For over 15 years, Dr Anthony Shum, a pulmonologist at the University of California, San Francisco has been studying a rare genetic disorder called the COPA Syndrome. It stands for coatomer subunit alpha and is a rare, inherited disorder that affects the lungs, joint, and kidney. The National Organization for Rare Disorder also notes that it is a genetic autoimmune disorder that is caused by mutations in the COPA gene. This disease affects families unpredictably—some individuals with the mutation develop severe lung damage early in life, while others remain completely healthy. Now, Shum’s team has discovered a protective genetic variant that may offer new hope for treatment.

A Breakthrough

Researchers found that some relatives of COPA Syndrome patients stayed healthy despite carrying the same COPA gene mutation that causes the disease. The key difference? These unaffected individuals had a protective version of another gene called HAQ-STING.

When scientists introduced HAQ-STING into diseased lung cells from COPA patients, the cells returned to a balanced state, suggesting that this gene could be used as a therapy.

“We really think HAQ-STING could be a gene therapy tool and a step toward a cure,” said Shum, whose findings were published in the Journal of Experimental Medicine.

Families Who Solved The Mystery

Shum’s journey into COPA Syndrome research began in 2011 when he treated a young woman, Letasha, who had severe lung bleeding. Her mother, Betty Towe, mentioned that Letasha’s sister, Kristina, had suffered from similar symptoms. Over the years, Betty had taken both daughters on a four-hour trip to UCSF for treatment. After tracing their family history, Shum discovered that their distant relatives in Texas and Oakland also had lung problems and arthritis. In 2015, Shum, along with scientists from Baylor College of Medicine and Texas Children’s Hospital identified the COPA gene mutation. They realized that it was the common factor behind the illness. However, only some of the 30 individuals with the mutation actually developed symptoms, leaving a major question unanswered.

The Domino Effect

It was established that it occurs when a mutated COPA gene causes another gene STING to go overdrive. The STING that helps fight infections in COPA patients, remain permanently active, which leads to chronic inflammation that damages the lungs, kidneys, and joints. In 2020, while studying STING’s role in the disease, researchers discovered a key variation: HAQ-STING. This version of STING, present in about one-third of the population, appeared to neutralize the harmful effects of the COPA mutation.

To confirm their theory, the scientists needed both affected and unaffected family members to participate in the testing. Letasha, Kristina and Betty immediately volunteered. The researchers then analyzed DNA samples from 26 COPA patients and their healthy relatives. They also conducted CT scans and blood tests to ensure that unaffected members did not have any hidden symptoms. When the findings were all clear, it was revealed that all the healthy individuals had HAQ-STING, while none of the COPA patients did. This was the first known case of a common gene variant completely protecting against a severe genetic disease.

Encouraged by this discovery, researchers tested HAQ-STING’s effects in a lab setting. They introduced it into diseased lung cells from COPA patients, and the cells returned to normal function.

Way Ahead

Shum believes HAQ-STING could lead to game-changing treatments, including:

• Prenatal gene therapy for babies diagnosed with COPA Syndrome before birth
• Aerosol delivery of HAQ-STING for adults, directly targeting the lungs

Before publishing their findings, Shum called Betty with the news—her own HAQ-STING gene had protected her from the disease. He also informed Letasha and Kristina, who were overwhelmed with relief and joy.

“We always believed Dr. Shum would get to the bottom of it,” said Letasha. “This discovery is going to change lives.”

Your DNA, or more specifically your genes, have fascinating interactions with your diet. These interactions are often bidirectional and form the basis of personalized nutrition through genomic biohacks.

This has impressive applications in solving some of the most stubborn health related challenges, including undesirable weight gain and obesity.

Here are the five ways by which your DNA could positively shape your diet:

Nutrigenomics

Nutrigenomics is the mechanism by which your diet affects your genes, and not the other way round. The process has massive implications for your health, and especially over how you can use specific dietary components to protect yourself against serious killer diseases like cancers and issues like faster aging.

Deficiency in key nutrients like Vitamin B9 or folate, Vitamin B12, choline & methionine can cause genomic instability and increased cancer risk.

In contrast, specific foods like curcumin, resveratrol, green tea, broccoli, Brussels sprouts etc can help with genomic stability and help fight inflammation, oxidative stress and cancers.

Nutrigenetics

These are the processes by which your genes affect your diet or consumed food and hence central to our theme here. At times, nutrigenetics is referred to by the wider umbrella term nutrigenomics.

Your gene variants determine how you process specific nutrients, which explains why the same diet works differently for different people. Genetic tests like Eplimo can easily find this out.

For instance, presence of certain variants of the SGK1 gene make those individuals more prone to high blood pressure from salt intake.

Similarly, variants in the FTO gene are strongly linked to obesity risk. Other very common examples are variants in the CYP1A2 gene that determine how fast you metabolize caffeine and mutations in the LCT gene that determines whether you are at risk of lactose intolerance.

Hunger & Satiety Hormones

Ghrelin, the hunger hormone, is produced mainly in the stomach and stimulates appetite, increases food intake as well as promotes fat storage.

The production of ghrelin hormone is governed by the GHRL gene, and a common variant in this gene called RS696217 is associated with unnecessary hunger and higher obesity risk.

Similarly, leptin is a hormone produced by the body’s fat tissues and regulates satiety or the feeling of fullness with regard to food.

Production of leptin is governed by the LEP gene, while its utilization is controlled by the LEPR (leptin receptor) gene. Variants in either, especially LEP, can cause severe, early-onset obesity.

Metabolic Pace

Genes play a significant role in determining your metabolic pace. Studies show that genes account for up to 60 percent of the variations seen in the Resting Metabolic Rate between individuals.

RMR is basically a measure of how much calories are burnt while you are sitting or doing light activities.

It is different from Basal Metabolic Rate (BMR) that requires fasting and bed rest. Hundreds of genetic variants work together to set your RMR.

These include variants in the UCP1 gene governing thermogenesis or heat production, the MC4R gene that influences how the body burns nutrients for energy, and genes governing mitochondrial efficiency.

Building more muscles is a proven way to counter the negative impact of such variants and boost RMR.

Gut Microbiome

Does your gut microbiome impact your genes more, or does your genes impact your gut microbes more? Definitely, it is the former, which is also a better known mechanism due to that greater impact.

But that doesn’t mean that the reverse impact, from your DNA to your microbiome which accounts for around 10 percent of its composition, is insignificant in any way.

For instance, your specific gene variants determine which bacteria thrive by influencing immune responses, metabolism, and food preferences.

Specific genes, such as the LCT gene, directly correlate with the abundance of beneficial bacteria like Bifidobacterium. Genetics also influence how you digest food and your dietary preferences, which in turn feeds specific bacterial species.

Other genetic factors too have been identified as having strong links to microbial diversity, which is a great marker for not only gut health, but overall health, performance and longevity.

The impact of social media on adolescents’ well-being is significant, said the World Happiness Report 2026 today, warning that the scale of harm is significant enough to affect entire populations.

The annual report, published by the Wellbeing Research Centre at the University of Oxford, points to overwhelming evidence of both direct and indirect harm.

Direct harms include exposing them to videos of graphic pornography and real-life violence, facilitating cyberbullying and deepfakes, promoting dangerous “challenges”, connecting them with sexual predators, and facilitating the purchase of illegal drugs.

The indirect harms involve rising levels of depression, anxiety, and reduced life satisfaction.

“The harms and risks to individual users are so diverse and vast in scope that they justify the view that social media is causing harm at a population level,” the report said.

The harmful "experiences are so common that they should also count as ordinary use,” it added.

Notably, the report called the major social media platforms such as Facebook, Instagram, Snapchat, TikTok, and X, "dangerous consumer products that harm adolescents at a massive scale”.

“The evidence of harm – both direct and indirect – is so strong and comes from so many sources in so many countries that we believe policymakers around the world now have enough evidence to justify action to protect children and adolescents,” the report said.

In line with this, countries such as Australia and Indonesia recently introduced legislative restrictions on social media use among young people. In India, states including Karnataka and Andhra Pradesh have announced bans, while Bihar is considering similar measures.

The report pointed out that social media is causing direct harms to millions of people globally. This includes:

• Addiction and problematic use
• Sleep deprivation
• Sextortion
• Sexual harassment

Impact on Youth Well-being

Research cited in the report shows a clear link between heavy social media use and lower life satisfaction among adolescents. Youth and teens who spent more time on social platforms reported poorer mental well-being compared to those who used less.

Overall, internet use was linked with negative effects, particularly among girls and in countries such as the UK and Ireland. Yet, among those who used the internet for communication, learning, news consumption, and content creation, higher life satisfaction was reported.

The report noted that negative emotions are becoming more common across all regions. Worry increased among young people, while the frequency of anger declined across both younger and older populations.

Despite these trends, positive emotions still occur about twice as often as negative ones globally.

Global Happiness Rankings

Finland has been ranked the world’s happiest country for the ninth consecutive year, followed by Iceland, Denmark, and Costa Rica. Other countries in the top 10 include Sweden, Norway, the Netherlands, Israel, Luxembourg, and Switzerland.

In contrast, when measuring changes in happiness among people under 25, countries in the NANZ region -- the United States, Canada, Australia, and New Zealand -- rank much lower, placing between 122 and 133 out of 136 countries.

Hormonal changes during menopause can significantly increase Alzheimer's disease (AD) risk in women, according to Dr Lisa Mosconi, a neuroscientist and women’s brain health specialist.

In a new The Journal of Clinical Investigation review, the renowned AD expert noted that menopause can change brain biology and metabolism and may contribute to amyloid plaques and tau tangles, which are key biological markers of AD.

Alzheimer disease is the most common cause of dementia, affecting over 55 million individuals worldwide, with projections exceeding 150 million by 2050 . Out of the reported cases, nearly two-third are made up of women, with the majority being postmenopausal women

Estrogen protects the brain by lowering inflammation, increasing neuronal survivals supporting non-amyloidogenic processing, and reducing amyloid-beta-related neurotoxicity, all of which are factors contributing to the development of AD.

However, when estrogen levels drop during menopause and follicle-stimulating hormone (FSH) and luteinizing hormone (LH) rise, the brain becomes more likely to develop AD-related damage.

Previous research has also shown that early menopause, especially before age 45, is linked with increased risk of dementia and the removing the ovaries before natural menopause could increase long-term dementia risk, with the greatest excess risk seen at younger ages, especially before 45.

READ MORE: Simple Blood Test Can Predict Dementia Risk in Women 25 Years Before Symptoms

What Is Alzheimer’s Disease?

Alzheimer's disease is one of the most common forms of dementia and mostly affects adults over the age of 65.

About 8.8 million Indians aged 60 and above are estimated to be living with Alzheimer's disease. Over seven million people in the US 65 and older live with the condition and over 100,00 die from it annually.

Alzheimer's disease is believed to be caused by the development of toxic amyloid and beta proteins in the brain, which can accumulate in the brain and damage cells responsible for memory.

Amyloid protein molecules stick together in brain cells, forming clumps called plaques. At the same time, tau proteins twist together in fiber-like strands called tangles. The plaques and tangles block the brain's neurons from sending electrical and chemical signals back and forth.

Over time, this disruption causes permanent damage in the brain that leads to Alzheimer's disease and dementia, causing patients to lose their ability to speak, care for themselves or even respond to the world around them.

While there is no clear cause of Alzheimer's disease, experts believe it can develop due to genetic mutations and lifestyle choices, such as physical inactivity, unhealthy diet and social isolation.

Early symptoms of Alzheimer's disease include forgetting recent events or conversations. Over time, Alzheimer's disease leads to serious memory loss and affects a person's ability to do everyday tasks.

There is no cure for this progressive brain disorder and in advanced stages, loss of brain function can cause dehydration, poor nutrition or infection. These complications can result in death.

Can You Detect Alzheimer's Early On?

The US Food and Drug Administration has approved the use of a blood test which can help diagnose Alzheimer’s disease in adults aged 55 and above.

The blood test, known as Lumipulse, can detect amyloid plaques associated with Alzheimer’s disease and has proven to be a “less invasive option” that “reduces reliance on PET scans and increases diagnosis accessibility.”

FDA Commissioner Martin A. Makary said of the landmark decision, "Alzheimer’s disease impacts too many people, more than breast cancer and prostate cancer combined.

"Knowing that 10 percent of people aged 65 and older have Alzheimer's, and that by 2050 that number is expected to double, I am hopeful that new medical products such as this one will help patients."

It remains unclear when this test will be available for commercial use across the world.