Fasting may reset your body, but can it reset your mind? The new trend of dopamine fasting claims it can. And wait, there's more. This trend also works against dopamine resistance, implying that things that did not make you happier before will now do. You see, dopamine is a part of the brain's reward system and plays an important role in your pleasure reception. While this neurotransmitter is not directly linked to an individual's happiness, it triggers feelings of satisfaction, motivation and pleasure.

However, a person can also reach a stage of dopamine resistance if they continue to indulge in activities that trigger its frequent or constant release. In this case, the individual stops feeling the impact of this neurotransmitter and thus, does feel good or happy.

So does dopamine fasting work?

Dopamine fasting is a practice where individuals limit their exposure to activities or stimuli that typically provide a surge of dopamine. The idea behind dopamine fasting is to reset or recalibrate the brain's reward system. This is usually done by abstaining from gratifying things or experiences like social media, junk food, and even sex. Proponents of dopamine fasting argue that continual overstimulation from digital devices, social media, and easily accessible indulgences has numbed our brain's reward pathways. By regularly denying ourselves these dopamine triggers, the idea claims, we might restore our ability to acquire fulfilment from life's basic pleasures.

How Does Dopamine Imbalance Affect Your Mental Health?

Having low levels of dopamine can make you less motivated and excited about things. In Parkinson's disease, there is not enough dopamine in the areas of the brain important for movement. This leads to problems with muscle stiffness and movements such as walking.

The symptoms of a dopamine imbalance depend on what is causing the problem. They include physical symptoms such as:

• muscle cramps, spasms or stiffness
• digestion problems, such as constipation or reflux
• pneumonia
• trouble sleeping
• moving or speaking more slowly than usual

• feeling tired and unmotivated, or sad and lacking hope
• having low libido (sex drive)
• hallucinations (experiencing something that's not real)

How Can I Adjust My Dopamine Levels?

Adjusting dopamine levels is complicated, as it is involved in many different roles in the brain. Your doctor won't measure your dopamine levels directly, and there is no simple test to measure it. Your symptoms will be the clues that tell your doctor if you have too much or not enough dopamine. They will then prescribe medicines to adjust your dopamine level, based on your symptoms, and make adjustments based on how your body responds and how you feel.

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Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, affects millions of people worldwide. The lifelong condition commonly begins in adolescence or early adulthood and can require repeated hospital treatment, long-term immunosuppressive medication, and, in some cases, surgery.

Despite advances in treatment, many patients cycle through multiple therapies without achieving lasting disease control, impacting their lives and costing healthcare systems millions.

Now, a team of UK researchers from the Universities of Oxford, Newcastle, and Cambridge has identified an important driver of inflammatory bowel disease (IBD).

The findings, published in the New England Journal of Medicine, suggest that inflammatory bowel disease is not a single condition but a group of biologically distinct diseases driven by different underlying mechanisms.

"Understanding what drives the inflammation provides a clear explanation for disease in this group of people and opens the door to new treatments that target the autoantibodies themselves or cells that produce those autoantibodies," said Professor Holm Uhlig, a pediatric gastroenterologist and director of the Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford.

What Did the Study Find?

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The researchers analyzed more than 4,900 patients with IBD and discovered that:

• A substantial subset of patients shows autoimmune responses to one of the guardians of the immune system, interleukin-10 (IL-10), which leads to uncontrolled inflammation.
• This damaging immune response is the mechanism for one of the strongest known genetic risk factors for IBD.

Antibodies that block interleukin-10 (IL-10), a cell-to-cell messenger that normally acts as one of the body's key controls on inflammation, effectively remove the immune system's natural "brake" on inflammation, allowing inflammatory responses to continue unchecked.

The researchers found high levels of anti-IL-10 neutralizing autoantibodies in the blood of about 3.5% of IBD patients, including those with Crohn's disease and ulcerative colitis, but not in healthy individuals. This could equate to 15,000–20,000 people with IBD in the UK carrying these autoantibodies.

The Genetic Link

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The researchers also found that the presence of these antibodies was strongly linked to carriage of a particular genetic variant known as HLA-DRB1*01:03.

The link between HLA-DRB1*01:03 and a severe form of inflammatory bowel disease was first identified by Oxford researchers 30 years ago.

The new findings show that people carrying this variant are far more likely to develop antibodies that block IL-10, helping explain how the gene contributes to disease.

What Could This Mean for Patients?

The researchers say the findings support the development of a blood test to identify this subgroup of patients, helping clinicians move quickly toward more appropriate treatment.

What Is IBD?

As per the Centers for Disease Control and Prevention (CDC), IBD refers to a group of lifelong diseases that affect your intestines. The main types of IBD are ulcerative colitis and Crohn's disease.

Ulcerative colitis affects the large intestine, while Crohn’s disease can inflame any part of the digestive tract. Both are lifelong conditions of unknown cause that trigger abdominal pain, diarrhea and other complications, with no known cure.

What Are The Symptoms Of IBD That People Usually Ignore?

• Diarrhea or changes in bowel movements
• Stomach pain
• Fatigue
• Nausea
• Weight loss

• Dehydration
• Increased risk of colon and rectal cancers
• Low red blood cell count (anemia)
• Reduced bone density
• Joint pain
• Skin changes
• Eye irritation
• Delayed or impaired growth in some children.

With modern lifestyle changes, delayed childbearing, and other factors, infertility among Indians as young as 25 has become a looming public health concern for the country. However, the issue does not stop at the present.

A recent study published by The Menopause Society in their journal Menopause found that infertility may lead to earlier menopause, raising questions about the long-term reproductive health implications of this demographic shift.

What is Menopause?

Menopause is the final stage of a woman’s reproductive lifecycle, when menstruation stops, and she can no longer get pregnant. When the ovaries stop producing estrogen and progesterone, and a woman misses her period for 12 consecutive months, she has officially reached menopause.

Although menopause is a regular part of ageing, women typically reach menopause between 45 and 55 years of age. If menopause occurs before age 45, it is considered early menopause. If it occurs before 40, it is termed premature menopause – rarer than early menopause but involves the same causes, symptoms, and health risks.

While previous studies have been conducted to find a link between infertility and both early and premature menopause, they have had mixed results and did not consider the effect of different types of infertility; this study focuses on women with a history of primary infertility, women who have never achieved pregnancy, and have difficulty conceiving.

What Did the Study Find?

For the study, researchers examined the reproductive lifecycle of nearly 700 women in the U.S. – 461 with primary infertility and 530 without infertility – who were otherwise demographically similar (age, education, smoking status, etc.). It found that the 461 women had a 25% higher likelihood of reaching natural menopause about 1.2 years earlier than the 530.

Researchers also noted that women with underlying endometriosis as a cause of their infertility reached menopause between 40 and 44 years, much sooner than the national average of the United States, i.e., 52 years.

Possible explanations include accelerated ovarian ageing, reduced ovarian reserve, or the effects of endometriosis on ovarian function. But no matter the causes, the implications for women’s long-term health are substantial.

Why Does This Matter?

All women are born with a finite, predetermined number of eggs, which are sensitive to age, environmental toxins, medications, hormonal imbalances, and lifestyle factors. When exposed to such risk factors, especially over a long period of time, the DNA inside the eggs is altered, causing permanent genetic damage and reducing the egg quality and quantity.

As a core part of the reproductive process, any damage to the eggs directly affects reproductive health and, in turn, long-term systemic health.

Infertility impacts more than the ability to conceive and go through a pregnancy; it is often a sign of underlying health conditions and potential chronic illnesses, acting as a biomarker of increased all-cause mortality. Experiencing infertility itself increases a woman’s risk of developing cardiovascular disease, metabolic disorders, gynecologic cancers, etc., but reaching menopause early on top of that puts them at further health risk, adding osteoporosis and cognitive decline to the mix, along with the emotional distress and mental health challenges.

Indian women already reach menopause earlier than women in Western countries, with the average woman experiencing menopause at 46.2 years of age. With fertility rates dropping across the country, this study highlights just how critical it is to increase fertility awareness. Early screenings and regular fertility testing can help detect risks early and enable timely intervention, not only to combat the ongoing crisis but to ensure that women live healthy, fulfilling lives without impending morbidity.

A new oral GLP-1 medication has delivered encouraging results in a Phase 2b clinical trial for people living with type 2 diabetes.

According to AstraZeneca, its experimental tablet, elecoglipron, significantly lowered blood sugar levels and helped participants lose an average of 10.5% of their body weight after 26 weeks of treatment.

The findings were presented at the 2026 American Diabetes Association Scientific Sessions in New Orleans and published in The Lancet on June 8.

Elecoglipron joins a growing wave of GLP-1 therapies being developed as pills, offering an alternative to injectable drugs such as Ozempic, Wegovy, Zepbound, and Mounjaro.

The first oral GLP-1 treatment, Rybelsus from Novo Nordisk, received FDA approval in 2019 for adults with type 2 diabetes. Since then, oral options have continued to expand. In December 2025, the FDA approved a tablet version of Wegovy for weight management, while Eli Lilly’s oral obesity treatment, Foundayo, gained approval in April.

Independent experts say AstraZeneca’s results highlight the growing potential of non-injectable GLP-1 therapies for both diabetes and obesity treatment.

“It’s encouraging to see another oral medication demonstrating the benefits of GLP-1 therapy without requiring injections,” said Dr. Pouya Shafipour, a family and obesity medicine specialist at Providence Saint John’s Health Center in California.

Dr. Marilyn Tan, an endocrinologist and professor of medicine at Stanford University, noted that the rapidly expanding GLP-1 market could soon welcome another oral treatment option if elecoglipron succeeds in Phase 3 trials and ultimately secures FDA approval.

How Does GLP-1 Drug Work?

GLP-1 is a natural hormone produced in the intestines that regulates blood sugar, appetite, and digestion. Now, every time you eat, your body produces various hormones, including GLP-1. These are called post-nutrition hormones, and they help you absorb the energy you just consumed.

GLP-1 travels to your pancreas, prompting it to produce insulin. It also travels to the hypothalamus in your brain, which gives you the feeling of being full or satiated. GLP-1 pills imitate that hormone, thereby silencing the food chatter in the brain. Interestingly, for some people, this food chatter is really quiet, and for others it is an outburst. So with GLP-1, silencing this self-talk in the brain, people tend to lose their appetite and eventually weight.

However, it is important to note that losing weight includes not just fat but muscle as well. Losing too much muscle can lead to reduced strength and a shorter life span. Notably, records show that most people who start taking them stop them at 12 weeks; therefore, it is important for some but not for others.

What Are The Side Effects?

The side effects of these pills include:

• Nausea is a frequent side effect, especially when starting or increasing the dose, and vomiting may occur along with nausea.
• Diarrhoea and abdominal discomfort also show up.
• It can reduce appetite but may also lead to unintended weight loss or reduced food intake, causing discomfort for some people.
• There are certain less common, but serious side effects, like Pancreatitis, or inflammation of the pancreas.
• This drug may also cause severe kidney issues, particularly if dehydration occurs from side effects like vomiting or diarrhoea.