Reddit deep dives can involve anything from TV show fan theories to DIY advice.

A new AI-assisted analysis now suggests that the 'front page of the internet' could help researchers spot potential side effects of GLP-1drugs used to manage weight and diabetes, such as Ozempic, Wegovy, Mounjaro, and Zepbound.

A team from the University of Pennsylvania analyzed more than 410,000 Reddit posts across a six-year span, looking for mentions of two active ingredients in widely used GLP-1-based drugs: "semaglutide" or "tirzepatide", or their brand names.

" Clinical trials are the gold standard, but by design, they are slow," says computer and information scientist Sharath Chandra Guntuku.

"This is not a replacement for trials, but it can move much faster, and that speed matters when a drug goes from niche to mainstream almost overnight."

When it came to potential side effects that doctors may not know about, two groups of complaints stood out: reproductive health issues (including irregular menstrual cycles) and temperature-related problems (such as chills and hot flashes).

The way the body's metabolism burns energy is known to impact temperature balance, so there is a real mechanism that potentially links the side effect to the drug in a causative way. But there is less research on how these drugs affect the menstrual cycle.

It's worth noting that these previously "unrecognized potential effects" were far from the most commonly reported on Reddit, and the researchers emphasize that they don't see their new analysis as a replacement for trials or clinical assessments.

However, the findings suggest that online boards and peer-to-peer conversations may be places where people feel able to discuss certain symptoms, some of which they might not mention to a doctor.

"Some of the side effects we found, like nausea, are well known, and that shows that the method is picking up a real signal," says Guntuku.

"The underreported symptoms are leads that came from patients themselves, unprompted, and clinicians could potentially pay attention to them."

This kind of large-scale data capture and interrogation is made possible by the latest AI models. Here, the researchers used GPT models from OpenAI to crunch through Reddit posts and find patterns.

That's no easy task, given the volume of text and the variety of ways people might talk about GLP-1 drugs and their side effects. These scans can be completed rapidly, identifying potential sources for investigation in future clinical trials.

With little else known about the Reddit posters involved, the research can't be definitive about whether drugs like Ozempic or Mounjaro are actually causing these symptoms.

However, these self-reported side effects are worth further investigation.

"These drugs are thought to work by engaging part of the brain called the hypothalamus, which helps regulate a wide variety of hormones," says psychologist Jena Shaw Tronieri.

"That doesn't mean the medications are necessarily causing these symptoms, but it could suggest that reports of menstrual changes and body temperature fluctuations are worth studying more systematically."

GLP-1 drugs are named after glucagon-like peptide-1, a natural hormone that the medications mimic. Specifically, the drugs limit appetite, slow down digestion, and trigger the release of insulin from the pancreas in response to high blood sugar levels.

While these treatments are associated with significant benefits in weight loss and diabetes management, research is ongoing into other potential consequences of GLP-1 use.

Those consequences potentially include protection against Alzheimer's, better cardiovascular health, and a greater risk of acute or chronic pancreatitis – so, quite the mix. We also know that regaining most of the weight after GLP-1 treatments is common.

The kind of online analysis done here may highlight problems that might otherwise be missed.

"The whole point of this kind of approach is that it can move quickly, and that's exactly when it's most valuable," says Guntuku.

Reddit tends to skew towards younger, male, US adults – but that doesn't mean it can't be useful for flagging problems that researchers need to know about.

Related: Ozempic-Like Drugs Can Help You Lose Weight, But There's a Catch

"Clinical trials generally identify the most dangerous side effects of drugs, but they can fail to find what symptoms patients are most concerned about," says computer and information scientist Lyle Ungar.

"Even though social media is not necessarily representative, a large collection of posts may reflect additional concerns."

The research has been published in Nature Health.

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A life that leads to dementia can take many paths, but there are some common risk factors that make a diagnosis more likely.

An extensive new study shows, however, that among older adults, the effect of those risk factors differs.

Some risk factors seem to hit women's cognition harder than men's, and accruing multiple risk factors over a lifetime seems to worsen women's brain function more so than men's.

In other words, certain risk factors may not mean the same thing in a woman's brain as it does in a man's, which has implications for dementia research and treatments.

It's well known that dementia is more common in women than in men, and longer life expectancy does not fully explain the gap.

There's something else going on that these findings could also help us understand.

"Our study suggests that women may be at greater risk of dementia because they experience a greater number of risk factors, and because these risk factors reduce cognition to a greater degree than [in] men," the researchers write.

Study co-authors Megan Fitzhugh and Judy Pa, two neuroscientists from the University of California, San Diego, say their results provide further evidence that dementia risk needs to be assessed and managed in a personalized way.

"Looking beyond which risk factors are most common, we found that some have a disproportionately larger impact on women's cognition," says Fitzhugh.

"This suggests that prevention efforts may be more effective if they are tailored not just to risk factor prevalence, but to how strongly each factor affects cognition in women versus men."

The researchers analyzed health data from 17,182 individuals aged 40 or older, examining 13 risk factors linked to dementia.

Depression, physical inactivity, and sleep problems were more common in women, compared to men.

Higher rates of hearing loss, diabetes, and heavy alcohol use, on the other hand, were more often reported by men.

Some risk factors were linked to greater reductions in cognitive scores in women – an indication that they affect women's brains more negatively than men's.

These factors included high blood pressure, hearing loss, and diabetes.

Higher BMI was also associated with poorer cognitive performance in women in their 50s and 60s, but not at older ages.

Amid that picture of cognitive decline, there were some positive trends suggesting that certain factors might help preserve cognitive function in women compared to men.

"Two risk factors, years of education and total cholesterol, showed positive associations with cognition, such that higher levels were correlated with greater cognition," write the researchers in their published paper.

Given their links to cognitive performance, it's possible these factors may be especially important to investigate in women's dementia risk.

However, this observational study can't prove cause and effect. A longer-term analysis could provide stronger evidence that these risk factors were contributing to the cognitive test scores.

While 'women' and 'men' are recognized as gender categories, this study uses these terms to refer to individuals' self-reported biological sex.

"It is important to distinguish between sex differences in the prevalence of risk factors and their impact on cognition, because prevalence and impact may not correspond," writes the team.

"Targeting only the most prevalent risk factors within each sex may overlook certain risk factors that more markedly influence cognitive decline."

The new findings fit with previous research suggesting that dementia risk factors may affect men and women in different ways, though these studies have tended to look at only one risk factor at a time.

Alzheimer's disease now affects an estimated one in nine US adults aged 65 and older, and two-thirds of those affected are women.

While the figures for dementia may be bleak, there are real and practical ways to reduce risk, while work on treatments continues.

The researchers emphasize that all these risk factors are potentially modifiable. That means they're real targets that people and their doctors can try to address, whether it's drinking less, moving more, or seeking help for depression.

Next steps here could include research to determine why women's cognition may be more vulnerable to certain factors.

Hormonal changes around menopause may be involved, but the mechanisms remain unclear.

Related: One Vital Bodily Function Could Link Many Dementia Risk Factors

"These differences highlight the importance of considering sex as a key variable in dementia research," says Pa.

The research has been published in Biology of Sex Differences.

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People have been consuming tobacco for millennia, though it wasn't until the late 1820s that nicotine was first extracted from tobacco plants.

Now, 200 years later, scientists have finally discovered how the tobacco plant makes those nicotine molecules.

The discovery could potentially transform products made from or using tobacco species, a practice known as 'plant molecular farming'.

Scientists have been engineering tobacco plants to produce therapeutic compounds and even vaccines, but the nicotine is problematic: it's highly addictive.

Understanding how nicotine is made could mean researchers could devise ways to prevent its production in plants.

"It is a big moment in plant science and biochemistry that we now have the answer we have been chasing for more than 200 years," says biologist Benjamin Lichman, from the University of York.

Lichman and colleagues at the University of Copenhagen in Denmark identified in their new study the genes and enzymes that help produce nicotine.

"With this new knowledge we can remove or repurpose the nicotine that is produced naturally by the plant and create better biotechnology tools," says Lichman.

"There is also exciting potential for the future to adapt tobacco's nicotine forming system to make useful pharmaceutical compounds."

Through a genetic analysis of tobacco (Nicotiana tabacum), the researchers flagged genes that sit close together in tobacco DNA, and activate at the same time as genes already known to be involved in nicotine production.

They then isolated the enzymes produced by these genes.

In both test tubes and living plants, the researchers demonstrated that these enzymes combined to form nicotine.

It turns out the enzymes work through a clever process that goes some way to explaining why they've remained hidden for so long.

Initially, a glucose molecule is attached to the building blocks of nicotine, putting them in the reactive state that's needed for nicotine assembly. That same molecule then snaps off after the process has finished – so the sugar does its essential job, then disappears.

The researchers also identified the two enzymes, NaGR and NicGS, that help assemble the nicotine molecule from its raw materials. Those materials are an amino acid linked to protein building and a vitamin-like compound.

"It is exciting because it has real-world applications," says Lichman.

"A close relative of tobacco, Nicotiana benthamiana, is already used in 'molecular farming' to produce life-saving drugs and vaccines."

"It opens up new ways to use tobacco plants for good: not in cigarettes, but for medicines and other valuable products."

Another recently published study backs up the findings: nicotine is created by glucose, helped by a chain of enzymes, before the glucose disappears.

That complete vanishing act, together with the unusual way glucose is used here compared to other plant processes, is what made the nicotine production process so elusive for so long, the researchers say.

There are still some questions about nicotine production in tobacco, but we now have the main steps and key ingredients sorted.

The researchers suggest the process could be tweaked to produce different chemical substances and tobacco with low levels of nicotine; however, previous attempts have stunted plant growth.

Related: Plants Stopped Thriving When Earth Warmed 56 Million Years Ago

Ultimately, these researchers have not only solved a 200-year-old mystery but also laid the groundwork for more advanced and precise bioengineering.

"Tobacco plants can be used in biotechnology as platforms for producing vaccines or other pharmaceutical products, but it is plagued by the presence of nicotine, which contaminates the products and requires processing to remove it," says Lichman.

The research has been published in Nature Communications.

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A diet designed for weight loss could offer a different bonus benefit, according to a new review.

Researchers from the University of Coimbra in Portugal looked at dozens of previous studies analyzing this diet and its relationship to neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's disease.

If you're on the ketogenic (or keto) diet, you'll be prioritizing fats and proteins, while cutting down on carbohydrates – and it turns out, at the same time you could be protecting your brain from disease.

The team also looked at research relating to the keto diet more generally, trying to pin down the effects of the high-fat, dairy-rich diet on the body's metabolism – how it stores and uses energy in the form of glucose (sugar).

Problems with processing glucose underpin several brain diseases, and the team concluded that the keto diet has real potential as a way of targeting these conditions.

They also acknowledge there are several challenges with using the diet as a treatment method.

"The ketogenic diet has emerged as a metabolically oriented strategy with potential preventive and therapeutic relevance in neurodegenerative diseases," write the researchers in their published paper.

"While preclinical studies have demonstrated encouraging results, significant gaps remain in understanding long-term effects, safety, and practicality of [the ketogenic diet] in clinical settings."

The keto diet works by getting the body to burn fat for energy rather than glucose (which we get mainly from carbohydrates). Biologically, this is known as a metabolic state called ketosis, where fat molecules called ketones are used instead of glucose.

It means weight can rapidly be lost, and the keto diet is actually prescribed for treating epilepsy in some cases.

As the researchers here summarize, there are multiple mechanisms through which it might protect against neurodegenerative conditions too.

Brains running on empty could use ketones as an alternative, emergency energy source, for example, as has been demonstrated in studies of Alzheimer's – thus going some way to restoring neuron stability and functionality.

Ketones have also been shown to reduce inflammation in mice models of Parkinson's and multiple sclerosis, boost an important cellular clean-up process called autophagy, and promote gut bacteria associated with better brain function.

Add all of that up, and there's plenty of evidence that the keto diet – and the metabolic changes that it brings about – can target some of the processes thought to contribute to several devastating brain diseases.

"The ketogenic diet may serve as a complementary metabolic intervention that supports disease-specific treatments by enhancing metabolic resilience and contributing to symptom management," write the researchers.

It's not quite as simple as using the keto diet with people at high risk of neurodegenerative problems, however. Most of the reviewed studies involved animals rather than people, so further investigation is required in terms of clinical trials.

The keto diet is also one of the most difficult to stick to, so getting patients to follow it might be a problem. It also tends to come with a variety of unpleasant side effects: it's been linked to constipation, insomnia, and high cholesterol in some people, for instance.

Past studies have found that the keto diet might cause harm in the longer term, and increase the risk of type 2 diabetes and heart disease. These downsides need to be weighed against any benefits that come along with the keto diet.

What this new review does is give us a 'state of play' in terms of scientific understanding right now. The multiple studies that were looked at offer solid evidence that following a keto diet and having better brain health are connected – though their results shouldn't be considered in isolation.

Related: Keto Diet May Have a Surprising Bonus Benefit, Mouse Study Suggests

"This review underscores the potential of [the ketogenic diet] for treating neurodegeneration on the basis of current scientific evidence while highlighting the need for further research to optimize its application and address existing gaps," write the researchers.

The research has been published in Translational Neurodegeneration.

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A diagnosis of multiple sclerosis (MS) comes with a wave of uncertainty about how the condition will progress.

Now, new research points to a potential mechanism and treatment target for those who are most severely affected.

MS damages nerve cells, stripping away their protective covering that keeps nerve signals firing.

The new study, from researchers in the Netherlands, suggests that in the most severe cases of MS, an immune cell usually in charge of repairing damaged tissue and clearing away waste becomes overloaded with fat droplets.

Known as "foamy microglia", these cells have been spotted in MS patients before, but it wasn't clear exactly what they were doing.

According to the findings from this latest study, they could be key drivers of MS at its worst.

MS is an autoimmune disease in which the body's immune system becomes overactive, mistakes its own cells as foreign, and starts causing damage through inflammation. But these foamy microglia suggest there's also more to the story.

"We found that patients with large numbers of these foamy microglia had a more severe disease course more frequently," says molecular physiologist Daan van der Vliet, from Leiden University in the Netherlands.

"It does not appear to be simply about the inflammatory response alone."

The team analyzed post-mortem brain tissue from 28 people with secondary progressive MS, where the disease has progressed to the point where cognitive and physical function are declining.

This tissue was compared against samples from 10 donated brains from people without the disease.

Using a combination of profiling techniques, the researcher created a map of proteins, fats, and active genes for the brain regions affected by MS lesions.

These lesions form when the fatty, protective coating around nerve fibers, known as myelin, is attacked by immune cells that have become too aggressive.

Not only was there a link between more foamy microglia and MS progression, but the researchers also found that the microglia were changing the mode of inflammation around the lesions – they had a different molecular signature in terms of proteins and enzymes.

The researchers suggest that as microglia arrive to try and repair the damage done to neurons, they get clogged up with fats (beginning with myelin) and become overwhelmed, which in turn, makes the inflammation worse.

"These cells are probably trying to do something good: clearing up damage," says van der Vliet.

"But they become overloaded, so to speak. As a result, they can no longer effectively contribute to repair."

The researchers also used a mouse model of MS, blocking one of the enzymes most active in foamy microglia. Tissue healing improved in these mice, further emphasizing the connection between these immune cells and worse MS progression.

We're still in the early stages of this research, and clinical trials with MS patients will be needed to see if the foamy microglia link holds up.

Researchers will also need to look at how these lesions that aren't repaired continue to develop over time.

However, these are promising findings in terms of figuring out why some people with MS live relatively normal lives for decades, while others become paralyzed sooner or develop more severe symptoms at a young age.

The study team is hopeful that the findings could help develop new MS treatments that target fat metabolism in cells.

There's also the potential, along with other lines of research, to identify more severe cases of MS at an earlier stage.

The researchers found signs of fats associated with foamy microglia floating around in cerebrospinal fluid, which they say could be measured as a marker of the disease.

Related: Scientists Identify Specific Bacteria Linked to Multiple Sclerosis

"That opens the possibility of developing biomarkers in the future that could help doctors identify earlier which patients are at risk of rapid decline – and which treatment would suit them best," says van der Vliet.

The research has been published in Nature Neuroscience.

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