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My last drop

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I was looking back in my diary, trying to find clues to why I was struggling with severe insomnia. I had just begun to take new antidepression medications, and something wasn’t right. I’d experienced insomnia before, and now I saw the common thread. In both cases, my psychiatrist had started me on new medications and had recommended that I temporarily stop drinking alcohol. Suddenly it hit me: The insomnia was a symptom of alcohol withdrawal. I was a functioning alcoholic. It was the wake-up call I needed, and I’ve been sober ever since. But now I worry that others, facing the stresses and sadness of the pandemic, may be starting down a similar path. Here’s my cautionary tale.

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ILLUSTRATION: ROBERT NEUBECKER

“It was the wake-up call I needed, and I’ve been sober ever since.”

Alcohol had long been a respite for me. During high school and into college, I drank heavily to cope with anxiety. Part of me knew this wasn’t a healthy approach, but it seemed to work. When I discovered a love of geochemistry, I eased up on my drinking. On weekdays, I chose to study rather than go to the bars. I still enjoyed drinking on weekends, but it was social drinking—nothing I was concerned about. Throughout grad school and my early years as a professor, I still sometimes drank too much. But it didn’t cause problems.

That started to change roughly 11 years into my faculty position, when my father died. Devastated by his loss, I began to suffer from depression, which in turn led to weight gain and sleep apnea. I became chronically sleep deprived and could no longer think clearly, which made it challenging to meet the intellectual demands of my job. I suffered from a short temper and strained relationships. I started to self-medicate with alcohol, which reduced my anxiety in the short term. But eventually I became so depressed that I no longer tried to restrain my drinking. I took up mixology as a hobby and started to drink cocktails every night.

Years passed, and I still felt deeply unhappy. I decided to see a psychiatrist, who began to treat me for chronic depression at first. It took me several more years to recognize I was an alcoholic.

An important clue came one morning when I awoke after an awards dinner at a conference feeling so hungover I wasn’t able to co-chair a session that morning as planned; I had to ask colleagues to go on without me. I had vowed not to drink too much. But my anxiety got the best of me. After multiple bottles of wine were placed on the table in front of me, I started to drink heavily, the conversation distracting me from realizing how much I consumed. Afterward, I was frustrated and confused by my lack of control, but I wasn’t quite ready to admit I had a serious problem.

That changed a few months later when I looked back on my diary and finally, with the help of my psychiatrist, named my problem. I immediately committed to abstinence. The first 6 weeks were especially hard, but I got through them by exercising regularly and spending time with my family. I was fortunate that I was on a sabbatical at that time, which gave me space to focus on my health and recovery. I started to practice mindfulness and meditation and attend Alcoholics Anonymous meetings. I also took time to learn about a new scientific discipline and start a new collaboration, which got my creative juices flowing again and helped me rediscover my thirst for research.

Now, nearly 10 years later, I live with less stress, have healthier relationships, and am happier and more productive. I still suffer from anxiety, but I find that regular exercise and meditation help me cope. When I attend conferences—at least, when I used to do so in person, before COVID-19—I avoid alcohol-centered events or decline the free alcohol tickets. Occasionally, I get odd looks from colleagues, but they quickly understand when I tell them I’m a recovered alcoholic. No one I’ve confided in has made me feel bad.

If you’re one of the many people who are currently struggling in the midst of the pandemic, take it from me: Alcohol may make you feel better temporarily, but it’s not a healthy way to cope with stress and anxiety. Ask for help instead.

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Science

Deep abiotic weathering of pyrite

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Getting rid of fool’s gold

Pyrite, also called fool’s gold, is an iron sulfide mineral that is very commonly found in rock but is almost nonexistent in sediments today. Pyrite oxidizes quickly and is a major source of sulfur to the ocean, but it is also a proxy for the oxygen content historically in Earth’s atmosphere. Gu et al. conducted a set of detailed observations of the pyrite oxidation process in a shale unit. The authors found that erosion tied to fracturing is just as important as the oxygen content for the dissolution process. They developed a model that helps determine the conditions in Earth’s past for which pyrite might have been stable and the role of microorganisms in the oxidation process.

Science, this issue p. eabb8092

Structured Abstract

INTRODUCTION

Oxidative weathering of pyrite, the most abundant sulfide mineral in Earth’s crust, is coupled to the biogeochemical cycles of sulfur, oxygen, carbon, and iron. Pyrite oxidation is key to these cycles because of its high reactivity with oxygen. Before the Great Oxidation Event (GOE), atmospheric oxygen concentrations were low on early Earth and pyrite was exposed at Earth’s surface, allowing erosion into sediments that were preserved in river deposits. Today, it oxidizes at depth in most rocks and is often not exposed at the land surface. To understand pyrite weathering through geologic time, researchers extrapolate the reaction kinetics based on studies from the laboratory or in acid mine drainage. Such work has emphasized the important role of microorganisms in catalyzing pyrite oxidation. But to interpret the oxidation rates of pyrite on early Earth requires knowledge of the rate-limiting step of the oxidation as it occurs naturally in rocks.

RATIONALE

We investigated the oxidation of pyrite in micrometer-sized grains, in centimeter-sized rock fragments, and in meter-scale boreholes at a small, well-studied catchment in a critical-zone observatory. Our goal was to determine the reaction mechanism of pyrite weathering in rocks as it occurs today. The slow-eroding catchment is underlain by shale, the most common rock type exposed on Earth. We determined weathering profiles of pyrite through chemical and microscopic analysis.

RESULTS

At the ridgelines of the shale watershed, most pyrite oxidation occurs within a 1-m-thick reaction zone ∼16 m below land surface, just above the depth of water table fluctuation. This is the reaction front at the borehole scale. Only limited oxidation occurs in halos around a few fractures at deeper depths. Above the depth where pyrite is 100% oxidized in all boreholes, rock fracture density and porosity are generally higher than below. However, the narrow parts of pore openings called pore throats remain small enough in oxidizing shale to limit access of microorganisms to the pyrite surface. During oxidation, iron oxides pseudomorphically replace the pyrite grains. High-resolution transmission electron microscopy (TEM) reveals that the oxidation front at grain scale is defined by a sharp interface between pyrite and an iron (oxyhydr)oxide (Fh) that is either ferrihydrite or feroxyhyte. This Fh then transforms into a banded structure of iron oxides that ultimately alter to goethite in outer layers. This complex oxidative transformation progresses inward from fractures when observed at clast scale.

CONCLUSION

Under today’s atmosphere, pyrite oxidation, rate-limited by diffusion of oxygen at the grain scale, is regulated by fracturing at clast scale. As pyrite is oxidized at borehole scale before reaching the land surface in most landscapes today, the oxidation rate is controlled by the movement of pyrite upward, which is in turn limited by the rate of erosion. Comparisons of shale landscapes with different erosion rates reveal that fracture spacing varies with erosion rate, so this suggests that fracture spacing may couple the landscape-scale to grain-scale rates. Microbial acceleration of oxidation globally today is unlikely in low-porosity rocks because pyrite oxidation usually occurs at depth, where pore throats limit access, as observed here for shales. Before the GOE, the rate of pyrite oxidation was instead controlled by the slower reaction kinetics in the presence of lower atmospheric oxygen concentrations. At that time, therefore, pyrite was exposed at the land surface, where microbial interaction could have accelerated the oxidation and acidified the landscape, as suggested by others. Our work highlights the importance of fracturing and erosion in addition to atmospheric oxygen as a control on the reactivity of this ubiquitous iron sulfide.

Schematic depiction of oxidative weathering of pyrite in rocks buried at meters depth.

Pyrite oxidation was studied from the molecular (TEM) scale of the pyrite―Fe oxide interface through clast and borehole scales to extrapolate to landscapes. The rate of oxidation of pyrite, limited at grain scale by oxygen diffusion through the shale matrix, is regulated at larger scales by fracturing and erosion.

Abstract

Pyrite is a ubiquitous iron sulfide mineral that is oxidized by trace oxygen. The mineral has been largely absent from global sediments since the rise in oxygen concentration in Earth’s early atmosphere. We analyzed weathering in shale, the most common rock exposed at Earth’s surface, with chemical and microscopic analysis. By looking across scales from 10−9 to 102 meters, we determined the factors that control pyrite oxidation. Under the atmosphere today, pyrite oxidation is rate-limited by diffusion of oxygen to the grain surface and regulated by large-scale erosion and clast-scale fracturing. We determined that neither iron- nor sulfur-oxidizing microorganisms control global pyrite weathering fluxes despite their ability to catalyze the reaction. This multiscale picture emphasizes that fracturing and erosion are as important as atmospheric oxygen in limiting pyrite reactivity over Earth’s history.

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Moving heart elements and cells

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Transposable elements comprise a large percentage of the human genome, with the endogenous retrovirus (ERV) subclass representing more than 8%. Using human pluripotent stem cell–derived cardiomyocytes and bioengineered micropatterning to recapitulate cardiogenesis, Wilson et al. found evidence that the primate-specific ERV MER41 is involved in primate heart development. A MER41-derived long noncoding RNA called BANCR is exclusively expressed in the fetal heart. When BANCR is eliminated, cardiomyocyte migration is disrupted. The cardiogenic transcription factor TBX5 and Hippo signaling factors TEAD4/YAP1 bind to a BANCR enhancer during fetal development. A related analysis in mouse shows that heart size increases with embryo BANCR knock-in.

Dev. Cell 54, 694 (2020).

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Science

Obesity and inflammation

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Accumulation of fat cells (shown in yellow in this micrograph) may be promoted by gene variants linked to inflammation.

IMAGE: DAVID M. PHILLIPS/SCIENCE SOURCE

Obesity is associated with chronic inflammation, which can trigger other diseases such as atherosclerosis, type 2 diabetes, and even cancer. There appears to be a genetic component to excess fat accumulation, and studies suggest that inflammatory gene variants may contribute. Karunakaran et al. found that single-nucleotide polymorphisms in the human receptor-interacting serine/threonine-protein kinase 1 gene (RIPK1) increase its expression and are causally associated with obesity. RIPK1 is a key regulator of inflammatory responses and cell death. Silencing of Ripk1 in mice on a high-fat diet reduced fat mass, body weight, and inflammatory responses in adipose tissue. This suggests that RIPK1-mediated inflammation (and possibly other functions) contribute to obesity and that RIPK1 could be a therapeutic target.

Nat. Metab. 10.1038/s42255-020-00279-2 (2020).

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