. According to their introduction in PLoS Biology:

Along with 93% of the global burden of vector-borne and parasitic diseases (VBPDs), the tropics host 41 of the 48 “least developed countries” and only two of 34 “advanced economies.”

They contend that economic growth falters when people get sick. (Seems reasonable.) And the spread of disease among humans, many scientists argue, can increase or decrease depending on factors in the natural environment, including biodiversity.

The more diverse an ecosystem, the greater the chance that a pathogen is diluted among numerous and potentially less-than-ideal host species and, therefore, the less abundant the disease. In 2002, researchers found this to be true with Lyme disease. NPR sums it up well:

If you have a rich community of tick hosts, like squirrels, mice and other small mammals, the disease is diluted among them. But if the habitat is degraded, and ticks carrying Lyme have only white-footed mice as hosts, the disease risk to humans can rise dramatically.

The Academy’s microbiologist, Shannon Bennett, weighed in on biodiversity’s impact on human diseases. In a recent email, she wrote:

I am sure biodiversity influences the transmission of infectious diseases one way or another.  Over 75% of new, emerging or re-emerging human diseases are caused by pathogens from animals, according to the World Health Organization. That means that the ecological communities we live in, and how pathogens cycle through the different players, are key to human health. Biodiversity is one way that we measure the complexity of these communities. In what way biodiversity is important, or how these communities specifically affect infectious diseases and risk, depends on the pathogen ecology and life history, and host species relationships.

Stanford researchers brought up this same point last month—“depends on the particulars,” as Bennett put it—in a study in Ecology Letters. A summary from the Stanford Report states:

The researchers found that the links between biodiversity and disease prevalence are variable and dependent on the disease system, local ecology and probably human social context.

The role of individual host species and their interactions with other hosts, vectors and pathogens are more influential in determining local disease risk, the analysis found.

That dovetails exactly with the research Bennett and Academy entomologist Durrell Kapan are conducting. They’re currently studying mosquito vector communities and the relationships between their biodiversity, the diversity of their microbes, and the presence of pathogens.

As for putting a price tag on biodiversity, Bennett encourages the PLoS study’s authors:

I find the authors’ argument intriguing and certainly a significant angle to consider in support of the health value of biodiversity, and one that is unique—no one has teased out the financial correlations between biodiversity and human societies. That it includes human health and infectious diseases is the angle I find particularly intriguing and worth following up on with empirical studies.

And on these studies of human disease and biodiversity in general? Bennett is excited about the possibilities of further research, including her own:

Increasingly we are recognizing and appreciating that humans are members of complex communities of other species, and that the make-up of these communities, whether they live inside of us or outside, can be very important to human health, as well as the health of all life. Human health and the health of life on this planet are coupled. We need to understand those coupling mechanisms better to ensure sustainability of that life, and the best way to understand those coupling mechanisms is with a multi-disciplinary approach, bringing together human health researchers with ecologists and evolutionary biologists, to name a few!

Some organizations have sprung up to do just that. Bennett points to two examples: the One Health Initiative and the EcoHealth Association. Whatever dollar value we assign to biodiversity and other ecosystem services, let’s wish these organizations luck in improving human health and well-being.

Image: CDC

At least that’s how it worked for Shinya Yamanaka, a Japanese scientist and senior investigator at Gladstone. Yesterday in a ceremony in Norway, he was awarded the Nobel Prize in Physiology or Medicine for his discovery of how to transform ordinary adult skin cells into cells that, like embryonic stem cells, are capable of developing into any cell in the human body.

“Cells that can develop into any cell in the human body can be used to replace specific damaged tissues, such as those involved in blindness and spinal cord injuries, and treat a whole range of diseases, from cancer to immune disorders to neurodegenerative disorders,” says the Academy’s Shannon Bennett. “The growing field of regenerative medicine depends on using these pluripotent cells—cells that can become almost anything.

“Up to now getting these cells has raised ethical concerns, because they are collected from fertilized human embryos which are destroyed by the process.   Adult stem cells are not as useful an alternative—they are already committed to the organ they come from. But now, Yamanaka has discovered a method to induce adult cells that have already developed—skin cells, for example—to become pluripotent, cells that can become virtually any cell in the human body!”

Yamanaka’s path to the Nobel Prize wasn’t as neat as you might think. He started his science career as a surgeon, “only to find he was not so good at it,” according to the New York Times.

He came to Gladstone in 1993 and worked with mice to research how to lower bad cholesterol. A hopeful treatment caused liver cancer in the mice, which led Yamanaka to research the cancer.

He needed stem cells to research the cancer in the mice and eventually the stem cells became his focus.

Which led him to his Nobel Prize-winning research.

Science often works this way—unexpected discoveries lead to new paths and questions. And Gladstone especially seems to embrace and understand this. From their website:

“The Gladstone philosophy has always been to allow scientists like Shinya Yamanaka the freedom to follow wherever their curiosity—and the science—leads,” says Robert Mahley, MD, PhD, Gladstone’s founding scientist… “As a postdoc, Dr. Yamanaka embraced that philosophy, which I think has played a big part in making him the scientist and the person he is today.”

Please stay tuned: the Academy and Gladstone will kick off a week-long festival in January 2013 called Brilliant!Science: Decoding Human Health—including lectures, events, family activities and opportunities to engage with active scientists.

“The Brilliant!Science festival will be a great collaboration and help demonstrate the synergies amongst all kinds of research, from human health to biodiversity,” says Shannon. “Whether its about the diversity of cells in the human body, the genes that compose us, the diseases that plague us, or the diversity of life forms around us, science unfolds in a similar pattern—with questions! We’ll share a week of exciting science from both Academy and Gladstone scientists, hosted around the city and at the Academy itself.”

Image: Gladstone Institutes/Chris Goodfellow

The experiment demonstrates natural selection at work. And because samples are frozen and available for later study, when something new emerges, scientists can go back to earlier generations to look for the steps that happened along the way.

Last month, Zachary Blount, Lenski and colleagues published a paper in Nature detailing a new evolution in E. coli—the ability to eat citrate.

Shannon Bennett, associate curator of the Academy’s Microbiology department, explains why this is so unusual.

E. coli doesn’t normally eat citrate unless it is desperate (there’s no glucose, no oxygen). But these E. coli did evolve the ability to eat citrate, in fact thrive on it, in the presence of both oxygen and glucose.

They were able to evolve to do this when certain individuals made mistakes and copied their citrate gene (which usually is turned on only under oxygen-poor conditions) to a different spot in the genome near a switch point that turns on in the presence of oxygen.

Blount was able to trace this new trait through generations and uncover a three-step process in which the bacteria developed this new ability.

The first stage was potentiation, when the E. coli accumulated at least two mutations that set the stage for later events (see Shannon’s explanation above). The second step, actualization, is when the bacteria first began eating citrate, but only just barely nibbling at it. The final stage, refinement, involved mutations that greatly improved the initially weak function. This allowed the citrate eaters to wolf down their new food source and to become dominant in the population.

“We were particularly excited about the actualization stage,” Blount says. “The actual mutation involved is quite complex. It re-arranged part of the bacteria’s DNA, making a new regulatory module that had not existed before. This new module causes the production of a protein that allows the bacteria to bring citrate into the cell when oxygen is present. That is a new trick for E. coli.

“It wasn’t a typical mutation at all, where just one base-pair, one letter, in the genome is changed,” he continues. “Instead, part of the genome was copied so that two chunks of DNA were stitched together in a new way. One chunk encoded a protein to get citrate into the cell, and the other chunk caused that protein to be expressed.”

Shannon explains why this study is so exciting:

This study is cool because it shows many of the important mechanisms in evolution, namely gene duplication and gene regulation (turning genes on and off at different times). It all went on in a series of test tubes, so it’s “artificial” evolution, but what’s nice about that is, they were able to freeze samples down at early time points through to the present, to trace the path of evolution, and that they used a model organism, Escherichia coli, that evolves very quickly (not as quick as viruses, but much faster that vertebrates). My work takes advantage of the same historical sampling and evolutionary speed, only I’ve focused on “natural” experiments in the viruses I work on.