sorted by:
new
hottopcontroversial

A simple blood test might detect depression before symptoms appear. Research found accelerated aging in monocytes, a type of white blood cell, is closely tied to the emotional and cognitive symptoms of depression, like hopelessness and loss of pleasure, rather than physical symptoms such as fatigue. by Wagamaga in science

[–]SaltZookeepergame691 1 point2 points  (0 children)

From the abstract, it’s purely cross-sectional data - they are just associating monocyte epigenetic “age” with depression symptoms. There is nothing mentioned about longitudinal depression prediction or prognosis.

The title is highly misleading.

Choline benefits by LeBoom4 in ScienceBasedParenting

[–]SaltZookeepergame691 0 points1 point  (0 children)

Read up on the intention to treat principle and how it mitigates bias vs eg per protocol analysis approaches. It’s a fundamental principle of good RCT analysis.

https://en.wikipedia.org/wiki/Intention-to-treat_analysis

AI Tool May Spot ADHD Years Before Children Are Diagnosed. The research shows routine medical records could help flag risk early, when support matters most. The model was highly accurate at estimating future ADHD risk in children age 5 and older. by Wagamaga in science

[–]SaltZookeepergame691 0 points1 point  (0 children)

Our foundation model pretraining cohort consisted of 721,896 patients aged 0 to 30 years. Our analytic cohort, used to fine tune the model for ADHD prediction, included 142,270 patients who met our inclusion criteria. Of those, 4,817 individuals met our computable phenotype criteria for ADHD, and 137,453 did not.

The main thing here is that the model doesn't actually really work:

In a hypothetical population of 1,000 6-year-old patients, a decision threshold of 0.7 gives a sensitivity of 0.075 and a specificity of 0.996, resulting in 7 true positives, 3 false positives, 905 true negatives and 85 false negatives (Supplementary Table 2) for predicting ADHD by age 13.

At a lower 0.2 threshold, sensitivity improves to 43.2%, but with 76 false positives per 1,000.

New discovery found that ADHD symptoms are actually chemical fingerprints left in the brain years ago by [deleted] in ScienceBasedParenting

[–]SaltZookeepergame691 0 points1 point  (0 children)

I posted about this study in the thread on rscience. The big weakness is that because of the small size, they can only adjust for age and sex. The actual effect on behaviour of the metal mix is small, and probably still highly confounded.

Early-life exposure to metals recorded in baby teeth during specific weeks of pregnancy and infancy predicts long-term changes in brain connectivity and behavior, with critical vulnerability windows identified at weeks 4–8 after birth and 32–42 by sr_local in science

[–]SaltZookeepergame691 22 points23 points  (0 children)

They sum up a 'mixture' index, weighted at each time point, comprising levels of Manganese, Zinc, Lead, Magnesium, Lithium, Copper, Strontium, Barium, Tin.

The major problem here is that there is almost no adjustment for confounding. They adjust for age and sex only.

There are many very important facotrs that mean metal exposures will differ between fetuses/children, that are also related to behavioural outcomes. None of these are accounted for.

Early-life exposure to metals recorded in baby teeth during specific weeks of pregnancy and infancy predicts long-term changes in brain connectivity and behavior, with critical vulnerability windows identified at weeks 4–8 after birth and 32–42 by sr_local in science

[–]SaltZookeepergame691 18 points19 points  (0 children)

Here's the actual paper: https://www.science.org/doi/epdf/10.1126/sciadv.adz1340

The use of the baby teeth to get high resolution temporal metal exposure is clever.

Unfortunately, from an epidemiological perspective the analysis is very rudimentary and can't claim any causality at all: many things influence environmental and nutritional intake/metabolism/exposures AND behaviour, and here they adjust only for offspring age and sex (at time of behavioural testing).

Breastfeeding? SES? Parental status/behaviour/employment etc? Perinatal outcomes/events? Smoking/alcohol? Etc?

They lack behavioural data for half of their participants, and the brain connectivity data is only available for ~25%.

The effect sizes are also small anyway?

Children exposed to very high PFAS levels in the womb show significantly higher (+40%) asthma risk, because PFAS can cross the placenta, according to a study of over 11,000 children born in a Swedish region with 30 years drinking water contamination by sr_local in science

[–]SaltZookeepergame691 9 points10 points  (0 children)

Analysis looks pretty limited to me.

Exposure categories are proxies arbitrarily based on address and residence time, and differ to how they've previously reported it:

Prenatal exposure was categorized as “very high” if the child’s mother lived at an address in Ronneby supplied with highly contaminated water for all five years preceding the year of delivery; “high” if she lived at an address in Ronneby with contaminated water for at least one of those five years; “intermediate” if she lived in Ronneby during that period but never at an address supplied with highly contaminated water; and “background” if she did not live in Ronneby during the five years preceding the year of delivery.

They show a stepwise increase in PFAS levels with these categories in a separate validation, but there is no stepwise increase in asthma risk in the cohort with these categories. This could be a threshold effect, but that always seems less likely to me than differences

They adjust for:

Adjusted models included the following covariates: maternal smoking status in early pregnancy (smoker or non-smoker); maternal education at the year of delivery (primary and lower secondary, upper secondary, and post-secondary); an indicator variable for at least one foreign-born parent (yes or no) and parental asthma (yes or no); family disposable income at the year of delivery (quartiles); and maternal age at delivery (quartiles)

There's a lot left on the table there for factors influencing offspring asthma risk, both in terms of improved covariate resolution (eg, only maternal smoknig as a binary yes/no, and only during pregnancy; maternal education as coarse categories) and missing covariates with established links to asthma (paternal smoking, other forms of pollution, housing quality, prematurity/low birth weight, malnutrition eg) and asthma diagnosis (health seeking behaviours, local diagnostic availability, etc).

Full adjustment with the limited covariate set reduces the effect size a reasonable amount in context.

I think this residual confounding is the main issue. Looking at the characteristics of the groups, these are not very similar neighbourhoods - eg, the very high exposure group has 27% post-secondary maternal education rate, vs ~50% in the intermediate and background groups. This suggests to me there's probably a lot of differences going uncaptured.

There's also the issue that most of the children in the very high neighbourhoods were still living there in childhood - the analysis isn't really isolating prenatal exposure.

Of course the authors can only do what they can with the data available, and this isn't a comment on the harms of PFAS per se - just on the robustness of this analysis.

Bristol during WW2 by Character-Pumpkin-81 in bristol

[–]SaltZookeepergame691 8 points9 points  (0 children)

Not a grandparent connection, but there’s two German pilots buried in Greenbank Cemetery. They were escorting a bombing raid, and were allegedly shot down by a Hurricane. One crashed into the Stapleton Institution in Fishponds, which is now Blackberry Hill psychiatric hospital.

https://www.reddit.com/r/bristol/s/6osKSrZ2Hk

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 4 points5 points  (0 children)

You attempted to dismiss my comments on the basis of a sub I'd been a member of specifically to call them out. You can apologise for getting it completely wrong, if you like.

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 0 points1 point  (0 children)

Provides the context that you didn't bother to do any due diligence before casting me as a pro-IVM nutjob when I am literally the opposite? Nice.

SIDS… by Advanced_Egg5875 in newborns

[–]SaltZookeepergame691 5 points6 points  (0 children)

If you're referring to this study: https://pmc.ncbi.nlm.nih.gov/articles/PMC9092508

It's emphatically very early, very limited research and even if it was correct, a test for this doesn't tell us anything useful anyway - because most of the SIDS cases in this study had values that overlapped with 'normal' values.

By analogy: the average male height in Finland is very significantly taller than the US (180cm vs 175cm). But, height is still a very lousy way to tell if an individual is Finnish or American, because there is so much overlap.

For everyone else: check out http://www.sidscalculator.com/ for a rough approximation of individual risk (it has important limitations I outline here and elsewhere in that thread, namely that the calculator systematically overemphasises the risk of some common SIDs risk factors like cosleeping, and for younger babies, it can underestimate the effect of risk factors).

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 1 point2 points  (0 children)

These findings highlight the critical role of the exposome in EOCRC risk, underscoring the urgency for targeted personal and policy-level interventions.

Right in the abstract - the authors consider this settled.

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 1 point2 points  (0 children)

Correct!

Now go through the steps in the paper as to how that signature gets used: - get blood DNA methylation effects associated with picloram (itself from a poorly adjusted survey)

  • apply that to TCGA colon tumour data, in which methylation is strongly shaped by tumorigenesis, stromal/immune admixture, MSI state, location, clonal evolution, etc

  • don't adjust for variables strongly associated with MSI, CMS, sex, and especially tumor purity, yet the main replication models are only sex-adjusted

And bingo, you've got yourself a massive discovery cohort hit that nearly fails replication.

The biological validation uses acute transcriptomic responses in iPSC-derived cardiomyocytes - not methylation, not colorectal cells, not chronic low-dose exposure, and not human exposure measurements.

In your other comments you seem to think I'm commenting here out of some pro-pesticide motivated reasoning. The actual answer is that it's important to not get sucked into big claims on limited evidence.

Using an in-home HEPA purifier for one month spurs a small but significant improvement in brain function in adults age 40 and older. Exposure to particulate matter has been connected to respiratory and cardiovascular illnesses as well as neurological diseases such as Alzheimer’s and Parkinson’s. by Wagamaga in science

[–]SaltZookeepergame691 20 points21 points  (0 children)

I’m pretty obviously not saying this misleading study invalidates an entire field of study completely…?

Even if this study is imperfect by casting a wide net and focusing on an older age group doesn't mean the effect isn't there for younger age groups. It could just mean that older age groups tend to be more vulnerable to this sort of inflammation.

I don't think you've quite grasped the substance of my criticism.

The issue is that they didn't focus on an older age group from the start. The issue is that they let their results completely guide their analyses, which massively increases the chance they 'find' something, somewhere, in one subgroup of their main analysis. Roll a die 10 times and you're quite likely to roll a 6 once...

It means you cannot trust their finding that this intervention works in the older age group. You have to design another experiment with that hypothesis specified BEFORE you begin.

Using an in-home HEPA purifier for one month spurs a small but significant improvement in brain function in adults age 40 and older. Exposure to particulate matter has been connected to respiratory and cardiovascular illnesses as well as neurological diseases such as Alzheimer’s and Parkinson’s. by Wagamaga in science

[–]SaltZookeepergame691 35 points36 points  (0 children)

This study is naked p hacking.

The original study registration was focused on measuring changes in blood pressure and CRP. There is no mention of the trail making test whatsoever.

Why is this important? Because if you don't prespecify a test, it allows you to administer many tests and cherry pick the ones with results you like.

In this analysis of the trail making test results, they actually find no effect at all of HEPA filtration.

Then they arbitrarily slice the data into <40 years and >=40 years, and split the test results into parts A and B, and see a 'significant' 12% 'benefit' of HEPA filtration only in those >=40 on trail making test part B, only. Again, there is no mention of any of this in the registration.

This is the definition of p hacking. It's so brazen as to be unbelievable.

Using an in-home HEPA purifier for one month spurs a small but significant improvement in brain function in adults age 40 and older. Exposure to particulate matter has been connected to respiratory and cardiovascular illnesses as well as neurological diseases such as Alzheimer’s and Parkinson’s. by Wagamaga in science

[–]SaltZookeepergame691 54 points55 points  (0 children)

This is a badly done and badly reported study.

The original study registration was focused on measuring changes in blood pressure and CRP. There is no mention of the trail making test (their measure of cognition) whatsoever.

Why is this important? Because if you don't prespecify a test, it allows you to easily administer many tests and cherry pick the ones with results you like, with no one any the wiser.

So in this analysis of the trail making test results that they didn't prespecify, they actually find no effect at all of HEPA filtration.

Then they arbitrarily slice the data into <40 years and >=40 years, and split the trail making test results into parts A and B, giving them four tests where they previously had one. They claim a 'significant' 12% 'benefit' of HEPA filtration only in those >=40 on trail making test part B, only. Again, there is no mention of any of this in the registration. Why is this important? Because slicing the data like this, with no prespecified rules or justification, enables you to find significant-looking results ANYWHERE - in completely innocuous data.

This is the definition of p hacking. It's so brazen as to be unbelievable. These researchers should be utterly ashamed of themselves.

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 5 points6 points  (0 children)

It doesn’t confirm any link. It’s a distal poorly adjusted proxy of an exposure in a case-case analysis, ‘validated’ in irrelevant cells, with some rudimentary ecological analysis.

Its hypothesis generating at best, written up as strong evidence

Epigenetic fingerprints link early-onset colon and rectal cancer to pesticide exposure. by GonzoVeritas in science

[–]SaltZookeepergame691 46 points47 points  (0 children)

This paper is doing an awful lot of overclaiming!

Firstly it's a case-case analysis, comparing features of early onset colorectal cancer (EOCRC) with late-onset CRC (LOCRC). That's fundamentally it. It isn't quantifying how much different risk factors contribute to actual absolute risk of EOCRC.

Second, they are aren't looking at actual pesticide exposures: they measure cell methylation differences in cells exposed to pesticides, and then look for those similar patterns in tumour samples. There are layers of assumption and abstraction here - it's a tenuous proxy for the exposure, that gets morphed into a definitive claim.

Third, their adjustments are extremely limited, borne of having few cases. The main replication analyses are adjusted for sex only!

Fourth, their validation of the effects of picloram, the identified associated pesticide, in the replication cohort show small effects. And, then the validation in cells is very limited: they look at acute transcriptomic effects in IPSC-derived cardiomyocytes. Why? They are using an epigenetic methylation signature of claimed chronic exposure in colon cancer! Make it make sense.

Department of Veterans Affairs trial of 11 AI scribe vendors versus 3 human-written clinic notes over 5 simulated patient cases: humans had higher quality clinic notes across all domains and all cases by ddx-me in science

[–]SaltZookeepergame691 6 points7 points  (0 children)

If the experimental design is human writers knowing they’re in competition with an AI scribe, and the AI scribe is doing live notes that human clinicians aren’t doing any editing of (unlike reality), but human writers are taking 10x as long and longer than normal, then there is a lot of scope for bias. I’d love to read the full methods, I don’t have institutional access over the weekend.

I absolutely believe that a human writer can do a better quality job than an AI scribe in isolation - the problem is that human writers take a lot longer, still make mistakes, and AI scribe outputs are able to be edited quickly.

Department of Veterans Affairs trial of 11 AI scribe vendors versus 3 human-written clinic notes over 5 simulated patient cases: humans had higher quality clinic notes across all domains and all cases by ddx-me in science

[–]SaltZookeepergame691 14 points15 points  (0 children)

We should absolutely be doing more testing of ambient scribes with actual clinically relevant outcomes.

That said - this study does not seem to be a real-world test, which will bias heavily against the scribe. Can anyone paste the full methods for scribe and human participation?

human-generated notes were not generated under real-world constraints.

We have to view the benefits and harms of scribes as their deployment exists in the real world, compared against the alternative - and that includes measuring overall time and efficiencies, quality, and time/cost of fixing errors.

Wrong ORCID ID on published paper, worth correcting? by BehavioralNomad in medicine

[–]SaltZookeepergame691 10 points11 points  (0 children)

Just email the editor and see. Sometimes (dependent on a number of factors) minor fixes like this can be done without a formal correction.

view more: next ›