YSM Issue 90.1

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COUNTERPOINT TIGHT JEANS? DON’T BLAME YOUR GENES ►BY LUCINDA PENG The prevalence of obesity and Type 2 diabetes has been increasing for at least 50 years. Attempting to explain this trend from an evolutionary perspective, researchers developed the “thrifty gene hypothesis”: the idea that evolution selected for genes that promote fat storage as an evolutionary advantage during famines. The hypothesis originated in 1962, when James Neel proposed that modern living conditions had created an evolutionary mismatch, which occurs when genes that once were advantageous become deleterious in a new environment. He concluded that this mismatch had contributed to an increase in Type 2 diabetes, and his hypothesis was the first widely discussed idea on the subject. However, in 1989, Neel reviewed his own work and realized that his hypothesis was probably incorrect, for famines occurred too infrequently to have generated significant selection pressure. Since then, the theory has been put aside in favor of other hypotheses, and the new results discussed below solidify that move. Guanlin Wang and John Speakman of the Chinese Academy of Sciences found genetic evidence opposing the thrifty gene hypothesis. They examined 115 single nucleotide polymorphisms (SNPs), or common genetic mutations, that had previously been found to be correlated with obesity. They used genomes from a database compiled by the 1000 Genomes Project, an international collaboration to document genetic variability among different ethnicities, to ensure that effects of specific subpopulations did not influence their results. When Wang and Speakman analyzed the SNPs associated with a higher body mass index (BMI) in obese and control populations, they found no significant selection for these genes, suggesting that evolution has not selected for obesity. In fact, of the nine genes associated with IMAGE COURTESY OF WIKIMEDIA COMMONS ►Calorie dense junk food has contributed to the rise of type 2 diabetes and obesity. BMI, five of them had decreased, rather than increased, fat storage. Their discovery is not consistent with the genetic basis of the thrifty gene hypothesis, increasing the plausibility of other theories about the underlying causes of obesity. Dr. Stephen Stearns, Yale professor of Ecology and Evolutionary Biology, cites two other hypotheses to replace the thrifty gene hypothesis: the thrifty phenotype and the hygiene hypotheses. Hales and Baker proposed the thrifty phenotype hypothesis in 1992, suggesting that the body uses information from the environment early in life to predict its needs for the future environment. These environmental conditions can induce epigenetic changes, or nongenetic mechanisms, that affect phenotypic (observable) traits. They found that babies born during the Dutch Hunger Winter, a six-month food blockade by the Germans in the Netherlands, were more prone to insulin resistance due to a nutritional deficit in the womb. Insulin promotes the absorption of sugar from blood into tissues, but under starvation conditions, nonessential tissues become less responsive to insulin so that the brain can receive enough sugar. When the Germans left, food was abundant, so the environment that the baby was prepared for did not match the environment it was born into. As a result, the people born in this period were more prone to diabetes and other diseases. “This trend can be observed under normal circumstances, too, as birth weight is a good predictor of the risk of being affected by diseases later in life,” said Dr. Stearns. The thrifty phenotype hypothesis addresses a major problem from the thrifty genotype hypothesis. If there had been continued, strong positive selection for increased fat storage, all humans would be obese because these genes would be fixed, or permanently added to the human genome. In contrast, with “thrifty phenotypes,” epigenetic factors are affected by the environment and can vary among people. The hygiene hypothesis relates the gut microbiota to metabolic diseases. The gut microbiota is composed of bacteria that help to break down macromolecules and absorb nutrients; it is sensitive to environmental stimuli. For example, babies born by C-section rather than vaginal birth have different microbiota because they were not exposed to the bacteria in their mother’s birth canal, and being breastfed or taking antibiotics can also affect a baby’s gut microbiota. These changes have been shown to affect their risk of obesity, insulin resistance, and Type 2 diabetes. With a lack of genetic evidence to support the claim that humans evolved to better store fat, the thrifty phenotype and hygiene hypotheses are now favored to replace the thrifty genotype hypothesis. Wang and Speakman’s paper provides more concrete evidence to refute the thrifty gene hypothesis, supporting what many scientists already believed. Because the thrifty phenotype and hygiene hypotheses explain why metabolic diseases can be inherited but are also heavily influenced by the environment, they provide a more robust explanation for the rise in obesity and Type 2 diabetes. 34 Yale Scientific Magazine December 2016 www.yalescientific.org
BLAST from the PAST Malaria: Finding the Missing Pieces of Malaria’s Migratory Patterns ►BY WILL BURNS In 1925, Spain’s Catalan Government set up a humble hospital in the Ebro Delta region. The hospital treated patients suffering from malaria. Ildefonso Canicio, a doctor at the hospital, spent decades diagnosing and treating patients. By drawing blood from patients, and placing a drop on a microscope slide, he could determine whether the blood contained Plasmodium, the parasite that causes malaria. Canicio threw away most of his slides, but he kept a few slides from the 1940s. Little did he know that seventy years later, these slides would provide insight into the global migratory patterns of the malaria Plasmodium. To fight malaria in the present day, researchers are looking to the past to understand how the parasite evolved over time, specifically exploring how human movements transmitted the parasite across the globe. Malaria was successfully eradicated from Europe after World War II. Thus, researchers have had to search for old, badly preserved slides from Europe’s preeradication era, hoping to find clues about the nowextinct parasite. Carles Lalueza-Fox, a paleo-genomics researcher at the Institute of Evolutionary Biology in Barcelona, reached out to Canicio’s family who gave him three slides to analyze. Back at the lab, he quickly realized that analyzing the slides would be difficult. “There were just a few drops of blood in the samples. Once they were extracted and sequenced, they were gone. The slides were fragile and covered with stains and oils,” said Lalueza-Fox. Despite the fragility and small size of the samples, Lalueza-Fox and his team successfully obtained a huge amount of genetic data from Plasmodium mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA is inherited only from the mother, so it is better suited for determining the maternal lineage and genealogy of a species. “As far as I know, this is the first study where such old slides were used and such an amount of genetic data from the pathogens was retrieved,” Lalueza-Fox added. Using the reconstructed European Plasmodium mtDNA genomes, Lalueza-Fox and his team shed light on certain controversies surrounding the parasite’s evolutionary history. “It was not clearly understood how the pathogen spread along different continents, because Europe was central to some of these dispersals but no data from Europe was available,” noted Lalueza- Fox. His team found surprising genetic similarities between European Plasmodium mtDNA and Indian Plasmodium mtDNA. Lalueza-Fox believes that malaria was transmitted from India to Europe when the Persian Empire expanded into India in the sixth century BCE. The team also found evidence that European, Central American, and South American parasites are genetically similar–indicating that, the exchange of food, plants, culture, and technology between the Old World and the Americas in the 15th and 16th may have helped spread malaria. Lalueza-Fox is now attempting to construct the nuclear genome of the European Plasmodium parasite. “So far, we have about 40 percent of the nuclear genome of the P. falciparum. I reckon we need four or five more slides,” Lalueza-Fox said. In Lalueza-Fox’s opinion, understanding the nature of parasites from 100 years ago is critical for understanding the resistance of modern parasites to treatment. “Plasmodium is a very dynamic organism and very difficult to tackle because of these mutations,” Lalueza-Fox added. His team will continue to search for the missing pieces of the Plasmodium “puzzle,” researching the extinct parasite to enhance our understanding of malaria. www.yalescientific.org December 2016 Yale Scientific Magazine 35
Page 1 and 2: Yale Scientific Established in 1894
Page 3 and 4: Yale Scientific Magazine VOL. 90 IS
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Page 7 and 8: in brief NEWS The Miller laboratory
Page 9 and 10: computational biology NEWS SOLVING
Page 11 and 12: medicine NEWS THE FLU SEASON CRAVIN
Page 13 and 14: environmental science FOCUS Surging
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Page 37 and 38: ALUMNI PROFILE DR. RALPH GRECO, M.D
Page 39 and 40: cartoon FEATURE ►BY ABHI MOTURI a

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