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A lot of our body’s functions depend on when we are defecating and how well our bowel movements are taking place. People have different pooping habits, with some people having a nightly routine and others enjoying a morning bathroom run. But is it normal for one to run to the bathroom after every meal? Not only is it inconvenient but it could be a sign of something going wrong with your body. Have you ever enjoyed a meal and immediately needed to use the restroom?
If so, you might be worried that something is wrong with you. But you don’t need to stress about this! It is actually quite common and doesn't necessarily indicate a health problem.
This phenomenon is called the gastrocolic reflex. When food enters your stomach, it triggers a series of signals in your digestive system. Your stomach stretches to accommodate the food, and sends signals to your brain through the vagus nerve. The brain then communicates with your large intestine, telling it to make room for the new food by moving its current contents along. In other words, you're not pooping out what you just ate, but what has been in your digestive system for a day or two.
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Metformin has been long used to manage diabetes. But a major analysis based on more than 256,000 adults with obesity and prediabetes has found that people who take GLP-1 medications like Ozempic and Mounjaro were less likely to develop type 2 diabetes than those taking metformin.
The study also found that people taking GLP-1 medications were more likely to return to normal blood sugar levels and had lower risks of heart attacks, strokes, heart failure and death from any cause compared to those taking metformin.
The findings come from preliminary research presented at the American Heart Association's (AHA) Scientific Sessions 2026. Researchers compared health records of adults to both obesity and prediabetes to examine whether GLP-1 medications could help prevent the progression to type 2 diabetes.
According to the AHA, the analysis included 256,492 adults, with an average age of 52 years. Women accounted for 76% of the participants.
About half of the participants were taking GLP-1-based medications, including semaglutide, tirzepatide, liraglutide and dulaglutide, while the remaining participants were taking metformin.
Researchers used electronic health records from the TriNetX global multicentre network, which included 104 institutions. The records covered the period from 2010 to 2023. The participants were followed for an average of approximately three years.
The researchers matched participants based on factors such as age, existing health conditions, including high blood pressure and sleep apnoea, nicotine dependence and other medications.
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Compared to people on metformin, those taking GLP-1 medications had a 31% lower risk of developing type 2 diabetes.
They were also 1.5 times more likely to return to normal blood sugar levels, suggesting that the medications may help reverse the progression from prediabetes in some people.
The analysis also identified differences in cardiovascular results. Compared to the metformin group, people taking GLP-1 medications had:
The risk of death from any cause was also 41% lower among people taking GLP-1 medications.
Most earlier research on GLP-1 medications has focused on people who already have type 2 diabetes. This analysis examined their benefits at an earlier stage, when blood sugar levels are higher than normal but have enough for a diabetes diagnosis.
Commenting on the findings, study author Vinicius de Sousa Barzon Serra, MD, a research fellow in the Department of Cardiovascular Medicine at Mayo Clinic in Scottsdale, Arizona, said, “The great news with prediabetes is that it’s still possible to reverse the progression of the disease.”
He added, “This research may add to the case for considering GLP-1 medications earlier for certain patients, rather than waiting until they develop Type 2 diabetes.”
However, Serra said the findings do not mean metformin should be replaced by GLP-1 medications.
“The main effect these findings could have is on the shared decision-making discussion between doctors and patients exploring various treatment options, and the pros and cons for each,” he said.
“Metformin is still a first-line treatment choice. It is safe, inexpensive and has a long track record. This is less about replacing one medication with another and more about discussing additional options with specific patients,” he added.
Serra also highlighted the importance of lifestyle changes in preventing diabetes.
“It's important to note that an essential component of prediabetes treatment is lifestyle changes to manage weight, including diet and exercise and considering medications, including metformin, based on each individual's overall health and any other medical conditions,” he said.
Robert Eckel, MD, FAHA, a former volunteer president of the American Heart Association and professor of medicine emeritus at the University of Colorado Anschutz Medical Campus, said the findings were not surprising. “The benefits noted in this study likely relates to the patients losing weight, which is known to help prevent Type 2 diabetes,” said Eckel.
He explained that preventing the progression from prediabetes to type 2 diabetes could also help reduce cardiovascular complications.
“Preventing the progression from pre-diabetes to Type 2 diabetes keeps patients from having Type 2 diabetes, and it also helps prevent heart attack and strokes,” he said.
Eckel added, “GLP-1s provide another option for prevention, perhaps as an add-on therapy. However, costs and access to these medications are important factors.”
The findings should not be interpreted as evidence that Ozempic or Mounjaro is superior to metformin for every person with prediabetes.
The American Diabetes Association's 2026 Standards of Care identify metformin as an option for people at particularly high risk of developing type 2 diabetes, including adults aged 25 to 59 years with a BMI of 35 or higher, higher blood glucose levels or a history of gestational diabetes.
The guidelines also say that metformin has the most robust evidence for pharmacological diabetes prevention. While GLP-1-based therapies can be considered for weight management in people with overweight or obesity, long-term evidence does not currently support using glucose-lowering medications other than metformin solely for the purpose of preventing type 2 diabetes.
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Obesity during the 20s and 30s can fuel the risk of many lifestyle disorders like type 2 diabetes, cardiovascular diseases, metabolic syndrome, non-alcoholic fatty liver disease, sleep apnea and many others.
But according to a large study published in Annals of Internal Medicine, obesity could also increase the risk of developing cancer before midlife. The study identified higher chances of thyroid, endometrial and ovarian cancers.
Researchers examined health records of 6,313,338 adults in South Korea, aged between 20 to 39 years, who had no previous history of cancer.
Participants were followed for an average of 11.2 years to study the relationship between body weight and cancer risk.
During the follow-up period, 151,893 cancer cases were recorded. The findings showed that cancer risk increased in people with higher body mass index (BMI).
The researchers found that the 10-year total incidence of cancer was 1.84% among people with normal body weight. This increased to 2.24% among those with class I obesity and 2.62% among those with class II obesity.
In other words, the 10-year cancer incidence was approximately 0.78 percentage points higher among people with class II obesity than among those with normal weight.
The researchers also found that people with abdominal obesity were at higher cancer risk than those who didn’t have.
Among people with class I obesity, the 10-year cancer incidence was 2.45% in those with abdominal obesity, compared with 2.13% in those without it.
“Because abdominal obesity may be an important indicator for distinguishing cancer risk, it is important to manage waist circumference along with weight from a young age,” the authors wrote.
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The study identified particularly strong associations between obesity and cancers involving the thyroid and female reproductive system.
Thyroid cancer: Excess body weight has previously been linked with changes in metabolic and hormonal changes that may affect thyroid cancer development.
Endometrial cancer: Obesity can increase oestrogen levels because fat tissue produces this hormone. Prolonged exposure to excess oestrogen can stimulate the growth of the uterine lining and increase the risk of endometrial cancer.
Ovarian cancer: The relationship between obesity and ovarian cancer is complex and may involve inflammation, insulin resistance and hormonal changes.
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Obesity causes several biological changes that may contribute to cancer development. One of them is chronic inflammation.
Excess fat tissue can fuel inflammation that may create an favourable environment for abnormal cell growth.
Obesity can also lead to insulin resistance, in which the body’s cells respond less effectively to insulin. This can cause higher insulin levels, which may fuel cell growth and proliferation.
Hormonal changes are also a factor. Fat tissue produces oestrogen, and higher levels of this hormone have been linked with cancers like endometrial and ovarian.
The study authors wrote, "Some cancers have recently become more common even among younger people, and this study confirmed that obesity in young adults is significantly associated with the development of these cancers."
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Scientists have discovered a previously unknown mechanism that could explain why high cholesterol diet makes it challenging for the liver to remove bad cholesterol from the bloodstream. Researchers have also identified an experimental drug that blocks this process, offering a new method for treating high cholesterol.
The findings are published in the journal Nature by researchers from the University of California San Diego School of Medicine. Their experiments showed that blocking a specific enzyme called cathepsin A (CTSA) helped retain the liver's ability to clear low-density lipoprotein (LDL), commonly known as bad cholesterol.
In mice, inhibiting this enzyme stabilised LDL receptors in liver cells, reducing LDL cholesterol.
"We've known for a long time that a high-cholesterol diet reduces the liver's ability to clear cholesterol from the blood, but we didn't fully understand why," said senior author Alan Saltiel, professor of medicine at UC San Diego School of Medicine. "This new discovery explains a critical piece of that puzzle."
The liver plays a key role in regulating cholesterol levels. It uses LDL receptors located on the surface of liver cells to capture LDL cholesterol from the bloodstream.
When fewer of these receptors are available, the liver becomes less efficient at removing LDL cholesterol, allowing it to increase in the bloodstream. The researchers discovered that consuming high amounts of dietary cholesterol activates a protein called Ral. This increases the activity of CTSA, an enzyme that breaks down LDL receptors.
As these receptors are lost, the liver's ability to clear bad cholesterol declines. When researchers blocked CTSA using a small molecule inhibitor, LDL receptors became more stable and LDL cholesterol levels decreased dramatically in mice.
The discovery has sparked interest as researchers have identified an experimental drug that targets CTSA. The drug was originally developed as a possible treatment option for heart failure. Although its development for that purpose was discontinued for other reasons, it had already completed a Phase 1 clinical trial, which evaluated its safety in humans.
This previous test could help researchers move towards studying its ability as a cholesterol treatment. However, the drug has not yet been shown to lower LDL cholesterol in humans.
"There's still a real need for new cholesterol-lowering options, since some people can't get to safe levels even with the drugs we have now," Saltiel said.
He added, "This new pathway we discovered is completely separate from anything that existing drugs target, so it gives us a new opportunity to fill that gap."
The researchers hope to test the experimental CTSA inhibitor in a Phase 2 clinical trial to determine whether it can safely and effectively lower cholesterol in people. If successful, the approach could offer another option for people who struggle to control LDL cholesterol despite using existing treatments.
Saltiel said, "Luckily, there's an experimental drug sitting on the shelf that's already been shown to be safe in humans."
"We hope to test whether this might be effective by conducting a clinical trial -- which could potentially bring a new treatment option to patients much sooner than would have been expected."
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