Saturday 15 December 2018
Looking for magical beasts? Just ask your nearest Darwinian apologist.
Prehoda's Goof: Mutational Fitness Effects Cannot Be Predicted
Evolution News & Views
Last February when we looked into the claims of University of Oregon biochemist Kenneth Prehoda, we saw him pounding Darwin's pulpit with righteous fervor. He practically shouted that you could get instant animals by chance. His team's discovery of a mutation that seemed to allow proteins to interact more easily in a choanoflagellate became the springboard for a sermon envisioning all the marvels of multicellularity without intelligent design.
Indeed, a breathless reporter from the Washington Post gave him credit for explaining human beings with that one random accident: "Every example of cells collaborating that has arisen since -- from the trilobites of 500 million years ago to the dinosaurs, woolly mammoths and you -- probably relied on it or some other similar mutation."
He has toned down the rhetoric a bit in the latest news from his lab. Maybe he didn't want to face another Twitter storm by engaging "the ire of anti-evolutionists" the way he did last time. "We've witnessed evolution," he had said. "Evolution is just a fact, hands down." Even his reviewers had gotten on his case for overstating the implications of his findings. We showed that there were plenty of empirical and logical reasons, not religious reasons, for doubting the significance of his instant-animal mutation.
This time, the news item makes more modest claims:
Just as the course of a drift boat can be irreversibly altered by a log in its path, a single mutation can send life in an entirely new direction.
That scenario, says UO biochemist Ken Prehoda, provides a window on how one mutation sparked a huge jump in the evolutionary course of a protein important for the evolution of animals.
Earlier this year, Prehoda was on a team that found that a random mutation 600 million years ago in a single-celled organism created a new family of proteins that are important for multicellular life. In a new paper, now online ahead of print in the Journal of the American Chemical Society, Prehoda and colleagues describe what the mutation did to the original protein family.
Mutations happen randomly. Most are bad news. But occasionally a mutation is good, helping an organism adapt to environmental changes or advancing overall fitness. Understanding such changes better, Prehoda said, could potentially point to new treatments for human diseases such as cancer.
Ah, yes; evolutionists can score extra points for claiming their otherwise esoteric research "could potentially" lead to cures for cancer. But we don't need to deduct those points; there are enough other vulnerable points at risk of lowering Darwin's score.
Prehoda's basic claim was that a point mutation in an enzyme called guanylate kinase gave it a new protein-interacting domain (PID), launching the GKPID family of enzymes used by all animals. And coincidentally, this mutation happened right when multicellular organisms were first appearing 600 million years ago. Could human beings be far behind?
Prehoda now reveals that all he found was that the mutation "stiffened" the GK enzyme a bit. One might think this to be a disadvantage, but he weaves a story that the stiffening of the enzyme's backbone actually was a good thing.
The mutation, which researchers labeled s36P, set off a cascade of events in which protein interactions took new routes and evolved into more complex multicellular organisms, Prehoda said. The mutation is still conserved in all animals today, he added.
"A lot of the proteins that do the work in our bodies can be thought of as molecular machines," Prehoda said. "They move in a way that is coordinated with function. Each protein spins in a circle or motors along filaments. Our protein, before the mutation, was an enzyme that had certain flexible movements related to its function. This one mutation fixed the protein's backbone, locking the molecule into a shape that is important for its new function."
Incidentally, the spinning machine is ATP synthase, and the motor is most likely kinesin. We find that out in the new paper, published this time not in eLife but in the Journal of the American Chemical Society, which does not include reviewer's comments. For obvious reasons, Prehoda does not try to evolve ATP synthase by single point mutations.
In the paper, Whitney, Volkman and Prehoda mere "suggest" that the mutation that stiffened the GK enzyme "might have been important" for instigating new functions by "tuning" its "conformational flexibility" in some way. Even so, they retain some epistemic modesty in this less audacious hypothesis: "Furthermore, even if flexibility was important in the functional transition from enzyme to PID, we do not know how it was altered or how doing so could lead to such a dramatic change in function."
Unfortunately, a new paper just appeared in the Proceedings of the National Academy of Sciences that undercuts their premise. Prehoda's team assumes that random mutations can be ranked as "good" and "bad" -- as if you can sort them like marbles into green jars and red jars. In this view, good things add up, and bad things get tossed out by natural selection. That was Darwin's view, too:
It may be said that natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and in organic conditions of life.
The new PNAS paper by Bank et al., "On the (un)predictability of a large intragenic fitness landscape," takes a serious look at the effects of mutational interactions. Mutations aren't like isolated red and green marbles. They interact in complex ways. "Epistasis" is a term referring to the combinatorial effects of mutations. For instance, two neutral mutations might interact to produce a benefit; that would be a case of positive epistasis. On the other hand, a seemingly beneficial mutation could have negative effects elsewhere in the organism; that's called negative epistasis. It won't improve an organism's fitness, for example, if a mutation for stronger muscles also produces heart attacks.
The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen. Because their conclusion has far-reaching implications for all evolutionary predictions, it bears quoting in full:
Originally introduced as a metaphor to describe adaptive evolution, fitness landscapes promise to become a powerful tool in biology to address complex questions regarding the predictability of evolution and the prevalence of epistasis within and between genomic regions. Due to the high-dimensional nature of fitness landscapes, however, the ability to extrapolate will be paramount to progress in this area, and the optimal quantitative and qualitative approaches to achieve this goal are yet to be determined.
Here, we have taken an important step toward addressing this question via the creation and analysis of a landscape comprising 640 engineered mutants of the Hsp90 protein in yeast. The unprecedented size of the fitness landscape, along with the multiallelic nature, allows us to test whether global features could be extrapolated from subsets of the data. Although the global pattern indicates a rather homogeneous landscape, smaller sublandscapes are a poor predictor of the overall global pattern because of "epistatic hotspots."
In combination, our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable, because there are multiple optima and the probability to reach any one of them depends strongly on the starting genotype. At the same time, evolution may become locally predictable with the population following obligatory adaptive paths that are a direct result of the creation of fitness valleys owing to epistatic interactions.
The empirical fitness landscape studied here appears to be intermediate between these extremes. Although the global peak is within reach from almost any starting point, there is a local optimum that will be reached with appreciable probability, particular when starting from the parental genotype. From a practical standpoint, these results thus highlight the danger inherent to the common practice of constructing fitness landscapes from ascertained mutational combinations. However, this work also suggests that one promising way forward for increasing predictive power will be the utilization of multiple small landscapes used to gather information about the properties of individual mutations, combined with the integration of site-specific biophysical properties.
From this, we can see that Prehoda's team has taken a leap to think that one mutation in one enzyme would start a path to animals. He has not taken into account the effects of epistasis. Bank et al. say that local fitness peaks would be more likely to strand the animal there, rather than let it progress. Walking right past the "danger" sign, Prehoda engaged in the "common practice of constructing fitness landscapes from ascertained mutational combinations." At best, he should only investigate a "small landscape" around the mutation to see what might happen. Maybe it would help a certain choanoflagellate. Beyond that, he is on dangerous ground making predictions.
Prehoda might have this comeback argument. He could say that his work on "ancestral protein reconstruction" shows that the mutation occurred right at the time multicellularity took off. It's a postdiction, therefore, not a prediction. This argument, however, commits the fallacy of "affirming the consequent" -- i.e., "If P, then Q. Q occurs. Therefore, P." You can't say P caused Q. That overlooks multiple other possibilities for Q. In fact, there could be an infinite number of causes for Q besides P. Prehoda could only argue Q if and only if P: specifically, that the emergence of animals required a specific mutation to guanylate kinase. That would be unwarranted even within neo-Darwinian theory. The best he can say is that the mutation is "consistent with" a scenario in which a stiffer enzyme contributed to new functions useful to multicellular organisms, assuming it avoided negative epistasis in the process.
Such clarification, however, would be unlikely to yield headlines in the Washington Post. Empirically speaking, Bank et al.'s yeast remain yeast, and Prehoda et al.'s choanoflagellates remain choanoflagellates.
Evolution News & Views
Last February when we looked into the claims of University of Oregon biochemist Kenneth Prehoda, we saw him pounding Darwin's pulpit with righteous fervor. He practically shouted that you could get instant animals by chance. His team's discovery of a mutation that seemed to allow proteins to interact more easily in a choanoflagellate became the springboard for a sermon envisioning all the marvels of multicellularity without intelligent design.
Indeed, a breathless reporter from the Washington Post gave him credit for explaining human beings with that one random accident: "Every example of cells collaborating that has arisen since -- from the trilobites of 500 million years ago to the dinosaurs, woolly mammoths and you -- probably relied on it or some other similar mutation."
He has toned down the rhetoric a bit in the latest news from his lab. Maybe he didn't want to face another Twitter storm by engaging "the ire of anti-evolutionists" the way he did last time. "We've witnessed evolution," he had said. "Evolution is just a fact, hands down." Even his reviewers had gotten on his case for overstating the implications of his findings. We showed that there were plenty of empirical and logical reasons, not religious reasons, for doubting the significance of his instant-animal mutation.
This time, the news item makes more modest claims:
Just as the course of a drift boat can be irreversibly altered by a log in its path, a single mutation can send life in an entirely new direction.
That scenario, says UO biochemist Ken Prehoda, provides a window on how one mutation sparked a huge jump in the evolutionary course of a protein important for the evolution of animals.
Earlier this year, Prehoda was on a team that found that a random mutation 600 million years ago in a single-celled organism created a new family of proteins that are important for multicellular life. In a new paper, now online ahead of print in the Journal of the American Chemical Society, Prehoda and colleagues describe what the mutation did to the original protein family.
Mutations happen randomly. Most are bad news. But occasionally a mutation is good, helping an organism adapt to environmental changes or advancing overall fitness. Understanding such changes better, Prehoda said, could potentially point to new treatments for human diseases such as cancer.
Ah, yes; evolutionists can score extra points for claiming their otherwise esoteric research "could potentially" lead to cures for cancer. But we don't need to deduct those points; there are enough other vulnerable points at risk of lowering Darwin's score.
Prehoda's basic claim was that a point mutation in an enzyme called guanylate kinase gave it a new protein-interacting domain (PID), launching the GKPID family of enzymes used by all animals. And coincidentally, this mutation happened right when multicellular organisms were first appearing 600 million years ago. Could human beings be far behind?
Prehoda now reveals that all he found was that the mutation "stiffened" the GK enzyme a bit. One might think this to be a disadvantage, but he weaves a story that the stiffening of the enzyme's backbone actually was a good thing.
The mutation, which researchers labeled s36P, set off a cascade of events in which protein interactions took new routes and evolved into more complex multicellular organisms, Prehoda said. The mutation is still conserved in all animals today, he added.
"A lot of the proteins that do the work in our bodies can be thought of as molecular machines," Prehoda said. "They move in a way that is coordinated with function. Each protein spins in a circle or motors along filaments. Our protein, before the mutation, was an enzyme that had certain flexible movements related to its function. This one mutation fixed the protein's backbone, locking the molecule into a shape that is important for its new function."
Incidentally, the spinning machine is ATP synthase, and the motor is most likely kinesin. We find that out in the new paper, published this time not in eLife but in the Journal of the American Chemical Society, which does not include reviewer's comments. For obvious reasons, Prehoda does not try to evolve ATP synthase by single point mutations.
In the paper, Whitney, Volkman and Prehoda mere "suggest" that the mutation that stiffened the GK enzyme "might have been important" for instigating new functions by "tuning" its "conformational flexibility" in some way. Even so, they retain some epistemic modesty in this less audacious hypothesis: "Furthermore, even if flexibility was important in the functional transition from enzyme to PID, we do not know how it was altered or how doing so could lead to such a dramatic change in function."
Unfortunately, a new paper just appeared in the Proceedings of the National Academy of Sciences that undercuts their premise. Prehoda's team assumes that random mutations can be ranked as "good" and "bad" -- as if you can sort them like marbles into green jars and red jars. In this view, good things add up, and bad things get tossed out by natural selection. That was Darwin's view, too:
It may be said that natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and in organic conditions of life.
The new PNAS paper by Bank et al., "On the (un)predictability of a large intragenic fitness landscape," takes a serious look at the effects of mutational interactions. Mutations aren't like isolated red and green marbles. They interact in complex ways. "Epistasis" is a term referring to the combinatorial effects of mutations. For instance, two neutral mutations might interact to produce a benefit; that would be a case of positive epistasis. On the other hand, a seemingly beneficial mutation could have negative effects elsewhere in the organism; that's called negative epistasis. It won't improve an organism's fitness, for example, if a mutation for stronger muscles also produces heart attacks.
The point of the study is that epistatic interactions are profoundly unpredictable. By performing one of the largest-ever surveys of epistasis on engineered mutations to Hsp90, a well-known protein, they concluded that it is extremely difficult to predict what will happen. Because their conclusion has far-reaching implications for all evolutionary predictions, it bears quoting in full:
Originally introduced as a metaphor to describe adaptive evolution, fitness landscapes promise to become a powerful tool in biology to address complex questions regarding the predictability of evolution and the prevalence of epistasis within and between genomic regions. Due to the high-dimensional nature of fitness landscapes, however, the ability to extrapolate will be paramount to progress in this area, and the optimal quantitative and qualitative approaches to achieve this goal are yet to be determined.
Here, we have taken an important step toward addressing this question via the creation and analysis of a landscape comprising 640 engineered mutants of the Hsp90 protein in yeast. The unprecedented size of the fitness landscape, along with the multiallelic nature, allows us to test whether global features could be extrapolated from subsets of the data. Although the global pattern indicates a rather homogeneous landscape, smaller sublandscapes are a poor predictor of the overall global pattern because of "epistatic hotspots."
In combination, our results highlight the inherent difficulty imposed by the duality of epistasis for predicting evolution. In the absence of epistasis (i.e., in a purely additive landscape), evolution is globally highly predictable because the population will eventually reach the single-fitness optimum, but the path taken is locally entirely unpredictable. Conversely, in the presence of (sign and reciprocal sign) epistasis evolution is globally unpredictable, because there are multiple optima and the probability to reach any one of them depends strongly on the starting genotype. At the same time, evolution may become locally predictable with the population following obligatory adaptive paths that are a direct result of the creation of fitness valleys owing to epistatic interactions.
The empirical fitness landscape studied here appears to be intermediate between these extremes. Although the global peak is within reach from almost any starting point, there is a local optimum that will be reached with appreciable probability, particular when starting from the parental genotype. From a practical standpoint, these results thus highlight the danger inherent to the common practice of constructing fitness landscapes from ascertained mutational combinations. However, this work also suggests that one promising way forward for increasing predictive power will be the utilization of multiple small landscapes used to gather information about the properties of individual mutations, combined with the integration of site-specific biophysical properties.
From this, we can see that Prehoda's team has taken a leap to think that one mutation in one enzyme would start a path to animals. He has not taken into account the effects of epistasis. Bank et al. say that local fitness peaks would be more likely to strand the animal there, rather than let it progress. Walking right past the "danger" sign, Prehoda engaged in the "common practice of constructing fitness landscapes from ascertained mutational combinations." At best, he should only investigate a "small landscape" around the mutation to see what might happen. Maybe it would help a certain choanoflagellate. Beyond that, he is on dangerous ground making predictions.
Prehoda might have this comeback argument. He could say that his work on "ancestral protein reconstruction" shows that the mutation occurred right at the time multicellularity took off. It's a postdiction, therefore, not a prediction. This argument, however, commits the fallacy of "affirming the consequent" -- i.e., "If P, then Q. Q occurs. Therefore, P." You can't say P caused Q. That overlooks multiple other possibilities for Q. In fact, there could be an infinite number of causes for Q besides P. Prehoda could only argue Q if and only if P: specifically, that the emergence of animals required a specific mutation to guanylate kinase. That would be unwarranted even within neo-Darwinian theory. The best he can say is that the mutation is "consistent with" a scenario in which a stiffer enzyme contributed to new functions useful to multicellular organisms, assuming it avoided negative epistasis in the process.
Such clarification, however, would be unlikely to yield headlines in the Washington Post. Empirically speaking, Bank et al.'s yeast remain yeast, and Prehoda et al.'s choanoflagellates remain choanoflagellates.
In OOL Science imagination has replaced evidence as a pillar.
Self-Replicating Droplets: Evidence or a Shot in the Dark?
Sarah Chaffee
When scientists judge explanations for the origin of life that employ strictly chemical means, the evidentiary bar often seems notably low. For example, consider a new article on the Chemistry World website, published by the Royal Society of Chemistry. It claims, "Key riddle of life's origin may be answered by primitive protocells that can divide," and references a study in Nature Physics.
Generally, chemical evolution theorists assume that three components must have been necessary for the first living cell: 1) metabolism, 2) RNA/DNA, and 3) a containment structure or primitive cell wall to separate the first two components from the outside world. This study aims to address the third issue.
Researchers found that droplets, when influenced by an energy source, grow by absorbing moisture from their surroundings and then divide when they reach a critical size. Supposedly, if RNA was contained in one of these droplets, the system could have sparked life.
The article goes on to note:
Evolutionary biologist William Martin of Heinrich Heine University of Düsseldorf, who advocates the idea that life originated in pores in hydrothermal vents, says: 'It's not clear to me what real biological system based on observations from nature that this might be emulating.' However, he adds: 'If we assume that hydrothermal vents provide a system of organic micro-compartments, and that these have collected hydrophobics, then it's certainly imaginable that there might have been properties of these droplets in the aqueous phase within a hydrophobic phase that might have been relevant. You never know.'
In origin-of-life theories the term "imagine" appears quite often to cover a giant gulf between what can be demonstrated and what is required to produce the first viable cell.
In this case, the differences between a chemical-rich droplet and a functional cell membrane are numerous. For instance, the latter must distinguish between fuel and waste, allowing only the right molecules to pass into the cell and the right molecules to exit. Even the most generous calculations indicate that the likelihood of droplets coalescing with the needed properties around an extremely rare (nonexistent?) RNA molecule are essentially nil.
In contrast, the appearance of a fantastically improbable set of molecules carefully configured together to achieve a function goal shows the unmistakable signs of intelligent design, a source of causation we know well from daily experience. Design, unlike unguided chemical processes, requires no strenuous exercise in imagination.
Sarah Chaffee
When scientists judge explanations for the origin of life that employ strictly chemical means, the evidentiary bar often seems notably low. For example, consider a new article on the Chemistry World website, published by the Royal Society of Chemistry. It claims, "Key riddle of life's origin may be answered by primitive protocells that can divide," and references a study in Nature Physics.
Generally, chemical evolution theorists assume that three components must have been necessary for the first living cell: 1) metabolism, 2) RNA/DNA, and 3) a containment structure or primitive cell wall to separate the first two components from the outside world. This study aims to address the third issue.
Researchers found that droplets, when influenced by an energy source, grow by absorbing moisture from their surroundings and then divide when they reach a critical size. Supposedly, if RNA was contained in one of these droplets, the system could have sparked life.
The article goes on to note:
Evolutionary biologist William Martin of Heinrich Heine University of Düsseldorf, who advocates the idea that life originated in pores in hydrothermal vents, says: 'It's not clear to me what real biological system based on observations from nature that this might be emulating.' However, he adds: 'If we assume that hydrothermal vents provide a system of organic micro-compartments, and that these have collected hydrophobics, then it's certainly imaginable that there might have been properties of these droplets in the aqueous phase within a hydrophobic phase that might have been relevant. You never know.'
In origin-of-life theories the term "imagine" appears quite often to cover a giant gulf between what can be demonstrated and what is required to produce the first viable cell.
In this case, the differences between a chemical-rich droplet and a functional cell membrane are numerous. For instance, the latter must distinguish between fuel and waste, allowing only the right molecules to pass into the cell and the right molecules to exit. Even the most generous calculations indicate that the likelihood of droplets coalescing with the needed properties around an extremely rare (nonexistent?) RNA molecule are essentially nil.
In contrast, the appearance of a fantastically improbable set of molecules carefully configured together to achieve a function goal shows the unmistakable signs of intelligent design, a source of causation we know well from daily experience. Design, unlike unguided chemical processes, requires no strenuous exercise in imagination.
Saturday 8 December 2018
When scientists attack?
Why Scientific Polarization? A Case Study
David Klinghoffer | @d_klinghoffer
David Klinghoffer | @d_klinghoffer
Here’s a scientific war that’s rending the fabric of polite disagreement. Scientists are divided against themselves, choosing sides in a highly polarized environment, charging each other’s “lobby” with denying or distorting evidence.
As the European Journal for Philosophy of Science summarizes, “The two sides of the controversy have never seen eye to eye, but over the past decade, the accusations and counter accusations have become increasingly belligerent and entrenched.” It’s not merely a scientific but a “legal and political battleground.”
Yes, it’s the bitter scientific dispute over…evolution? Nope. Climate change? No, silly, over Lyme disease!
Debate and Death Threats
The specific issue is the existence and treatment of “chronic Lyme disease.” Our friend Alex Berezow at the American Council on Science and Health notes, “The man who discovered Lyme disease, Allen Steere, was skeptical of the chronic Lyme diagnosis as well as long-term antibiotic therapy. So, he started receiving death threats from patients who were convinced he was wrong.” The aforementioned journal article takes this debate, previously unknown to me, as a model of how disagreement arises even among scientists — you know, those models of cool, rational deliberation — and tends increasingly toward irrational polarization. Berezow writes:
The authors employ a mathematical model to show that, even when scientists are acting in good faith over the correct interpretation of evidence, polarization is still a likely outcome. How so?
Suppose a scientist believes that Hypothesis X is more likely to be correct than Hypothesis Y. He may perhaps come to believe that other scientists who also accept Hypothesis X are slightly more reliable than scientists who accept Hypothesis Y. Over time, this slight initial bias against data provided by scientists who believe Hypothesis Y can morph into outright distrust. Once that happens, a stable state of polarization develops, in which neither side can “win” the debate, even if the facts clearly support one hypothesis over the other.
The authors reach a rather disturbing conclusion:
“We do not need to suppose that anyone is a bad researcher (in our models all agents are identical), or that they are bought by industry, or even that they engage in something like confirmation bias or other forms of motivated reasoning to see communities with stable scientific polarization emerge. All it takes is some mistrust in the data of those who hold different beliefs to get scientific polarization.”
In other words, everybody acting in good faith can result in a society in which we cannot agree on a common set of facts.
Berezow cites the parallel of our contemporary political scene where Left and Right often appear not just to hold different opinions but to live in alternative universes. You can compare these, dizzyingly, by switching rapidly back and forth between Fox News and CNN.
Strengths and Weaknesses
I would add that the evolution debate presents another illustration, equally stark. Berezow again: “Over time, this slight initial bias against data provided by scientists who believe Hypothesis Y can morph into outright distrust. Once that happens, a stable state of polarization develops, in which neither side can ‘win’ the debate, even if the facts clearly support one hypothesis over the other.”
I honestly don’t think that most advocates of intelligent design are unable to recognize merits in the other side’s case. If we were unable, we wouldn’t speak of the alternative neo-Darwinian theory’s “strengths and weaknesses.” Yes, it has strengths. In explaining the emergence of biological novelties, the choice between Darwin and design is not a no-brainer.
This most sound unfair if you know little about the evolution debate. However, from long experience, I do believe that many evolution proponents are so committed to their view with its unacknowledged philosophical underpinnings, so mistrustful of other interpretations, that arguing with them is likely a waste of time.
A friend explained recently that this appears to be so, not least, with theistic evolutionists of a certain profile. See “No Escape from Theistic Evolution?” When we do argue with these people, the purpose is not to convince them, which is probably hopeless, but to persuade the unpersuaded who, we know, are listening or reading.
Denis Noble says time to rebuild rather than repair Darwinism.
Denis Noble: Why talk about replacement of Darwinian evolution theory, not extension?
Posted by News under Darwinism, Evolution, Intelligent Design
In new book on the Royal Society’s Public Evolution Summit,, Oxford’s Denis Noble explains,
The reasons I think we are talking about replacement rather than extension are several. The first is that the exclusion of any form of acquired characteristics being inherited was a central feature of the modern synthesis. In other words, to exclude any form of inheritance that was non-Mendelian, that was Lamarckian-like, was an essential part of the modern synthesis. What we are now discovering is that there are mechanisms by which some acquired characteristics can be inherited, and inherited robustly. So it’s a bit odd to describe adding something like to the synthesis ( i.e., extending the synthesis). A more honest statement is that the synthesis needs to be replaced.
By “replacement” I don’t mean to say that the mechanism of random change followed by selection does not exist as a possible mechanism. But it becomes one mechanism amongst many others, and those mechanisms must interact. So my argument for saying this is a matter of replacement rather than extension is simply that it was adirect intention of those who formulated the modern synthesis to exclude the inheritance of acquired characteristics. (p. 25)
That’s why the fat’s in the fire and smoking hot. Darwinism (or whatever the term du jour is) has been a totalistic system, enforced as such. But the evidence today simply doesn’t support it.
Reading Mazur’s book, I was struck by two things:
The genuinely interesting nature of alternative evolution proposals contrasts sharply with the science media release where fairly dull researchers have come up with a casuistical explanation of how Darwinism can account for various phenomena. And one realizes that for those individuals, that is evolution. That is science. Science is about reaffirming and finding evidence for the teachings of the Great One. And deploring or attacking anyone who doubts his teachings, irrespective of the state of the evidence.
The new approach is not exclusive or totalistic. It does not behave, as Darwinism does, as a metaphysic. Among many assemblies of evidence, some will naturally prevail, as more persuasive than others. But for once, evidence exists to understand living things better rather than to understand Darwin better.
Ladies and gentlemen, place your bets. This’ll be fun.
Posted by News under Darwinism, Evolution, Intelligent Design
In new book on the Royal Society’s Public Evolution Summit,, Oxford’s Denis Noble explains,
The reasons I think we are talking about replacement rather than extension are several. The first is that the exclusion of any form of acquired characteristics being inherited was a central feature of the modern synthesis. In other words, to exclude any form of inheritance that was non-Mendelian, that was Lamarckian-like, was an essential part of the modern synthesis. What we are now discovering is that there are mechanisms by which some acquired characteristics can be inherited, and inherited robustly. So it’s a bit odd to describe adding something like to the synthesis ( i.e., extending the synthesis). A more honest statement is that the synthesis needs to be replaced.
By “replacement” I don’t mean to say that the mechanism of random change followed by selection does not exist as a possible mechanism. But it becomes one mechanism amongst many others, and those mechanisms must interact. So my argument for saying this is a matter of replacement rather than extension is simply that it was adirect intention of those who formulated the modern synthesis to exclude the inheritance of acquired characteristics. (p. 25)
That’s why the fat’s in the fire and smoking hot. Darwinism (or whatever the term du jour is) has been a totalistic system, enforced as such. But the evidence today simply doesn’t support it.
Reading Mazur’s book, I was struck by two things:
The genuinely interesting nature of alternative evolution proposals contrasts sharply with the science media release where fairly dull researchers have come up with a casuistical explanation of how Darwinism can account for various phenomena. And one realizes that for those individuals, that is evolution. That is science. Science is about reaffirming and finding evidence for the teachings of the Great One. And deploring or attacking anyone who doubts his teachings, irrespective of the state of the evidence.
The new approach is not exclusive or totalistic. It does not behave, as Darwinism does, as a metaphysic. Among many assemblies of evidence, some will naturally prevail, as more persuasive than others. But for once, evidence exists to understand living things better rather than to understand Darwin better.
Ladies and gentlemen, place your bets. This’ll be fun.
Russia's tattered reputation re: religious liberty regresses to full blown dumpster blaze
Mass Arrests and Detentions Continue in Russia
During the month of October 2018, local and federal police raided more than 30 homes throughout western Russia. Six brothers and two sisters were arrested and sentenced to pretrial detention for so-called extremist activity. Consequently, there are now 25 brothers and sisters unjustly imprisoned, and 18 others are under house arrest.
October 7, Sychyovka, Smolensk Region—Local police and masked special forces searched four homes and arrested two sisters, 43-year-old Nataliya Sorokina and 41-year-old Mariya Troshina. Two days after their arrest, the Leninsky District Court sentenced our sisters to pretrial detention through November 19, 2018. Then, on November 16, 2018, the Leninsky District Court extended the sisters’ pretrial detention for an additional three months, that is, until February 19, 2019.
October 9, Kirov, Kirov Region—At least 19 homes were raided. Five congregation elders were arrested and later sentenced to pretrial detention. Four of the brothers (Maksim Khalturin, Vladimir Korobeynikov, Andrey Suvorkov, and Evgeniy Suvorkov) are Russian nationals, and one, Andrzej Oniszczuk, is a Polish citizen. Brother Oniszczuk is the second foreigner, after Dennis Christensen from Denmark, to be unjustly detained in Russia for his Christian beliefs.
October 18, Dyurtyuli, Republic of Bashkortostan—Police raided at least 11 homes and seized money, bank cards, photographs, personal letters, computers, SIM cards, and cell phones. Anton Lemeshev, an elder, was arrested and then sentenced to pretrial detention for two months. On October 31, 2018, he was released from prison and transferred to house arrest, where he remains at present.
Despite the ongoing threat of raids and unlawful seizure of their belongings, local brothers and sisters continue to pray for those imprisoned and to provide them and their families with practical help when possible. Until the situation is resolved, our international brotherhood will supplicate Jehovah in behalf of all his faithful servants in Russia, even mentioning some by name.—Ephesians 6:18.
Darwinism's glass jaw and the Cambrian explosion's challenge.
In Cambrian Explosion Debate, ID Wins by Default
Evolution News | @DiscoveryCSC
Evolution News | @DiscoveryCSC
Sometimes you win a game by default. The loser might not acknowledge losing, but fails to show up.
Picture a world champion prize fighter who has command of the media. He hears a challenger who claims to have a knockout punch, but refuses to get into the ring with him. Instead, he runs to the media and tells them there is indeed a big challenge, and it “might” be winnable. That’s it. Reporters run with the story and report, “The Fight Might Be Winnable.” Nothing is said about the challenger or his knockout punch. Question: under these circumstances, who wins the fight?
This is the impression you get reading the mainstream media regarding the debate about the Cambrian explosion. Stephen Meyer offered a big challenge in Darwin’s Doubt, claiming that Darwinian evolution is not only incapable of explaining the Cambrian event, but that the hierarchical information required to explain almost 20 new body plans that appeared suddenly in Cambrian layers gives positive evidence of intelligent design. His challenge was not lost on Darwin proponents. The book created a strong backlash by evolutionists in blogs, but only one Darwinian got into the ring with Meyer, so to speak, but at least by taking on his challenge. That was “heavyweight” paleontologist Charles Marshall, and a gentlemanly interchange resulted. Meyer answered the response by demonstrating that it did not explain the main point: the origin of the information required to create hierarchical body plans (see Debating Darwin’s Doubt, Section III). The challenge stood.
Still Waiting Engagement
The rest of Debating Darwin’s Doubt responded to various critics who had taken potshots outside the ring. None of them defeated Meyer’s challenge. Paul Nelson wrote in Chapter 34, “Still Waiting Engagement”:
Thus, at the end of the day, it really doesn’t matter whether the contemporary evolutionary theorists that Meyer discusses in Darwin’s Doubt are attempting to supplement neo-Darwinian theory, replace it with something fundamentally new, or replace some, but not all, parts of the theory. What matters is whether any of these theories can explain what needs to be explained: the origin of novel animal body plans and the biological information necessary to produce them.
That was in 2015. In the four years since, evolutionists have had plenty of opportunity to “engage” and offer their explanation, yet every paper reported here at Evolution News has simply dodged the issue. They pretend the challenge doesn’t exist. Instead, they mutter among themselves that “the fight might be winnable,” and give the media the impression that Darwin remains the world champion in the heavyweight category of scientific explanation.
The latest is an essay by Michael S. Y. Lee and James B. Dorey in Current Biology, “Evolution: Dampening the Cambrian Explosion.” Lee and Dorey practice all the same old moves that failed before. They rely on two recent papers, one already addressed by Evolution News: the one by Deline et al: and another by Graham Budd, who has been cited several times in these pages, most recently here.
A List of Moves
Here’s a list of the moves in the new Current Biology paper. This is the latest response by Darwinians about the Cambrian explosion. Keep your eye on the right hook (the origin of biological information) and see if they are ready for it.
The Small Explosion move: “Cambrian diversity was not greater than living diversity — at least for arthropods, the most diverse group of animals then and now.”
The Soft Touch: Sure, arthropods and vertebrates developed hard parts that accelerated their diversification, but “most phyla have either soft bodies (e.g. annelids, nematodes) or simple and relatively inert skeletons (mollusks, brachiopods), and remain largely confined to aqueous environments.”
The Distraction: The Burgess Shale Cambrian animals failed to fit into living phyla, but “when viewed from the perspective of the Cambrian explosion, modern birds and beetles would appear even more bizarre.”
The “Got All Day” feint: “Animal disparity is still increasing, and the extent of post-Cambrian innovation rivals the Cambrian explosion, though admittedly occurring over a longer timeframe.”
The Promise-to-Fight Later tactic: “more complex phyla indeed have larger genomes” —a result from analysis that “should therefore provide fertile ground for further testing.”
The Churchill Strategy: “History is written by the victors,” Churchill said. Twisting this principle in support of Darwin, they allege that “focusing only on living taxa can give a very distorted view of the dynamics of evolutionary radiations.” What we see as an explosion might just be an artifact of having only survivors in the record. Darwin was as busy at the beginning as he is now!
Punch at random: “Budd and Mann further speculate that if speciation rates are correlated with rates of morphological and molecular change — an association which has been much debated — then surviving clades would also exhibit elevated rates of phenotypic evolution and genetic change, again due to chance alone.”
That’s it. Did you see any response to the origin of biological information for new body plans? There’s a lot of punching at the air, and hitting at the soft gloves of the sparring partner. Basically, they reaffirm Darwin as the undisputed champion, even without a fair fight. Here’s the ending paragraph. They acknowledge a big challenge is afoot, but they tell the media not to overestimate it, promising them that “the fight might be winnable.”
While there is little doubt that the Cambrian explosion represented a massive and rapid proliferation of animal forms and lineages, the two studies caution against overestimating its magnitude [i.e., Meyer “might” be a pushover.] The empirical work of Deline and colleagues demonstrates that the Cambrian did not represent the zenith of animal diversity, and that major innovation continues to this day, while the theoretical study of Budd and Mann suggests that elevated rates in speciation at the base of such radiations might be at least partly attributable to stochastic upswings rather than unusual evolutionary mechanisms.
“Innovation” or Chance Miracles?
You can always trust Darwin to be the world champion eventually, they promise. In Darwinspeak, “innovation” refers to chance miracles, like new body plans appearing suddenly. Those miracles evidently happen more quickly in periods of “stochastic upswings” within the “usual evolutionary mechanisms” (you know: sheer dumb luck). Sometimes, by chance, sheer dumb luck runs faster!
Most amusing in this paper is a suggestion that actually handicaps Darwin more. It’s the idea that there might have been even more body plans at the Cambrian that we don’t see! This makes perfect sense — if you believe that blind chance has infinite creative power. Since Darwin is always on the move, they speculate, and since history is written by the victors, the explosive evidence in the fossil record might just be an artifact of what survived. Logical, right? Commenting on the Deline paper, they say:
In a major challenge to the view of unsurpassed Cambrian diversity, all Cambrian fossils fall near (between or within) living phyla: for instance, the famously bizarre Anomalocaris helps link modern velvet worms and arthropods. Thus, at least some gaps between the different body plans of modern phyla are artefacts of extinction of ‘intermediate’ taxa, rather than fundamental evolutionary discontinuities.
How this will help Darwin in the “major challenge” he admittedly faces (Darwin called the Cambrian explosion “the most obvious and serious objection which can be urged against the theory”) is anyone’s guess.
Furthermore, the morphospace occupied by Cambrian forms is much smaller than the morphospace occupied by living forms, even after accounting for non-preservation of soft features in most fossils.
But again, that is not the challenge Meyer makes. It’s about disparity, not diversity. They can call it small, but the morphospace includes at least 20, and up to 30, new body plans, each distinctive, bearing complex systems like muscles, nerves, digestive systems, sensory systems, locomotion, and reproductive systems with no precursors in the Precambrian. They all appear suddenly. Where are the “intermediate taxa”? They are nowhere in the rock record, 158 years after Darwin had hoped they would be found.
So that’s the situation going on six years after Meyer’s challenge. Marshall tried a few practice punches after the book came out, but then left. Bloggers have hooted and hollered from the stands, nothing more. Meyer still stands alone in the ring. He wins by default.
Sunday 25 November 2018
Brainy cells v. Darwin.
Memory — New Research Reveals Cells Have It, Too
Evolution News | @DiscoveryCSC
Evolution News | @DiscoveryCSC
Without memory, our lives would be exceedingly troublesome, and dangerous if not impossible. What if you had to look up what “green light” means every time you saw one? Many of us have had to witness loved ones suffering from dementia, including its common symptom of short-term memory loss. Human memory is somehow facilitated by the organ of the brain, where Alzheimer’s disease and other forms of dementia take their toll. Cells have no brains. Yet biochemists are increasingly finding that cells do have memory.
Stem Cell Memory
The old picture of stem cells was that they remain pure and static, until signals trigger cell division and differentiation. Ongoing research reveals a new, more dynamic picture of stem cells: cells that can remember things and respond to their surroundings. According to Monique Brouilette in Quanta Magazine:
Stem cells, famous for replenishing the body’s stockpile of other cell types throughout life, may have an additional, unforeseen ability to cache memories of past wounds and inflammation. New studies in the skin, gut and airways suggest that stem cells, often in partnership with the immune system, can use these memories to improve the responses of tissues to later injuries and pathogenic assaults.
“What we are starting to realize is that these cells aren’t just there to make tissue. They actually have other behavioral roles,” said Shruti Naik, an immunologist at New York University who has studied this memory effect in skin and other tissues. Stem cells, she said, “have an exquisite ability to sense their environment and respond.”
Most tissues have small reservoirs of stem cells that can replenish cells as they age or die. They can differentiate into any one of the cell types of the tissue. That’s been their primary function, Brouilette writes, to serve as “miniature factories” for tissue regeneration. It was thought they had to remain “blank slates” that were unchanged from their histories. “But now a new picture is starting to emerge.”
Studies of people with chronic inflammatory diseases led to the discovery of stem cell memory. Stem cells extracted from the nasal cavities of people unable to recover from chronic sinusitis showed activity in the genes for allergic inflammation long after the pathogen was gone. Did these stem cells remember a previous threat?
The fact that the targeted genes were active in stem cells meant that the stem cells were apparently in direct communication with the immune system. A hunch that this communication might have an effect on the chronic nature of the disease led the researchers to a further set of experiments.
They removed cells from the airways of allergy patients, grew them in culture for about five weeks, and then profiled their gene activity. They found that the genes involved in allergic inflammation were still active, even though the allergic threat of dust and pollen was long gone. In addition, the researchers described many of the cells as “stuck” in a less-than-fully-mature state.
Apparently these stem cells transfer their memories to future generations of cells. This can be a good design feature; it allows the cells to “retain a record of past assaults to sharpen their responses next time.” In the sinusitis patients, however, the stem cells were apparently stuck in a feedback loop, “perpetually signaling to the immune system that an attacker is there,” the scientists deduced. The only way they would do that would be if they had remembered a prior threat and had modified their genomes to deal with it.
“This opens a new paradigm,” an outside immunologist commented, “where we don’t only focus on the self-renewal potential of these cells but on their potential interaction with their surroundings.” Another said, “we are realizing that cells can be tuned” to adapt to their environment more rapidly and effectively. For instance, inflamed skin on mice that was allowed to heal was found to heal 2.5 times faster the next time at that same spot. The “memory” lasted as long as six months. Moreover, the stem cells also appear to communicate with the immune system to work as a team.
How memory is stored in a cell is not known. It probably involves epigenetic factors, such as the packing of the genes for access, or changes to gene regulators. The picture that is emerging is one of stem cells in a wide range of tissues engaging in “chemical dialogues” with each other, “pooling their information to cope most effectively with changing conditions.”
Whatever the details of those conversations might be, all the evidence points to stem cells playing a central role in helping to make tissues more adaptable by preserving some record of their history.
“It makes more sense that a tissue would just learn from its experience,” Naik said. “That way it doesn’t have to reinvent the wheel every single time.”
Egg Memory
Another discovery about cell memory comes from the University of California, Davis. What researchers there found was an aspect of “oocyte quality control” that involves remembering when daughter cells, on the way to becoming eggs, experienced less-than-optimal repair after DNA damage. Such cells might lead to defective offspring, so as part of the “oocyte selection process,” they are culled early. A gene named Rnf212 signals them to undergo apoptosis (programmed cell death).
In mice, as in humans, developing females initially form very large number of oocytes. Around six million oocytes enter meiosis in humans, but a stunning 5 million are culled by birth. By puberty, the ovaries contain only around 250,000 oocytes, which are steadily depleted until menopause.
This drastic reduction reflects selection for only the highest quality oocytes. Oocytes that experienced defects in meiosis, including damage to their DNA, are culled. Only those that pass through quality control checkpoints can continue and become established in the ovarian reserve.
The selection process includes a “cellular memory” of DNA damage, the press release explains. Slow DNA repair triggers RNF212 to tag these cells so that they become sensitive to apoptosis. The memory has to be able to count to ten:
The researchers found that RNF212 prevents the repair of lingering breaks to create a “cellular memory” of defects that occured in earlier stages of development. This allows the cell to assess how bad the defects were. If the number of unrepaired breaks passes a critical threshold of around ten, the cell is deemed to be of poor quality and undergoes apoptosis. If there are only a few lingering breaks, repair is reactivated and the oocyte is allowed to progress and become part of the ovarian reserve.
“It seems counterintuitive that a cell would actively impede DNA repair, but this is how oocytes gauge the success of earlier events. High levels of lingering breaks means there was a problem and the oocyte is likely to form a low quality egg,” Hunter said.
Having more eggs in the reserve is not helpful if they are of low quality. “Thus, the reproductive system must balance quality and quantity of oocytes for optimal fertility.” Mice without RNF212 tended to have more eggs, because more snuck through the quality-control process. But they were also more at risk of miscarriage and congenital defects in the offspring.
A Programmed Design Feature
The culling process appears to represent a programmed design feature to minimize the effects of mutations. Geneticist John Sanford, who organized the 2014 conference Biological Information: New Perspectives at Cornell (see Synopsis), where Douglas Axe, William Dembski, and Robert Marks spoke, gave a lecture last month to the National Institutes of Health (NIH) about mutational load and genetic entropy (see it on YouTube). Mutations are not increasing fitness, Sanford concludes: they are driving humans extinct. This fits the theme of Michael Behe’s upcoming new book Darwin Devolves (preorder it here to get the associated free perks).
Without cells having rigorous, multi-part, irreducibly complex systems to repair damage, minimize mutational degradation, and maintain genetic integrity, we likely would not still be here to experience the awe of cellular memory.
Be grateful for your eyes' flawless design.
This Thanksgiving, Be Grateful for the Intelligent Design of Your Eyes
David Klinghoffer | @d_klinghoffer
With Thanksgiving falling this week, if you’re looking for one more thing to express gratitude for, look no further than…your eyes.
We take them for granted, but our ability to interact with the world through vision is beyond remarkable. At the same time, the eyes are an evolutionary icon, in two senses. In a powerful short video written and directed by our old colleague Rachel Adams, we consider the scientific evidence around the question of eye evolution.
Darwin expected that eyes must have developed from simple forerunners through the usual (hypothesized) series of gradual steps. But at the Cambrian explosion some 530 million years ago, we find clear evidence of both compound and camera eyes already in use by creatures among the first animals in the fossil record. BOOM: There they are.
To deal with and demote the exquisite sensitivity of our vision — the ability to detect a single photon — Darwinists claim that vertebrate eyes are built backwards in testimony to the haphazard ways of evolution. But as biologist and Zombie Science author Jonathan Wells explains, evolutionists are working with outdated science. It’s not ID proponents, but entirely mainstream research, that increasingly reveals the optimal design of our eyes.
David Klinghoffer | @d_klinghoffer
With Thanksgiving falling this week, if you’re looking for one more thing to express gratitude for, look no further than…your eyes.
We take them for granted, but our ability to interact with the world through vision is beyond remarkable. At the same time, the eyes are an evolutionary icon, in two senses. In a powerful short video written and directed by our old colleague Rachel Adams, we consider the scientific evidence around the question of eye evolution.
Darwin expected that eyes must have developed from simple forerunners through the usual (hypothesized) series of gradual steps. But at the Cambrian explosion some 530 million years ago, we find clear evidence of both compound and camera eyes already in use by creatures among the first animals in the fossil record. BOOM: There they are.
To deal with and demote the exquisite sensitivity of our vision — the ability to detect a single photon — Darwinists claim that vertebrate eyes are built backwards in testimony to the haphazard ways of evolution. But as biologist and Zombie Science author Jonathan Wells explains, evolutionists are working with outdated science. It’s not ID proponents, but entirely mainstream research, that increasingly reveals the optimal design of our eyes.
On saving it for marriage.
Couples who wait report better sex lives
The Globe and Mail
First comes love, then comes marriage. Where should sex fit in?
Couples who wait until they are married to have sex appear to be much happier than those who race to get it on, according to a new study in the American Psychological Association's Journal of Family Psychology.
The study was based on 2,035 married individuals who participated in an online assessment, which included questions such as, "When did you become sexual in this relationship?"
A statistical analysis of participants showed that couples who wait until they put a ring on it enjoy significantly more benefits than those who had sex earlier: relationship stability was rated 22 per cent higher; relationship satisfaction was rated 20 per cent higher; sexual quality of the relationship was rated 15 per cent better and communication was rated 12 per cent better.
"There's more to a relationship than sex, but we did find that those who waited longer were happier with the sexual aspect of their relationship," lead study author Dean Busby, a professor in Brigham Young University's School of Family Life, said in a release.
Why does waiting produce these benefits?
"I think it's because they've learned to talk and have the skills to work with issues that come up," Prof. Busby said.
The benefits were about half as strong for couples who became sexually involved later in their relationship but before marriage, according to the release.
If you're thinking it's because couples who choose to wait do so because of religious beliefs - and those are responsible for all the extra happy feelings - you're wrong. The study's analysis controlled for religion.
"Regardless of religiosity, waiting helps the relationship form better communication processes, and these help improve long-term stability and relationship satisfaction," Prof. Busby said.
Proverbs5:18,19 "Let thy fountain be blessed: and rejoice with the wife of thy youth.
Proverbs5:18,19 "Let thy fountain be blessed: and rejoice with the wife of thy youth.
19 Let her be as the loving hind and pleasant roe; let her breasts satisfy thee at all times; and be thou ravished always with her love."
On saving it for marriage II:Non-theist edition
7 Reasons Why Atheists Wait Until Marriage
August 14th, 2011 by LeoWhy on earth would an atheist ever choose to wait until they were married to engage in the wonderfully pleasurable world of sex!? Well I happen to be an atheist and I happen to have decided to wait until I’m married. Does this make me crazy? Maybe. But here’s a list of 7 very sane, very logical reasons that suggest otherwise.
1. Logic
Logic might seem like a strange reason for a person to wait until they’re married but when we examine the statistics it makes much more sense. Couples that do wait have only a fraction of the divorce rate that others do. I personally think divorce would be a miserably unpleasant thing to experience and would like to increase my chances of a successful union wherever I can. Couples who wait also enjoy better communication, rank their relationships as more fulfilling, and even claim to enjoy BETTER SEX. If I’m being perfectly honest, anything that even slightly promises better sex in a lifelong partner seems worth pursuing. So looking at things objectively it does make sense to wait.
2. Setting an Example
Although sex is a private thing, your decision to wait doesn’t have to be. In fact you can use your decision to influence others you care about. According to the statistics mentioned above anyone who waits has a better chance at a successful marriage. I personally want my own children and even my siblings and friends to have the best shot at a happy marriage possible. I have a little sister and I don’t want her to grow up seeing her brothers sleep their way through the local population. Others that are inspired by you will hopefully go on to inspire their own children and friends. It feels good to set such a positive example!
3. Healthy Self Image
Does sex make you feel better about yourself? I have no idea. What I do know is that many people do look for sex for the self-esteem boost it can provide. Knowing what you want in life (such as a strong relationship) leads to higher self-awareness and in turn a higher self-esteem. If you know yourself then it’s highly unlikely that you’ll feel the need to seek out sexual relationships for a pick me up. Having control over your image is a powerful thing indeed. It gives you the razor sharp focus you need to pursue other goals like education, a career, and meaningful relationships.
4. Rebellion!
I personally love this reason. In a culture that is steeped in cheap sleazy dime-a-dozen sex I like to be the one that smirks at everyone else. I go to the same bars and clubs as everyone else does but when I see them all grinding like rabbits in heat I can take pride in the fact that I am not one of them. Nonreligious individuals are already rebelling against something so it’s only natural that they would withdraw even further from the majority.
(Or as a modern philosopher put it "it's hip to be square.")
5. Respect
Respect goes two ways. The first is the idea that I respect my future wife (even though we’ve probably never met) enough that I want her to take solace in the knowledge that I am all hers. I think most girls would agree that a guy who has waited for them is pretty cool. That goes both ways. Guys will think it’s pretty awesome too! The second reason I abstain out of respect is because most girls are going to be someone’s future wife! I respect those will-be unions enough to not interfere. Plus I don’t want guys pushing themselves on my wife to be!
6. Idealism
One definition of idealism states, “conforming to an ultimate standard of perfection of excellence; the idea of something that is perfect; something that one hopes to attain.” While idealism is a highly romantic notion, it is universally shared by people that are waiting, religious or otherwise. We all are seeking that perfect union, that ultimate standard of perfection. The idea of ‘the one,’ a single person that will compliment you better than anyone else is highly idealistic. While a person may experience love in many relationships throughout their lives reserving physical intimacy for only one of those loves places it above the rest.
Dedicating one’s life to an ideal — especially one that aims to make another person feel so special — is a very unique and selfless choice. It will make whoever chooses to follow this path feel like they are on a quest. While it will not be easy eventually the person they wind up with will love them all the more for it.
7. Poetry
While this may seem very similar to idealism it is really the essence of the ideal mind. Poetry is the heart and soul of waiting. It is the romance, the true love, the life partner; these things all sing poetry. Living a poetic life is to live for beauty itself. When we see elderly couples holding hands we can’t help but sigh. It is comforting to see two people, so in love, after so much time. Beauty is inspirational and for this reason more than any others on this list is why someone who is nonreligious might choose to wait. Without the ideal of heaven, and the everlasting love of an eternal father there isn’t a whole lot of beauty left in the world. Except for one thing. Love.
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