Eggs are less likely to crack when dropped on their side, according to science
NEW YORK (AP) — Eggs are less likely to crack when they fall on their side, according to experiments with over 200 eggs.
What does this mean for the best way to crack an egg for breakfas t? Not much, since a break around the middle is the best way to get the golden yolk and runny whites to ooze out.
But scientists said it could help with hard-boiling eggs in a pot: Dropping eggs in horizontally may be less likely to cause a stray crack that can unleash the egg's insides in a puffy, cloudy mess.
It's commonly thought that eggs are strongest at their ends — after all, it's how they're packaged in the carton. The thinking is that the arc-shaped bottom of an egg redirects the force and softens the blow of impact.
But when scientists squeezed eggs in both directions during a compression test, they cracked under the same amount of force.
'The fun started when we thought we would get one result and then we saw another,' said Hudson Borja da Rocha with Massachusetts Institute of Technology, who helped run the experiments.
The researchers also ran simulations and dropped eggs horizontally and vertically from three short heights up to 0.4 inches (10 millimeters).
The egg result? The ones dropped horizontally cracked less .
'The common sense is that the egg in the vertical direction is stronger than if you lay the egg down. But they proved that's not the case,' said materials scientist Marc Meyers with the University of California, San Diego who was not involved with the new study.
Scientists found that the egg's equator was more flexible and absorbed more of the energy of the fall before cracking. The findings were published Thursday in the journal Communications Physics.
Eggs are also usually nestled top-down into homemade contraptions for egg drop challenges as part of school STEM projects, which partially inspired the new study. It's not yet clear whether the new results will help protect these vulnerable eggs, which are dropped at much loftier heights.
It's a bit counterintuitive that the oblong side of an egg could hold up better against a tumble, said study co-author Tal Cohen with Massachusetts Institute of Technology.
Countless broken eggs show 'the courage to go and challenge these very common, accepted notions,' Cohen said.
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The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute's Science and Educational Media Group and the Robert Wood Johnson Foundation. The AP is solely responsible for all content.
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Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending June 13, 2025, John Mandrola, MD, comments on the following topics: Listener feedback on cardiac sarcoidosis, SA node ablation, surgical AF ablation, chronic kidney disease protection, and recruiting for clinical trials. One of the best parts of this podcast is the listener feedback I receive. This week, David Birnie, MD, the division chief of cardiology at the University of Ottawa and an academic electrophysiologist, active in cardiac sarcoid research, sent me feedback on a paper from Dutch and American authors that I covered 2 weeks ago on May 30. 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And the title of that paper was: 'Treatment with corticosteroids was associated with an increase in ventricular arrhythmia burden in patients with clinically manifest cardiac sarcoidosis: Insights from implantable cardioverter-defibrillator diagnostics.' He adds that most of us in the field regard this subgroup as an exception to any sort of late gadolinium enhancement (LGE) cutoff or pattern 'rule.' Indeed, due to increased awareness and CMR and PET, we are increasingly diagnosing these patients earlier and earlier and there are reports where the PET scan is positive and the MRI is actually negative (Eur J Nucl Med Mol Imaging. 2016 Feb;43(2):259-269). That is, the disease is picked up so early in the process that scar has not yet formed. These findings led Dr Birnie to strongly recommend that all patients in this sub-group are recommended to have an ICD regardless of LGE. 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This study included authors who were employees of AtriCure, the company that makes the linear ablation device. It was not randomized, not blinded, and included no sham procedures. The control arm of endocardial ablation we know does not work. My take of this space and condition is that research should be focused on the causes of IST. I warn my colleagues not to run amok with PFA. I understand the urge to do something aggressive for these patients, because IST causes a lot of symptoms. Care of these patients requires tons of empathy, honesty about uncertainty, patience, and reassurance that it will likely improve with time. IST is similar in some ways to postural orthostatic tachycardia syndrome (POTS) and things like supine exercise often works. But not right away. PFA makes it easier to destroy cardiac tissue, that's good in the left atrium (LA) because we can avoid atrioesophageal fistula. But IST should infuse us with great caution. 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Not only because it's potentially very helpful, but also because it can be incomplete, or, what I call willy-nilly ablation to add an extra CPT code. This is especially bad because it can lead to LA flutters or poor atrial transport function. A recent retrospective, observational comparison study published by a number of academic surgeons in the Annals of Thoracic Surgery has stirred some conversation online. It's stirred conversation because the group who received surgical ablation had a significant survival advantage. The data source came from Medicare. Patients who had ablation at the time of coronary artery bypass grafting (CABG), which also includes hospital and surgeon volume as well as the surgeon's preference for doing ablation. Some do it a lot; others do it very little. That is a hint. The primary endpoint was all-cause mortality, which I often like because it is free of ascertainment bias — alive or dead. But it is not a great AF ablation endpoint because exactly zero non-HF trials of AF ablation show mortality reduction. That's because reducing AF burden is unlikely to reduce death, because of competing causes of death. That too is a hint. This study had a twist, though, in the comparison, which is necessary, because literally everyone knows that healthier patients are more likely to get concomitant ablation. The authors did something else to try and sort out the obvious confounding. They did an instrument variable analysis wherein the authors used surgeon preference for ablation as the "instrumental variable" (IV variable). Here's how it works: Some surgeons frequently perform ablation (> 40% of their cases) Some surgeons rarely perform ablation (< 5% of their cases) A patient's treatment depends partly on which surgeon they happen to see, and this creates — from a patient perspective — a "quasi-randomization." Then the authors do two parallel analyses: both require propensity matching techniques. As-treated analysis, which is a direct comparison of patients who got ablation vs. those who didn't. This is the traditional and highly biased approach. Surgeon-preference analysis: a patient with AF is sort of randomized in which surgeon operates on them. And if surgical AF ablation reduces mortality, surgeons who do more often should have lower mortality. This approach is interesting because if both analyses show similar results, it somewhat strengthens confidence that the findings are real rather than due to selection bias. And that's exactly what they found: As-treated analysis : 4.40 months survival advantage Surgeon-preference analysis: 4.96 months survival advantage The concordance between led the authors to conclude: 'Our findings support current guidelines recommending for surgical ablation during CABG in patients with atrial fibrillation and it highlights that ablation is currently underused in contemporary practice.' I am very warm to the possibility that concomitant surgical AF ablation may be a good thing to do for some patients with coronary artery disease (CAD) and CABG and AF. But this study does not support anything, nor does it suggest AF ablation is underused. Despite doing an IV analysis, which sounds great, this is still a non-randomized comparison. There is likely selection bias that cannot be overcome by matching. For instance, surgeons who do more AF ablation may see different types of patients, they may work at a better hospital and do better follow-up. These are things that randomization takes care of. That's not the main reason I don't put any weight on this study: the main reason is that the authors found no difference in the incidence of stroke in the two groups with either the as-treated or surgeon preference analysis. So, I ask, if the ablation of AF is not good enough to reduce stroke, how does it reduce death? I don't see a mechanism for reducing death — especially given all the other competing risks. What's more, the Whitlock meta-analysis of 23 RCTs showed no reduction in death with surgical ablation. So, your prior belief has to be extremely pessimistic and therefore it would take strong evidence to change. About 100 times stronger data than this. What's more, the mortality curves separate (by only 4 months) after 5 years. That seems a) like a minimal difference and b) separation over that long a time seems more related to healthier patients getting surgical ablation or better health systems. I want to continue my friendships with the cardiac surgeons. They do important work. But I would also suggest as humbly as possible that they need to improve when it comes to evidence generation. To me, there seems a huge need for proper RCTs of standardized AF ablation techniques. Endpoints should not be all-cause death. It should be AF burden and stroke incidence. Given the increasing prevenance of AF and CAD, I would think this would be a fantastic place for the new NIH leadership to invest money in. I realize that TWIC is a cardiology podcast, but we have yet another big randomized controlled trial of finerenone, the newest mineralocorticoid receptor antagonist, or MRA. As an EP doctor in the Southeastern United States, are unhealthiest geography, I see many patients for AF who also have type 2 diabetes (T2D) and chronic kidney disease (CKD). It goes with the territory. If you are an AF patient obese enough to have T2D, you likely have some CKD. I scratch my head these days, because in T2D there are so many drug classes available. Which one should we use, or should we use both—as if the drugs were generic $4 per month tablets. New England Journal of Medicine published the CONFIDENCE trial last week. I discuss it because it provokes me to think about science questions vs marketing efforts. Here is the deal. Patients with T2D who were taking an ACE inhibitor or ARB and had CKD as defined by an increased urinary albumin-to-creatinine ratio. I know, cardiologists don't use this number. Just think about it as enough CKD to spill protein, which is bad, and correlates with CV outcomes. The study treatment arms were finerenone alone, empagliflozin alone, or the combination of the two. The primary outcome was change in the urine albumin-to-creatinine (UACR) ratio. About 800 patients were randomized in the three arms. The main result was expressed in relative risk reduction: At day 180, the UACR ratio results were: Finerenone alone had a 32% reduction Empagliflozin alone: 29% reduction And the combination therapy had a 52% reduction from baseline So, the reduction with combination therapy was 29% greater than that with finerenone alone and 32% greater than that with empagliflozin alone; both were highly statistically significant. Adverse events and drug discontinuation were similar, though there was a decrease in the estimated glomerular filtration rate (eGFR) of greater than 30% at day 30 in two times more patients in the combination group, though GFR improved at study end when the drugs were stopped. In addition: 'the frequency of hyperkalemia, was relatively lower by approximately 15 to 20% with combination therapy.' For the optimistic or maximizer-docs, the previous model was sequential initiation of these two drug classes. This trial shows that simultaneous initiation worked better. But there were many critical appraisal issues — so many in fact, that it makes me wonder whether this was a marketing exercise. The most obvious issue is the endpoint. While we can say that cholesterol levels, or blood pressure (BP), or creatinine, these are surrogate markers that most patients don't care about. The UACR ratio is even more esoteric and likely even less of a surrogate marker than LDL or BP. The point of kidney protection strategies is to lower kidney outcomes — new dialysis, even doubling of the creatinine, or CV events. I realize UACR ratio is easier and may be an earlier sign, but I will quote the authors own words to underscore the uncertainty: Quote: 'We speculate that, taken together, these data suggest that the reductions observed with combination therapy with empagliflozin and finerenone will probably correlate with meaningful reductions in the risk of progression of chronic kidney disease.' I mean, that is truly remarkable in the NEJM. We speculate, probably . Wow. Then there is the matter of a 6-month trial. These were 67-year-old patients How long are we supposed to use these two classes of meds? Forever? Really? Then there is the matter of the 44-day screening period before randomization. They screened 1600 patients and excluded half. Why? They don't say. Highly selected patients, though, is not nefarious — lots of trials pick the perfect patient. But I mention the screen to randomized information because it speaks to the generalizability of this data. Finally, and I sound like a broken record, whenever finerenone is used in a trial, there should be an arm for spironolactone or eplerenone. That way, we would have an idea of the incremental value, if any, of the new nonsteroidal finerenone. In the end, I think CONFIDENCE was a marketing exercise. It does not change practice, and 6-month data of a very surrogate endpoint hardly meets any regulatory standard. Two UK Cardiology Trials Struggle to Recruit Patients Journalist Sara Freeman reports from the meeting of the British Cardiovascular Society meeting in Manchester, which I was lucky enough to be asked to speak last year, on a session describing difficulty in recruiting patients for two important clinical trials. This is an important topic. I can add a third trial that is also noting slow enrollment. In the UK, the CRAAFT-HF trial compares surgical vs catheter ablation in patients with HF. This is a hugely important question. For multiple reasons: the first is that despite my friendship with Nassir Marrouche, Christian Sohns, and Philipp Sommer, the principal investigators of CASTLE and CASTLE HTx, the numbers of HF patients in trials of AF ablation are few. The event rates are low, and the evidence for AF ablation in HF is limited. CRAAFT-HF would add to that evidence base. What's more, patients with HF often have atrial structural disease making them less likely to be pulmonary vein isolation (PVI) responders. And surgical AF ablation could also remove the left atrial appendage epicardially, a maneuver proven effective in the LAAOS III trial. I think surgical AF ablation could beat catheter-based ablation. The main problem with recruitment is the strict entry criteria. Indeed, this is a problem in HF and AF, as the chief weakness of the CASTLE trials was the highly selective entry criteria. The second UK trial having problems is the BRITISH trial of using scar on CMR to determine ICD implantation in patients with non-ischemic cardiomyopathy (NICM). BRITISH has a really brave trial protocol. Patients with NICM LVEF < 35% who have a scar on CMR would be randomized to either ICD or CRT-D vs implantable loop recorder (ILR) or CRT-P. (Basically no backup ICD). This is exactly what we want to know. It's a beautiful study question. The third trial that I traveled to Berlin to speak about this winter is the bravest of them all: The PROFID trial, which seeks to replicate the MADIT-II trial 20 years after. MADIT-II was ischemic CM with ejection fraction < 30% and the ICD reduced mortality with a number needed to treat of < 25. The idea behind PROFID is that sudden death rates in HF have fallen, medical therapy has improved, and the delta between the ICD arm and medical therapy arm is surely less. Well, PROFID also has had slow enrollment, for a couple of reasons: one is that there aren't that many terrible ischemic CM patients out there anymore, thanks to the IC community and rapid percutaneous coronary intervention (PCI) during ST-elevation myocardial infarction (STEMI). The second issue is that, at least in Germany, if you are a doc who randomizes a patient to PROFID and they are randomized to the medical arm, you lose reimbursement for the ICD. I highlight this topic mostly for my EP colleagues. While PFA holds all the excitement, we have stalled in terms of new major evidence development. PFA is nice, especially for patients, but if we are to maintain are stature as a profession, we need to support those who seek to answer important questions, like CRAAFT-HF, BRITISH, and PROFID.
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