New Turmoil Over Predicting the Effects of Genes

Promising efforts at disentangling the effects of genes and the environment on complicated traits may have been confounded by statistical problems.

https://www.quantamagazine.org/new-turmoil-over-predicting-the-effects-of-genes-20190423/?utm_source=Quanta+Magazine&utm_campaign=984df15895-RSS_Daily_Biology&utm_medium=email&utm_term=0_f0cb61321c-984df15895-389846569&mc_cid=984df15895&mc_eid=61275b7d81

Jordana Cepelewicz

Staff Writer

April 23, 2019

Various innovations in the field of genomics over the past few decades have given researchers hope that resolutions to long-lasting debates might finally be on the horizon. In particular, many have become optimistic about the prospects for disentangling the threads of “nature” and “nurture” — that is, about determining the extent to which genes alone can explain differences within and between populations.

But two recent studies are now calling some of the methods underlying those aspirations into question.

A key breakthrough was the recent development of genome-wide association studies (GWAS, commonly pronounced “gee-wahs”). The genetics of simple traits can often be deduced from pedigrees, and people have been using that approach for millennia to selectively breed vegetables that taste better and cows that produce more milk. But many traits are not the result of a handful of genes that have clear, strong effects; rather, they are the product of tens of thousands of weaker genetic signals, often found in noncoding DNA. When it comes to those kinds of features — the ones that scientists are most interested in, from height, to blood pressure, to predispositions for schizophrenia — a problem arises. Although environmental factors can be controlled in agricultural settings so as not to confound the search for genetic influences, it’s not so straightforward to extricate the two in humans.

Not to be thwarted, over the past two decades experts have come up with robust statistical techniques to address the issue, using data collected from thousands of individuals. This approach has become particularly prevalent in human genetics, as researchers hope to predict, say, someone’s risk for a disease based on their genome. Some groups have even used these methods to probe how natural selection might have led to observed differences in height (and other traits) among populations. The findings generated further excitement about the potential applications in medicine and evolutionary biology for GWAS.

But now, two results published last month have cast doubt on those findings, and have illustrated that problems with interpretations of GWAS results are far more pervasive than anyone realized. The work has implications for how scientists think about the interactions between genetic and environmental effects. It also “raise[s] the ghosts of the possibility that we overestimate … how important genetics is in contributing to differences between people,” said Rasmus Nielsen, a biologist at the University of California, Berkeley.

Predictions and Dreams

The warning signs started quietly. Genome-wide association studies had already proved incredibly successful at identifying genetic markers for a wide array of traits, even in complex cases where it wasn’t obvious what the many, many variants were doing.

What had also emerged from that research as an “obvious, beguiling offshoot,” according to Nick Barton, an evolutionary biologist at the Institute of Science and Technology Austria, was a specific prediction known as a “polygenic score.” Beyond the associations themselves, GWAS could provide estimates of how individual variants in the genome corresponded to measurable changes in a trait; polygenic scores constituted the sum of all those tiny effects. For instance, with height, having a guanine base instead of a cytosine one in a particular DNA region might correlate with being 0.1 millimeter taller than average. The polygenic score would take all those approximations, add them up and spit out a prediction for some individual’s actual height.

Polygenic scores offer a tantalizing opportunity to predict a person’s risk of developing a given disease, which could help inform when and how often to screen for it, what preventive measures to take and even which treatments to try. Some evolutionary biologists have hoped to use the scores to get a better picture of the phenotypes that were encoded in ancient genomes, and to better understand histories of adaptation in various populations.

The methods developed so far really think about genetics and environment as separate and orthogonal, as independent factors. When in truth, they’re not independent.

Gil McVean, University of Oxford

Five years ago, a series of analyses on a European database made these dreams seem within reach. People of northern European ancestry are on average taller than those of southern European ancestry. Researchers wanted to explore whether those differences were a result of natural selection. They found that the polygenic scores for height did indeed increase from southern to northern Europe, much more so than would be expected from the random fluctuations in variant frequencies called genetic drift. That pattern supported the idea that genetics could explain a significant portion of why someone of Swedish descent was likely to be taller than someone with Italian roots — and, it seemed, those genetic differences reflected some process of natural selection and adaptation.

Of course, to reach these conclusions, the researchers had to make sure they weren’t being accidentally misled by subtle environmental factors instead. Take an oft-cited, trivial example: Imagine you have chosen to study the genetics underlying motor skills by investigating how well people use chopsticks. A naïve approach would yield strong associations between chopstick use and certain genetic markers — yet those markers might simply be common among groups of east Asian ancestry who have used chopsticks more often, rather than having anything to do with intrinsic motor skills.

But the scientists had ways to correct for those biases, and the signal of selection on height remained. “We were really excited about that, because we were finally getting to look at … adaptation operating on complex traits,” said Graham Coop, an evolutionary geneticist at the University of California, Davis, who led some of that work along with Jeremy Berg, an evolutionary biologist now at the University of Chicago. Several studies, including one that used sibling data (the closest thing to a “control” experts have in this line of research), replicated their results.

And then the two recent papers in eLife, both relying on a newer database called the U.K. Biobank, saw that signal disappear.

The Vanished Signal

That database was larger and more homogeneous than the one that had driven the previous findings, and had been compiled much more systematically, reducing some of its biases just a bit. As a result, it yielded slightly different estimates for the small effect sizes associated with each of the variants, which weren’t a big deal in individual cases but added up to significantly different overall polygenic scores.

Graham Coop, an evolutionary geneticist at the University of California, Davis, uses genome-wide association studies to investigate complex traits in humans — but his work recently raised new questions about how to analyze those results.

Courtesy of Graham Coop

“The new studies are really quite disconcerting,” Barton said, because they demonstrated that scientists had been mistaking biases in the polygenic score calculations for something biologically interesting. Their statistical methods of accounting for population structure were not so adequate after all.

Though it was always understood to be a problem, “no one realized how big of a problem it was,” said Shamil Sunyaev, a computational geneticist at Harvard Medical School who performed one of the new eLife analyses with his graduate student Mashaal Sohail and their colleagues.

“It was just that sort of feeling where the world shifts under your feet slightly,” said Coop, who with Berg and their colleagues coauthored the other eLife paper to try to confirm their earlier research. “It’s fairly humbling to see all of that work go away.”

Barton agreed. “The whole thing is tricky, because the origins of genetic variation in any population are really complicated,” he said. “Now you really can’t take at face value any of these methods over the last four or five years that use polygenic scores.”

“Maybe the Dutch just drink more milk, and this is why they’re taller,” Sunyaev added. “We can’t say otherwise with this analysis.”

And when the trait being studied isn’t height, that can be dangerous. It means that trying to use estimates made about the effects of variants on diseases in one population might not apply to individuals in another population. That’s particularly worrisome because the vast majority of genome-wide association studies rely on data from people of white European ancestry. “People are not homogeneous, and it can come back to haunt you,” said Magnus Nordborg, a population geneticist at the Austrian Academy of Sciences.

Shamil Sunyaev, a computational geneticist at Harvard Medical School, helped identify persistent statistical problems in GWAS interpretations.

Courtesy of Shamil Sunyaev

Given that some experts want to roll out polygenic scores in the clinic, it’s already clear that this flaw could deepen the disparity in health care. In a study published last month, researchers found that trying to translate insights gleaned from European data to make health predictions in people of African descent led to as much as a 4.5-fold drop in accuracy. Others have tried using polygenic scores to make poorly supported claims about differences in behavioral and social traits between populations (such as IQ and education attainment, which are far more difficult to define and unpack than height is, yet are being used to potentially inform future policymaking decisions). “It’s kind of scary,” said Sarah Tishkoff, a geneticist at the University of Pennsylvania who emphasized how critical it is to collect more underrepresented genomic information.

The eLife work underscores an urgent need for future studies to involve more people, a greater diversity in data and more family-based replication analyses. It also calls for more sophisticated statistical methods that can better control for population structure and other environmental factors — something researchers are already working on as they continue to delve into exactly what went wrong with the initial analyses. “The methods developed so far really think about genetics and environment as separate and orthogonal, as independent factors. When in truth, they’re not independent. The environment has had a strong impact on the genetics, and it probably interacts with the genetics,” said Gil McVean, a statistical geneticist at the University of Oxford. “We don’t really do a good job of … understanding [that] interaction.”

That’s not to say that genome-wide association studies do not have incredible power. They can still identify important markers for traits of interest. The small intrinsic biases don’t invalidate the thousands of regions of DNA such studies have already implicated in diseases and other conditions and traits. But the strengths of those individual and collective associations are general estimates. It’s when they’re accumulated to make inferences about differences between populations, both in evolutionary and medical contexts, that things can go wrong.

“We have to go back to the thinking box,” Nielsen said. “This is a major wake-up call … a game changer.”

Update added on April 24, 2019: The contributions of Mashaal Sohail and others to the work with Shamil Sunyaev were no

Viruses Have a Secret, Altruistic Social Life

Researchers are beginning to understand the ways in which viruses strategically manipulate and cooperate with one another.

https://www.quantamagazine.org/viruses-have-a-secret-altruistic-social-life-20190415/?utm_source=Quanta+Magazine&utm_campaign=709cbe4b60-RSS_Daily_Biology&utm_medium=email&utm_term=0_f0cb61321c-709cbe4b60-389846569&mc_cid=709cbe4b60&mc_eid=61275b7d81

[[Everything is always much more complicated than we thought.]]

Viruses might seem like the ultimate selfish parasites to their hosts, but researchers are discovering that they can have extensive social interactions with one another, including some behaviors that seem like altruism.

Viviane Callier

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April 15, 2019

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AbstractionsBiologyCooperationEvolutionGame TheoryViruses

Social organisms come in all shapes and sizes, from the obviously gregarious ones like mammals and birds down to the more cryptic socializers like bacteria. Evolutionary biologists often puzzle over altruistic behaviors among them, because self-sacrificing individuals would at first seem to be at a severe disadvantage under natural selection. William D. Hamilton, one of the 20th century’s most prominent evolutionary theorists, developed a mathematical theory to explain the evolution of altruism through kin selection — for instance, why most individual ants, bees and wasps forgo the ability to reproduce and instead pour all their efforts into raising their siblings. Bacteriologists developed game-theory models to explain why bacteria in groups produce metabolites for their neighbors, even though some cheaters take advantage of the situation.

But until recently, no one had considered that simple viruses, too, have social lives that influence their fitness and their evolution. “From a theoretical perspective, there is clearly huge potential for viruses to interact socially, leading to possibilities for cooperation and conflict,” wrote Stuart West, a biologist at Oxford University who studies the evolution of social behaviors, in an email to Quanta. “However, there has been relatively little attempt to tackle this empirically.”

In a recent study published in Nature Microbiology, Rafael Sanjuán, an evolutionary geneticist at the University of Valencia in Spain, and his colleagues used a combination of theory and experiments to explore viral cooperation and conflict. They found that the spatial structure of a viral infection — the way that different sets of viruses can be isolated in separate compartments of the infected body — matters tremendously. In an evenly mixed system, altruistic viruses fall victim to “cheaters” that take advantage of their sacrifices, but if pockets in the body can isolate and shelter the altruists, they have a shot at survival.

Abstractions​ navigates promising ideas in science and mathematics. Journey with us and join the conversation.

Consider the vesicular stomatitis virus (VSV), a less dangerous member of the same viral family as rabies. Viral infections usually stimulate the cells of their mammalian hosts to produce interferons, the signaling proteins that raise neighboring cells’ antiviral defenses and interfere with viral replication. The wild-type VSV has evolved ways to suppress its host’s innate immune system, but at the cost of reproducing more slowly. Still, that ability enables the population of suppressive viruses to thrive — unless a “cheater” variant comes along.

The cheater does not have the ability to suppress its host’s defenses; in fact, its presence stimulates the release of interferons. But it still reaps the benefit of a lowered immune response because of the nearby VSVs that suppress interferon release. Because the cheaters don’t pay the reproductive cost of interferon suppression, they can outcompete the wild-type virus in the short term. From a social behavior standpoint, as Sanjuán and his colleagues pointed out in their paper, the wild-type VSV’s suppression of interferon qualifies as an altruistic act because in effect the wild type sacrifices itself for the cheater.

Eventually, the host’s interferon response overwhelms both types of viruses and kills them. It might seem like natural selection would therefore always weed out the ability to suppress interferon because its altruism would perversely leave viruses that had it at a disadvantage.

Sanjuán’s modeling study shows, however, that is not necessarily the case: The altruistic interferon-suppressing virus can still evolve and thrive if it and the cheater are physically segregated. Structures and barriers in the body can create havens where the interferon-suppressing viruses can survive, safe from the damage that cheaters would otherwise bring down upon them.

From a theoretical perspective, there is clearly huge potential for viruses to interact socially, leading to possibilities for cooperation and conflict.

Stuart West

To model the specific conditions in which innate immune suppression can occur, the researchers used the theoretical framework that Hamilton developed. According to Hamilton’s rule, altruism evolves when r × B > C, where B is the benefit to the recipient, ris the recipient’s relatedness to the giver, and C is the cost to the giver.

The researchers also used a parameter to indicate that the benefit, B, depends on whether a virus is surrounded by wild-type or cheater neighbors. Applying Hamilton’s rule to well-mixed and spatially segregated combinations of the two VSV variants, they could empirically estimate the parameters in Hamilton’s equation.

“For innate immune suppression to evolve, you need spatial structure,” Sanjuán said. Because both the virus and the host’s interferon response spread out from cell to cell, it’s actually quite difficult to avoid the emergence of spatial structures during infection. Limitations on the rate of diffusion of viral particles and interferon molecules, as well as physical barriers in the body’s tissues, easily create spatial heterogeneity, thus allowing for the evolution of innate immune suppression.

In animals with complex behaviors and in bacteria with relatively complex communication systems, the outcomes of evolutionary scenarios are influenced by many factors. In the case of viruses, “it’s much simpler,” Sanjuán said. “Everything is dictated by spatial structure. There is no other known process that can affect the outcome of the system. If the viruses are mixed, then this altruism cannot evolve, and if they are segregated, then the altruism can evolve.”

Another aspect of social evolution of viruses that Sanjuán is investigating is why multiple viral particles sometimes gather and infect a cell together. The trade-off is that, if the viral particles assemble, there are fewer units to infect different cells. So “in principle, this is costly because it limits diffusion capability,” Sanjuán said. But his team found, to their surprise, that the aggregated viruses grow faster and produce more progeny. This result was dependent on cell type: In tumor cells that have no innate immunity, being aggregated was costly. But in normal cells, which do mount an innate immune response, being aggregated was beneficial for the viruses because it allows the viruses to overwhelm the innate immune response, Sanjuán suggested.

Although the strategy of aggregation for infection seems beneficial for the virus, it too can lead to the evolution of cheaters. For example, if one virus in the aggregate loses a few genes, then it can replicate more quickly, and with that advantage it can outcompete the other viruses in the aggregate. These gene-deficient viruses are known as defective interfering particles (DIPs): Many of them lack about 90 percent of the viral genome and survive as just a small piece of RNA that can replicate very quickly inside a host (they cannot ordinarily infect a new host because they are so incomplete). In cell cultures with a high density of viral infections, the DIPs take over and soon represent more than 99 percent of the viral population, Sanjuán said.

The existence of DIPs may touch on another puzzle: Do viruses adjust their manipulations of one another in keeping with the needs of their life cycle? Raul Andino, a virologist at the University of California at San Francisco, points out that early in its invasion of a host, a virus might want lots of company because multiple simultaneous infections would increase its odds of success.“But then they want to reduce the possibility of high multiplicity of infection at a later stage, to reduce the possibility of production of these defective particles,” he said. “This is something we don’t fully understand, but it is a really interesting problem.”

New Fossil Human Species Thwarts Core Darwinian Predictions

Günter Bechly

April 19, 2019, 4:19 AM

https://evolutionnews.org/2019/04/new-fossil-human-species-thwarts-core-darwinian-predictions/

[[Note passages below that I put in bold. D.G.]]

The rewriting of the evolutionary narrative of human origins is proceeding at such an unbelievable pace that I am running out of new ways to introduce my comments on the latest findings. Just a few weeks ago, for Evolution News and ID the Future, I discussed the ongoing rewriting of human fossil history in Asia (Bechly 2018, 2019, Klinghoffer 2019). Now a new fossil species of our genus Homo from the Late Pleistocene of the Philippines has been described in Nature by Détroit et al. (2019), and guess what, the media again report this discovery as they’ve done in the past, saying that it “…May Rewrite Human History” (Joyce 2019), etc. I can hardly resist the temptation to say “I told you so,” or to jokingly remark, “Oops, they did it again.” Let’s instead have a closer look at the actual evidence and the implications of this new discovery.

Remains from Callao Cave

The digs were led by Dr. Armand Mijares from the University of the Philippines and the study conducted by Dr. Florent Détroit from the National Museum of Natural History in Paris. In their Naturepaper they describe the new species Homo luzonensis from 7 isolated teeth, 2 finger bones, 3 feet bones, and a thigh fragment. The remains were discovered in Callao Cave on Luzon Island, in the Philippines. These hominin fossils were recovered during excavations in 2007, 2011, and 2015, and have been radiometrically dated to a Late Pleistocene age of 50,000-67,000 years. A foot bone unearthed in 2007 was already described by Mijares et al. (2010) and similarities to Homo floresiensis and Homo habilis mentioned, but it was not yet named as a new species and an attribution to Homo sapiens was not ruled out. Last year the discovery of stone tools documented that hominins were present on Luzon since more than 700,000 years ago (Ingicco et al. 2018, Hawks 2018). That would predate the supposed origin of Homo sapiens and thus suggests an origin from a more archaic hominin form. This is also indicated by the anatomical character analysis of the Homo luzonensis fossils, which revealed similarities of several tooth characters and the curved shape of the toe with the ape-like genus Australopithecus rather than the human genus Homo (Stoddart 2019). Such curved toes are typical for those early australopithecines that were still adapted for climbing in trees rather than elegant bipedal walking.

The actual evidence for the establishment of a new human species may seem a bit thin. However, the strange combination of characters indeed suggests a new species, even though other researchers such as Dr. Bernard Wood are still skeptical. They emphasize that “it’s really at the lower end of the amount of evidence that you would want to base a new species” (Zimmer 2019). Nevertheless, distinguished paleoanthropologist John Hawks, who was one of the team of scientists that described Homo naledi, agrees that “No other known species shares the whole set of features found at Callao” (Hawks 2019c) and “Together, they represent a mash of features that are confusingly reminiscent of a huge range of other hominins, and together make for something new and hard to classify” (Hawks 2019b). In any case the discovery shows that the fossil history of humans was much more diverse and complex than previously believed. Paleoanthropologist Yousuke Kaifu from the National Museum in Tokyo is quoted in a National Geographic article (Greshko & Wei-Haas 2019) as saying that this new hominin “further highlights remarkable diversity of archaic (primitive) hominins once present in Asia, in a way beyond my expectation.”

A Mosaic Pattern

The mosaic pattern of primitive and derived characters in Homo luzonensis also shakes up the phylogenetic tree (Hawks 2019b). Actually, there is no well-established tree of fossil humans, as is nicely documented by the fact that John Hawks put question marks at almost every node in his most recent tree (Hawks 2019a). This embarrassing fact is mostly based on the problem that fossil humans show all kinds of strange combinations of characters that do not align well with a nested hierarchy. Even worse, they do not allow us to order human fossils in a gradually progressive and smooth transitional lineage from ape-like forms to modern humans. They also do not fall into a temporal cline from older primitive to younger derived forms. Some early australopithecines not only exhibit the expected ape-like features but also some very modern human characters, while some late representatives of Homo (e.g., Homo naledi) still have very primitive characters. Thus fossil humans do not form a transitional series like the famous horse series. They are a frustrating mess for evolutionists, and the new species from Luzon makes the situation even worse.

So what did scientists say about the potential affinities of Homo luzonensis? The authors of the original description refrain from saying anything about its relationships. Hawks (2019b) speculated about whether the SE Asian island hominins might be related to the elusive Denisovans. But in my view two arguments point against such an affinity: phylogenomic studies have shown that Denisovans are relatively modern members of the genus Homo, closely related to Neanderthal man, while the anatomical data suggest that the island hominins belonged to a much more primitive habiline grade (see below); furthermore, the small body size of the Flores and Luzon populations may suggest an already dwarf-sized ancestor, while the few Denisovan fossil remains (including the recently discovered first skull fragment, Jones 2019) document a large body size. Both arguments also point against an affinity with Homo erectus.

The Hobbit Man

The new discovery of course reminds one of another East Asian island hominin, the famous hobbit man, Homo floresiensis, discovered on the Indonesian island of Flores in 2003. Homo luzonensis not only shares with Homo floresiensis the estimated tiny height of less than 4 feet (1.2 meters), but also the strange (but different) mixture of primitive and derived traits, which may suggest a common origin from an early australopithecine-like form similar to the controversial wastebasket taxon “Homo” habilisthat may rather represent an australopithecine according to many critical paleoanthropologists. It is interesting that the most recent phylogenetic analysis (Argue et al. 2017) of Homo floresiensis revealed that it is not a dwarf descendent of Homo erectus, as had become the majority view, but a descendent of an archaic African hominin close to Homo habilis. It should neither exist at that remote place outside of Africa nor at that late time more than 1.75 million years after the supposed extinction of such forms (Australian National University 2017). Likewise, Homo luzonensis was found at the wrong place and at the wrong time. Such a primitive hominin should not have been living on the Philippines at all, and certainly not just 50,000 years ago as a contemporary of modern humans. So much for the popular evolutionist myth that there are no out-of-place fossils thwarting Darwinian expectations.

Another obvious problem that bothers scientists is: How did this primitive man get there at all? Some have suggested that archaic hominins reached SE Asian islands like Flores, Luzon, and Sulawesi (Talepu site stone tools from 118,000 years ago, van den Bergh et al. 2016, Greshko 2016), as well as the Mediterranean island of Crete (Associated Press 2011, Davis 2018), accidently with driftwood during storms or tsunami events, while others say that these extinct humans were smarter than we thought and could deliberately build ocean-going rafts. Hawks (2018, 2019b, 2019c) agrees and remarks that this would better explain three independent colonizations of East Asian islands that could not all have been reached by land bridges. However, the earliest archaeological evidence for boat building (the famous Pesse canoe from the Netherlands) is only from the Mesolithic period, less than 10,000 years ago. 

Last but not least, I would like to disagree with a critique of the new discovery that is, in my humble opinion, not warranted. Blogger and writer Dr. J.R. Miller is cited at Uncommon Descent (Anonymous 2019) with the claim that the Wall Street Journal article (Hotz 2019) strips its headline (“Fossil Evidence of New Human Species Found in Philippines”) of any meaning. He lists four quotes from the article to support his claim:

• “Small-jawed with dainty teeth, able to walk upright but with feet still shaped to climb, these island creatures were a mix-and-match patchwork of primitive and advanced features in a unique variation of the human form, …”
• “So far, the scientists haven’t found evidence that these creatures used tools to hunt or to process their food…”
• “The scientists also have been unable to isolate DNA from the bones and teeth that could be used to understand how closely they were related to other human species.”
• “The scientists also don’t know how these creatures reached the island.”

However, the first point actually confirms the status as a new species, and the other three points are mostly irrelevant to the claim in the Journal’s headline and the title of the scientific paper. I mention this because I think that skeptics of Darwinism should be careful not to cavil about new evolutionary studies, but should rather strive to accurately point out real scientific flaws and limits, and most of all show how an inference to the best explanation of all the scientific evidence indeed points against Darwinism.

Not Junk Science

This new discovery is highly interesting and by no means junk science. It confirms that the fossil evidence supports neither an unambiguous phylogenetic tree of fossil humans nor a smooth directional evolutionary trajectory from ape-like to human-like forms. Furthermore, the fossils occur at the wrong place and the wrong time. Therefore, we see three core predictions of neo-Darwinian evolutionary theory again refuted by empirical data. That’s how good science is supposed to work according to the late great philosopher of science Sir Karl Popper (1963): Conjectures and Refutations! If a theory and its proponents stubbornly refuse falsification by an ever increasing body of substantial conflicting evidence, the theory degenerates into a textbook example of dogmatic pseudo-science. The neo-Darwinian theory of macroevolution has failed on all fronts, from mathematical feasibility, to theoretical plausibility and explanatory power, to empirical support.

References:

• Anonymous 2019. Shakeup! New Human Find From Over 50,000 Years Ago Shows Our Ancestors Were Smarter Than Once Thought. Uncommon Descent April 11, 2019.
• Associated Press 2011. Cretan tools point to 130,000-year-old sea travel. NBC News Jan. 3, 2011.
• Argue D, Groves CP, Lee MSY, Jungers WL 2017. The affinities of Homo floresiensis based on phylogenetic analyses of cranial, dental, and postcranial characters. Journal of Human Evolution 107: 107-33.
• Australian National University 2017. Origins of Indonesian Hobbits finally revealed. Science Daily, April 21, 2017.
• Bechly G 2018. Rewriting Human Origins, Ongoing in East Asia. Evolution News, Nov. 28, 2018.
• Bechly G 2019. Günter Bechly: Human Evolution’s Once “Indisputable Facts” Now “Dead Theory.” ID the Future, March 20, 2019.
• Davis N 2018. Homo erectus may have been a sailor —and able to speak. The Guardian, Feb. 20, 2018.
• Détroit F, Mijares AS, Corny J, Daver G, Zanolli C, Dizon E, Robles E, Grün R, Piper PJ 2019. A new species of Homo from the Late Pleistocene of the Philippines. Nature 568, 181-186.
• Greshko M 2016. Stone Tools Point to Mysterious Neighbor of Flores “Hobbit”. National Geographic, Jan. 13, 2016.
• Greshko M, Wei-Haas M 2019. New species of ancient human discovered in the Philippines. National Geographic, April 10, 2019.
• Hawks J 2018. Looking at Luzon hominins, from the perspective of 1985. John Hawks Weblog, May 3, 2018.
• Hawks J 2019a. Three big insights into our African origins. Medium Jan. 4, 2019.
• Hawks J 2019b. New Hominin Shakes the Family Tree — Again. Sapiens, April 10, 2019.
• Hawks J 2019c. New species of hominin from Luzon. John Hawks Weblog, April 10, 2019.
• Hotz RL 2019. Fossil Evidence of New Human Species Found in Philippines. Wall Street Journal, April 10, 2019.
• Ingicco T et al 2018. Earliest known hominin activity in the Philippines by 709 thousand years ago. Nature 557, 233-237.
• Jones N 2019. First Confirmed Denisovan Skull Piece Found. Sapiens, March 1, 2019.
• Joyce C 2019. Ancient Bones And Teeth Found In A Philippine Cave May Rewrite Human History. NPR, April 10, 2019.
• Klinghoffer D 2019. Bechly: Lessons from the Ongoing “Rewrite” of Human Origins. Evolution News,March 21, 2019.
• Mijares AS et al. 2010. New evidence for a 67,000-year-old human presence at Callao Cave, Luzon, Philippines. Journal of Human Evolution 59(1), 123-132.
• Stoddart C 2019. These bones belong to a new species of human. Nature Video, April 10, 2019.
• Van den Bergh G et al. 2016. Stone Tools Point to Mysterious Neighbor of Flores ‘Hobbit’. Nature 529, 208-211.
• Zimmer K. New Species of Human, Homo luzonensis, Identified in the Philippines. The Scientist, Apr. 10, 2019.

Photo: Callao Cave, by Ervin Malicdem [CC BY-SA 4.0], via Wikimedia Commons.

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WHAT A MAAMIN SHOULD DO

I don’t think I get an original idea too often and when I do, there is no guarantee that it’s necessarily a good one. A few weeks ago was one of those very rare occasions in my life when I got one that actually checked both boxes. I still called the Gateshead Rav, shlita, and several other Rabbanim to make sure. Shavuos had just ended. I enjoyed enormously the people I had met at the hotel program where I had been speaking. Then I thought of the next significant event in the Jewish calendar and my good mood vanished. Shivah Asar B’Tammuz and the start of the Three Weeks was coming up next. Harav Moshe Feinstein, zt”l, famously got upset when he heard Jews uttering the phrase, “Shver tzu zayn a Yid — It’s hard to be a Jew.” His distress is understandable. “How many Jews left the Torah,” he would ask, “because all day long they heard their parents utter those awful words!” But then, the Three Weeks are a return to a time when repeatedly, over and over, the phrase that caused Reb Moshe distress seems to describe our situation perfectly. We just don’t seem able to solve the “Three Week” problem. I wrote a book about this last year. Building Tomorrow discusses sinas chinam and how to get rid of it for good. To paraphrase the Talmud Yerushalmi in Yoma: If you live in a generation where Shivah Asar B’Tammuz is on the calendar, you are doing the same things as those who put it there in the first place. But of course I wrote that book before I had my lightbulb moment. Maybe if I’d had my epiphany and then submitted the manuscript, things would have been different! At this point you are probably wondering what on earth I’m talking about. I know it’s unfair to keep you in suspense, but before I reveal my intention I have to tell you a story. Soon after I moved to the U.S., the job for which I had moved here ran out of money, leaving me unemployed. Our financial situation was desperate and I went to discuss it with Harav Mattisyahu Salomon, shlita. I have known him for over 40 years. I outlined my predicament. Then I said, “I don’t know why I am so worried. I think I am a maamin, but if I really am a maamin, why am I so worried?” He looked at me thoughtfully as I finished, “I the view WHAT A MAAMIN SHOULD DO feel such a fraud.” Rav Mattisyahu considered for a long moment and said, “Maybe you are a fraud!” Then he resumed the smile I know so well. The conclusion we came to was that maybe this had happened to me precisely to make me consider what sort of relationship I actually have with Hashem. After all, if I really do have emunah and bitachon, why wasn’t I talking to Him about my desperate financial situation? And that is the eureka moment I would like to share with you, in order to remove the fast of 17 Tammuz from our calendars once and for all. Sinas chinam and lashon hara have stuck tenaciously to us for 2,000 years. Tragically, our inability to change that fact makes “shver tzu zayn a Yid” seem to fit us perfectly. So the next time someone upsets you and the need to tell someone swells up inside you like a bomb about to explode … go ahead! Only make sure you tell it to the only One who can really do something about it. Tell Hashem. Now I know this sounds silly, but Chazal tell us that the Satan falls for his own tricks! As long as he got you to speak lashon hara, he thinks he’s won and leaves you alone, even if it was to Hashem! I have tried this out and it really works. Let Hashem know exactly what happened (you won’t be telling Him anything new). Pour out your heart. Make it clear you aren’t trying to “convict” anyone, just express why you’re so upset. The strange thing is, in telling it all to Him you really won’t feel the need to tell anyone else. After all, isn’t that precisely what a maamin would do?  Rabbi Rubinstein is a renowned author and lecturer. He lives in New York and travels all over the world to speak and teach. And that is the eureka moment I would like to share with you, in order to remove the fast of 17 Tammuz from our calendars by RABBI Y. Y. RUBINSTEIN 30 Sivan 5779 9