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No one looks forward to a colonoscopy, but it can save your life. So you might be wondering whether a home test is a good alternative.
These tests involve mailing a stool sample to a lab. Older types of tests check for blood, which could signal a cancerous growth. Precancerous polyps are harder to find with these tests, because they tend not to bleed. Newer types of stool tests look for changes in DNA that could be signs of cancer. They’re also better at finding advanced polyps. You’ll need to have a colonoscopy if a home test shows any positive results.
‘Virtual’ colonoscopy
Because they can’t detect a problem as early as imaging does, home stool tests are typically appropriate for people who have only an average risk of colorectal cancer and no history of polyps or colon disease.
Imaging tests, on the other hand, can find very small polyps, which can then be removed and tested for cancer. And they don’t need to be repeated as often as home stool tests, which must be done every one to three years. Imaging tests are repeated every five to 10 years, depending on the type of imaging done and whether any polyps are found.
There are differences among imaging tests, but all involve bowel prep. With a traditional colonoscopy, a flexible tube with an attached camera internally examines the entire colon. Flexible sigmoidoscopy is similar, but reaches only part of the colon. Another option is a “virtual” colonoscopy, which is non-invasive. It allows the doctor to see your colon from outside your body, but if any polyps are seen, you’ll need a traditional colonoscopy to remove them.
Despite these different choices, a very real problem exists, experts warn: Many people are still not having any type of colorectal cancer screening. If you’ve been putting it off, take the first step and talk to your doctor about your options.
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Tiny bits of DNA collected from waters off the West Coast allowed scientists to identify more species of marine vertebrates than traditional surveys with trawl nets. They also reflect environmental shifts such as unusual ocean temperatures that affect the organisms present, new research shows.
The findings published in Frontiers in Marine Science demonstrate that environmental DNA, or eDNA, can add valuable detail to longstanding marine surveys. They revealed the presence of important species that usually evade trawl nets such as great white sharks and salmon. Ongoing collection of eDNA can also help detect environmental changes when marine life shifts habitat with changes in the ocean, the study found.
“eDNA is adding details that we might not get any other way, and giving us a more complete picture,” said Collin J. Closek, an Early Career Science fellow at the Center for Ocean Solutions at Stanford University. Closek is lead author of the paper with other scientists from Stanford University, University of California Santa Cruz, and NOAA’s Southwest Fisheries Science Center.
Increasingly Powerful Genetic Tool
Marine life constantly sheds bits of genetic material into surrounding water. eDNA techniques capture that DNA from water samples and identify the species it comes from. New laboratory sequencing methods help scientists examine many samples at once. They have made eDNA an increasingly powerful tool for detecting the range of species that have passed through the water.
In fact, Closek said that collecting water samples and archiving them can provide a lasting record of the DNA record at a particular place and time. This allows scientists to tap that data years later.
“This helps us most in identifying species distribution,” said Elliott Hazen, a research ecologist at the Southwest Fisheries Science Center and coauthor of the study. “With rapid sampling at unprecedented scales, once we understand what it is telling us, we can get a lot of information about marine life across a large area relatively quickly.”
The method does not provide all the answers, though. For example, current eDNA sequencing results do not yet allow researchers to count the number or abundance of each species. They do not identify the age or size of the species represented. This means that eDNA will not replace traditional monitoring such as trawl or acoustic surveys any time soon.
Closek and his colleagues worked aboard the NOAA Ship Reuben Lasker in 2016 and 2017. They joined NOAA Fisheries’ Rockfish Recruitment and Ecosystem Assessment Survey, which has evaluated the California current forage community since 1983. The eDNA team collected 131 one-liter samples of water in roughly the same places where the ship deployed trawl nets. They collected samples of juvenile rockfish and other forage species. Observers aboard the ship also simultaneously counted the number of marine mammals and seabirds seen during daytime hours. The scientists then compared the results.
It was the first survey of eDNA across such a wide geographic scale on the West Coast.
eDNA Identified Most Species Overall
The trawl surveys identified 28 types of fish over the two years, 11 of which were identified only in the trawl surveys and not by eDNA. By itself, eDNA identified 65 different marine vertebrates, both fish and marine mammals. Together eDNA and trawl surveys identified 80 different fish and marine mammals. They included baleen whales, porpoises, dolphins, seals and sea lions, said John Field, a research fisheries biologist at the Southwest Fisheries Science Center.
“The eDNA analysis detected both the fish and marine mammals in the habitats that we would expect to find them, which gives us greater confidence in the technology to provide accurate details of the species present across the ecosystem,” he said. “It may sound basic, but this is an important step in validating this powerful new method of surveying marine life.”
Comparing 2016 to 2017, there were differences between the organisms present and their distribution. In 2016 the remnant warmth from a marine heat wave known as “the Blob” was dissipating. Unusual warm-water species were widely spread through West Coast waters.
In 2017, more normal conditions returned. Many of those unusual organisms diminished and eDNA found greater differences between the marine vertebrates present in different areas. These results indicate that eDNA results can help track changes in the environment.
“We don’t have the resources to survey everywhere for everything, and eDNA expands our reach,” said Alexandria Boehm, a professor in the Department of Civil and Environmental Engineering at Stanford and senior author of the new study. “Now that we know that the methods are in some agreement, it validates the methods so that people feel more confident using eDNA.”
A longstanding goal in neuroscience is to classify the brain’s many cells into discrete categories according to their function. Such categories can help researchers understand the complex neural circuits that ultimately give rise to behavior and disease. However, there’s little consensus about what metrics should define a cell’s identity.
In a new study, a collaboration born in part from the Neural Systems & Behavior (NS&B) course at the Marine Biological Laboratory tests the notion that a cell’s identity can be described solely by the genes it expresses. The study, published in Proceedings of the National Academy of Sciences, advocates a more “multimodal” approach to defining cell identity.
By using popular and powerful RNA sequencing techniques, researchers can take a snapshot of all the genes that are currently turned on inside a cell. But it’s becoming increasingly clear that such strategies may be limited in their ability to give a complete picture of cell identity, or represent changes over time.
Along with their collaborators, NS&B instructors Hans Hofmann, David Schulz, and Eve Marder put two popular RNA-based methods to the test: single-cell RNA sequencing and quantitative RT-PCR. They applied these techniques to two well-studied nerve clusters in the crab Cancer borealis — the stomatogastric and cardiac ganglia — which allowed them to compare the results from the RNA-based approaches to other known metrics of cell identity.
They found that the cell identities generated by the complete RNA profiles, or “transcriptomes,” did not match the existing cell identities they had compiled over years of observation. In fact, categorizing cells based on their entire transcriptome ultimately yielded “scrambled” identities.
However, as the researchers further refined their selection of key genes to input into their analysis, the RNA profiles began to more closely resemble the identities gleaned from other attributes, such as innervation patterns, morphology, and physiology. Thus, this multimodal approach has the potential to reveal a more accurate portrayal of cell identity than RNA sequencing alone.
According to Hofmann, most studies don’t bother to validate transcriptomic data with other metrics of cell identity like morphology and physiology. “Classification and characterization of cell types is often performed within the context of specific studies, and not based on a systematic approach,” he says. “We really have to collect a lot of additional data, even across species, to come up with a robust taxonomy of cell types.”
“RNA sequencing is tremendously promising and powerful, but this study provides a valuable and necessary check,” Schulz adds. “Rather than relying entirely on analytics applied blindly to cell type, whenever possible it’s important to consider multiple modalities of information as well.”
The trick, Hofmann and Schulz agree, is knowing which data are indicative of cell identity, and which are simply noise that will interfere with accurate classification.
Researchers must also eventually agree on a definition of “cell identity.” Drawing firm boundaries between cell types is useful in many ways, but may ultimately be problematic.
“Soon,” Schulz says, “we’ll start to see the limitations of trying to impose very discrete categories on the spectrum of cell types within and across individuals.”
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Adding a medication used to treat epilepsy, bipolar disorder and migraines to a blood pressure medicine reversed some aspects of breast cancer in the offspring of mice at high risk of the disease because of the high fat diet fed to their mothers during pregnancy. Conversely, this treatment combination increased breast cancer development in the offspring whose mothers had not been fed a high fat diet during pregnancy. The study by Georgetown Lombardi Comprehensive Cancer Center researchers appeared December 30, 2019, in Scientific Reports.
The key drug in the study regimen was valproic acid which, among several targets, inhibits histone deacetylase (HDAC), an important epigenetic silencer of genes. In contrast to mutations that permanently disrupt the normal functions of genes, epigenetic modifications are reversible. Valproic acid was combined with the blood pressure medication hydralazine that inhibits another critical epigenetic regulator, DNA methyltransferase (DNMT). Early treatment studies in people have shown that these two drugs can work in tandem to disrupt tumor growth.
“We believe that our research is the first to show that we can reverse some aspects of increased breast cancer risk found in offspring of mouse mothers fed a high fat diet during pregnancy,” said Leena A. Hilakivi-Clarke, PhD, a professor of oncology at Georgetown Lombardi. “This finding may have important implications in people because exposures in the womb to certain chemicals, or a mother’s high fat diet, or being obese, can subsequently increase a daughter’s breast cancer risk.”
These research findings demonstrate how impactful an epigenetic methyl group addition or subtraction from DNA can be. Compounds that reduce methylation of tumor suppressor genes that are excessively methylated (hypermethylated) can be beneficial. However, these drugs can have the opposite effect if tumor suppressor genes are not hypermethylated; they may remove methyl groups from cancer-causing genes, making these genes more active and potentially leading to more aggressive cancers.
The other key aspect of this finding involves the potential impact of diet on cancer risk. Many fruits and vegetables have compounds (such as flavones) that chemically react in the same ways as the HDAC- and DNMT-inhibiting drugs in this study. Some compounds in these foods, especially folic acid, have opposite effects. This research suggests that exposure to a high fat diet or endocrine disrupting chemicals in the womb might be reversed by the consumption of foods high in DNMT and HDAC inhibitors, while those who have not had such exposures might also gain a cancer protective benefit from consuming foods high in folic acid. The scientists note, however, that their findings, particularly as they relate to diet, need to be studied in people.
“Our next step will be to try to identify biomarkers in humans that indicate an exposure in the womb to diets or endocrine disrupting chemicals that could increase breast cancer risk later in life,” said Hilakivi-Clarke. “If we can identify such biomarkers, we’ll look to see if specific foods consumed by women can reverse epigenetic changes to their DNA that might lead to increased breast cancer risk.”
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The American coot is a somewhat drab water bird with gray and black feathers and a white beak, common in wetlands throughout North America. Coot chicks, however, sport outrageously bright orange and red feathers, skin, and beaks. A new study explains how the bright coloring of coot chicks fits in with the reproductive strategy of their less colorful parents.
Previous research had shown that coot parents preferentially feed the brightly ornamented chicks over those whose plumage has been manipulated to be less colorful, giving the ornamented chicks a survival advantage. This parental preference within families can drive the evolution of ornamentation in the offspring, just as female mate choice can result in ornamented males in the context of sexual selection (peacocks being the classic example of that).
Left unresolved by the earlier research, however, was why coot parents would have a preference for ornamented chicks in the first place, and whose fitness interests are served by the ornamentation, said Bruce Lyon, professor of ecology and evolutionary biology at UC Santa Cruz and first author of the new study, published December 30 in Proceedings of the National Academy of Sciences.
“It’s an interesting question, because there are theories about conflicts of interest between parents and offspring suggesting that it could be the chick manipulating the parents to get more food,” Lyon said. “Having shown that the parents really care about the ornamentation, we focused in this study on the natural variation in chick coloring.”
At their field sites in British Columbia, Lyon and coauthor Daizaburo Shizuka from the University of Nebraska-Lincoln were already conducting studies that involved collecting eggs from coot nests and hatching them indoors. Using a photospectrometer, they were able to get precise color measurements of almost 1,500 coot chicks. For every chick, they knew the family it came from, the egg laying and hatching order, and in many cases whether or not it was a parasitic egg.
Lyon has spent years studying birds that lay eggs in the nests of other birds. Called brood parasitism, this practice is rampant among coots, with most females laying some eggs in the nests of other coots in addition to laying a clutch in their own nest.
“We thought the parasitic chicks might be more colorful to gain an advantage,” Lyon said. “Instead, we found that the parasites are actually less colorful. That was a bit of a shock.”
A key finding came from looking at the chicks’ coloring in relation to the order in which they hatched. Coots lay about ten eggs, one per day, and the eggs hatch in the order in which they were laid. It turns out that the later a chick hatches the more colorful it is.
“That tells us the chicks can’t be controlling their coloration, because they don’t know where they are in the laying order. This is a maternal effect, presumably due to the mom putting more carotenoid pigments in the later eggs,” Lyon said.
So why would coot mothers want to mark their chicks in this way? The answer has to do with the American coot’s brutally harsh reproductive strategy. Coots lay a lot of relatively small eggs, producing more chicks than the food supply can support in most years. As a result, chick mortality is extremely high, with about half of each brood dying of starvation.
“It’s very efficient for coots, because their eggs are not very costly to produce. By laying an optimistic clutch size and then culling the brood to bring it in line with the food supply, they’re always raising as many chicks as they can,” Lyon said.
The culling takes place mostly during the first ten days after the eggs hatch, when the parents do not show any feeding preferences and feed whichever chick reaches them first when they have food. The first chicks to hatch get a head start on growth, so most of the mortality is among the later hatched chicks.
Everything changes, though, at about ten days after the last chick hatches. At that point, the parents start controlling food allocation to make sure the remaining runts in the brood get enough food to survive. Each parent chooses a favorite who gets preferential feeding, and these favored chicks are the most colorful, later-hatched chicks. Their larger, early-hatched siblings, meanwhile, endure a form of parental aggression called tousling (shaking them by the back of the neck) to keep them from hogging too much food. The favored chicks are initially much smaller than their siblings, but the extra feeding allows them to catch up and sometimes exceed the others in body mass.
“The male and female divide up the brood, with each parent exclusively feeding their half of the brood, and each parent also picks a favorite. Color predicts which one they choose, so the ornamentation may serve as a signal to tell them which chick needs the most help,” Lyon explained. “They start by creating an uneven playing field, which allows them to cull the brood, and then they intervene to level the field. The orange plumage seems to be a feature that helps them do that.”
The effect of laying order on coloring also explains why the parasitic eggs are less colorful. The eggs a female lays in a stranger’s nest are the first ones in her laying sequence, so they get the least pigment. The parasitic egg-laying behavior is opportunistic, so the female may not know when she’s forming an egg whether she will be laying it in her own nest or someone else’s.
“They’re complicated birds. For over 20 years, we’ve been chipping away at understanding their reproductive behavior, and this is another interesting aspect of that,” Lyon said. Lyon described parental preferences for ornamented chicks in a 1994 Nature paper, and he and Shizuka described coot parents’ food allocation strategies in a 2013 Ecology Letters paper.
The new work was supported by the National Science Foundation, the National Geographic Society, the Chapman Fund, and the Sigma Xi Society.
Writing in the December 30, 2019 online issue of Neurology, researchers at University of California San Diego School of Medicine and Veterans Affairs San Diego Healthcare System report that accumulating amyloid — an abnormal protein linked to neurodegenerative conditions such as Alzheimer’s disease (AD) — occurred faster among persons deemed to have “objectively-defined subtle cognitive difficulties” (Obj-SCD) than among persons considered to be “cognitively normal.”
Classification of Obj-SCD, which has been previously shown to predict progression to mild cognitive impairment (MCI) and dementia, is determined using non-invasive but sensitive neuropsychological measures, including measures of how efficiently someone learns and retains new information or makes certain types of errors.
The new findings, say authors, suggest that Obj-SCD can be detected during the preclinical state of AD when amyloid plaques are accumulating in the brain, neurodegeneration is just starting, but symptoms of impairment on total scores on thinking and memory tests have not yet been recorded.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” said senior author Mark W. Bondi, PhD, professor of psychiatry at UC San Diego School of Medicine and the VA San Diego Healthcare System. “These findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.
“This work, led by Dr. Kelsey Thomas, has important implications for research on treatment targets for AD, as it suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
Study participants were enrolled in the Alzheimer’s Disease Neuroimaging Initiative (ADNI), an on-going effort (launched in 2003) to test whether regular, repeated brain imaging, combined with other biological markers and clinical assessments, can measure the progression of MCI and early AD. Seven hundred and forty-seven persons were involved in this study: 305 deemed cognitively normal, 153 with Obj-SCD and 289 MCI. All underwent neuropsychological testing and both PET and MRI scans.
The research team found that amyloid accumulation was faster in persons classified with Obj-SCD than in the cognitively normal group. Those classified as Obj-SCD also experienced selective thinning of the entorhinal cortex, a region of the brain impacted very early in Alzheimer’s disease and associated with memory, navigation and perception of time. Persons with MCI had more amyloid in their brain at the start of the study, but they did not have faster accumulation of amyloid compared to those with normal cognition. However, those with MCI had more widespread temporal lobe atrophy, including the hippocampus.
Broadly speaking, scientists believe that for most people, AD is likely caused by a combination of genetic, lifestyle and environmental factors. Increasing age is a primary, known risk factor. The amyloid hypothesis or amyloid cascade model posits that accumulating amyloid protein plaques in the brain kill neurons and gradually impair specific cognitive functions, such as memory, resulting in AD dementia. However, many scientists are now questioning the amyloid hypothesis given the large number of clinical trials in which drugs targeted and successfully cleared amyloid from the brain but did not impact the trajectory of cognitive decline.
The ability to identify those at risk for AD before significant impairment and before or during the phase of faster amyloid accumulation would be a clinical boon, said authors, providing both a way to monitor disease progression and a window of opportunity to apply potential preventive or treatment strategies.
Currently, both approaches are limited. Some risk factors for Alzheimer’s can be minimized, such as not smoking, managing vascular risk factors such as hypertension or following a healthy diet with regular exercise. There are a handful of medications approved for treating symptoms of AD, but as yet, there is no cure.
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use or not available to those with certain medical conditions,” said first author Thomas, PhD, assistant professor of psychiatry at UC San Diego School of Medicine and research health scientist at the VA San Diego Healthcare System.
“A method of identifying individuals at risk for progression to AD using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening.”
What is catnip and how much of an effect does it have on our feline friends?
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How many goals should you have? How many is too many… or too few?
Does it even make sense to ask this type of question?
Suppose we try to come up with a decent number. We could say that the answer will depend on many factors:
Very quickly we see that the answer is going to be something like, Well… it depends.
The truth is that there are too many factors, there’s too much unpredictability, and there’s too much inherent chaos in the goal setting and achievement process to come up with an ideal formula for all situations. Answering this question numerically looks pretty hopeless.
But let’s not give up so quickly.
Suppose you ask me how many goals you should have, and I confidently say that you should have 42 goals. The answer you seek is 42.
You might ask, “Why 42? Why not 41 or 43? Does it make that big of a deal?”
And suppose I respond, “Nope – 41 is too few, and 43 is too many. You need 42. No more, no less.”
Then you’d probably want to know why. What’s wrong with any other number? What makes 42 so special?
Now I could give you all sorts of reasons for why 42 is the perfect number of goals for you. I could tell you that having 42 goals has always worked for me and that other numbers of goals have always let me down. I could quote a study that showed that 42 was the perfect number for most people. I could tell you that 42 works because it’s the answer to life, the universe, and everything. But no matter what I said, you would no doubt remain unconvinced. You’d find a way to poke holes in any answer I gave you. You’d tell me why your situation is different. You’re ornery that way, aren’t you? But of course you’d be right.
The problem with this question is the question itself. If we modify the question slightly, the problem becomes easier to see.
A goal is a result or an outcome, so the question of how many goals to have is very similar to asking, How many results should I have?
Obviously the answer is still 42. You should have 42 results. That sounds even more nonsensical, doesn’t it?
Let’s rephrase this question again slightly. Try asking instead, How many results could I have?
And again suppose I say 42. You could have 42 results. Now it sounds like you’re asking permission, doesn’t it? If I say you could have 42, you’ll probably resist having any limit placed upon the number you could have.
If you think about it, there’s really just one answer that makes sense now.
And that answer is one.
In terms of your life path, at any given time it makes sense to say that you’re experiencing a result. And there’s really just one result. That one result is the state of your life as it stands right now.
That one result is like a giant snapshot that includes the state of your body, your mind, your emotions, your finances, your home, your social relationships, your devices and all of their data, and everything else that’s part of your reality.
If your life were a video game, and we clicked the “save game” button right now, your one result would be that saved game file. No matter how much data that’s needed to define the current state of your life, such that we could reload it later and have it all look and feel identical to the way it is now, that data could still be saved in just one file. It would be a really big file, but we’d only need sufficiently large file to store everything that defines your result at any given time.
Asking how many goals to have is like asking how many elements are saved in that file. The answer depends on how granular you get in thinking about the individual pieces of data.
How would we define your body in terms of data points, for instance? These data points could include your weight, height, skin color, flexibility, strength, and so on. We could compile a long list of stats to define your body like we’d use to define a character in a role-playing game.
If we loop back and apply this same idea to goal setting, we can see more clearly why the number question is of little use. You could define just one physical goal, like weighing a certain amount, or you could take that same goal and split it into 10 or 100 goals, like how strong, fast, or flexible you want to be with respect to different movements. The number of goals depends on how you’d subdivide that one big file into meaningful data points.
But defining these data points is mostly arbitrary. We can have one compound goal or 10 or 100 smaller goals, and they could all define the same outcome. This applies to career goals, financial goals, relationship goals, health goals, and more.
But no matter how many goals we set, we can still view this through the lens that says: It all combines into one big result. No matter what, the whole thing reduces to a single saved game file. One file. One result.
Now a goal is actually an intended result, not necessarily an experienced result. But it’s still interesting to think about goal setting through the lens of defining your desired save game file.
If you think about having one goal only, that’s equivalent to thinking of the overall vision of your life. How would you define that vision? Even if that vision had lots of details, how would you summarize the key points?
Suppose you were playing a game and you saved it somewhere along the way, and a friend asks you, “Hey, how far did you get?” How would you describe the point at which you saved the game? What details would matter to you? What are the meaningful data points? The keyword here is meaningful, as in meaningful to you.
Would you say that your character just reached level 14? Would you say that you saved the game in an inn outside a certain village? Would you say that you’re halfway through a particular quest? Or would you mention all of these things? You’d be right no matter how you chunked it down.
Turning your goals into a numbered list is similar. The number really doesn’t matter. The only number that matters here is the number one – your one overall vision.
So let’s go back over the key questions again.
How many results could you have? One. You have one data file. One result. One outcome. You could have different results at different times, just like you could have billions of saved game files if you wanted to, but it’s really just one result at any given time.
How many results should you have? Still one. One life. One result.
How many goals should you have? One. If you need a numerical answer, then the answer is one. When we reach this particular question though, we could say that zero is a valid answer too, which would mean not setting any goals and letting the universe decide how things turn out. But in that case we could still say you have one goal, which is to see what happens if you don’t consciously set any goals. But this distinction isn’t really that important.
This answer is actually more useful and practical than it first appears. Instead of fussing over your quantity of goals, think more deeply about your one goal to rule them all. How would you define your overall mega-result? You can have 42 subgoals if you’d like, but if you sum them all together, what do you get? What’s the grand vision? What’s your one goal?
Now that’s a scary question! And the scariness of it can easily send us fleeing back to the comfort of a less scary question like, How many goals should I set?
What’s the scariest answer we can give to that question by the way? It’s one, isn’t it? That’s the answer we really don’t want to hear. And yet it’s also the simplest.
If you’ve been avoiding directly asking and seriously trying to answer this bigger question, notice that one way you’ll try to stop yourself is by asking blocking questions that you can’t actually answer. Those blocking questions serve as your objections that prevent you from facing the scarier and more difficult question. Why? Because if you don’t answer the bigger question, you don’t have to act on it yet. If you did actually answer that bigger question with a reasonable degree of intelligence, and if you achieved a reasonable degree of clarity there, what’s comes after that? Next you have to have take some serious action in that direction. You’ll know that it’s time to step up in the biggest way possible. And that’s going to run you right into your deepest, darkest fears.
Are you ready to go there yet? Or would rather play it safe a while longer and keep asking blocking questions?
Also note that you already are answering this bigger question. You already have a saved game file. You’re already getting a result that’s pretty specific. You may not like your current game state, and you might want to change that, which is fine, but the real lesson here is to catch yourself when you’re asking a blocking question in order to avoid the scariness and immensity of a more powerful question. You may recognize that this is a form of retreating to truth when you have a power challenge ahead of you.
But in the meantime, if you’re still concerned about setting just the right number of goals, go with 42. It works every time! In fact, WordPress informs me that this article has 42 paragraphs – spooky. 😉
Debate over the benefits and drawbacks of daily low-dose aspirin has flared in recent years, with guidelines now generally urging against the regimen to prevent a first heart attack or stroke in healthy people.
But some people with good heart health still might benefit from taking daily low-dose aspirin, a new study from New Zealand argues.
About 2.5% of women and 12% of men would likely benefit from daily aspirin during a five-year period, based on an analysis of more than 245,000 heart-healthy New Zealand residents.
“In our study, we were able to predict for each individual, by taking into account their personal characteristics, their propensity to benefit from or be harmed by aspirin,” said lead researcher Vanessa Selak, an epidemiologist with the University of Auckland in New Zealand.
“Using this personalised approach enabled us to identify specific individuals who were likely to benefit from aspirin after weighing up aspirin’s effects on both cardiovascular events and serious bleeding,” Selak continued.
That would seem to contradict new guidelines issued earlier this year by the American Heart Association (AHA) and the American College of Cardiology (ACC).
The two groups concluded that for older adults with healthy hearts, the risk of bleeding that comes with aspirin therapy outweighs any heart benefit.
“We used to say aspirin generally yes, occasionally no. Now we say aspirin generally no, occasionally yes,” said Dr Amit Khera, who served on the ACC/AHA committee that wrote the guidelines.
However, Khera feels this new study actually supports the new guidelines.
“This modelling exercise confirmed it’s a very small group of the population that potentially could be eligible for aspirin,” said Khera, a professor of cardiology with UT Southwestern Medical Center in Dallas.
These guidelines are not for people who’ve had an emergency regarding their heart health. Those people do derive overall benefit from aspirin, he said.
“If you’ve had a heart attack or stroke, continue to take your aspirin,” Khera said.
But clinical trial data that emerged in 2018 showed that daily aspirin taken by people in good heart health only reduces their risk of heart attack and stroke by 11%, but increases their risk of dangerous bleeding by 43%, he added.
“I want to be clear that I’m not talking about nosebleeds,” Khera said. “I’m talking about needing a transfusion, being hospitalised, bleeding in the brain. Big stuff.”
To take a closer look at the potential benefits of aspirin, Selak and her colleagues studied hundreds of thousands of New Zealanders without heart disease who had their heart health risk calculated between 2012 and 2016.
The net effect of aspirin was calculated for each person by subtracting the number of heart emergencies the person was likely to have over five years from the number of major bleeds aspirin could cause.
After personalising the risk-versus-benefit calculation, the researchers found that a select group of people would have a net benefit from aspirin if one heart health emergency that led to hospitalisation or death was considered equal to one major bleed that led to hospitalisation or death.
The percentages increased to 21% of women and 41% of men if a heart health emergency was considered equal to two major bleeds, the findings showed.
“This research suggests that decisions regarding the use of aspirin among people who have not already had a cardiovascular event should be made after undertaking a personalised prediction of cardiovascular benefits and bleeding harms from aspirin,” Selak said.
That’s already standard procedure under the US guidelines, Khera said.
“No one is saying aspirin doesn’t help. It just doesn’t help as much as we used to think, and you have to appreciate the bleeding penalty,” Khera said. “Some people are more concerned about heart attack risk and are willing to pay the bleeding penalty, especially if they’ve never had any bleeding problems. It’s still OK for them to consider it.”
Both Selak and Khera recommended that people talk with their doctor about the risks and benefits before starting to take daily aspirin. Calculators are available that help physicians weigh your risk of heart attack and stroke against the risk of bleeding.
“In many ways, people think of aspirin as this benign thing because it’s been around for centuries. Anybody can get it over the counter,” Khera said. “But if you’re going to take it every day for the next couple of decades, there are definite penalties to it.”
The new study was published online in the Annals of Internal Medicine.
Image credit: iStock
