We all must have come across the phase: this is why women live longer than men. These are all over the social media, where men are performing more often than not, some experiments, without gears, just for fun, "in the name of science". The caption reads: this is why women live longer. However, is there really a science to it, other than the fact that women choose to do things more safely?

In the United States, women have a life expectancy of about 80, whereas men have 75. Women outlive men and this holds true regardless of the country women live, the money they make, and other factors. In fact, it is true for most other mammals too.

Dr Dena Dubal, a professor of neurology at the University of California, San Francisco told the New York Times, "It is a very robust phenomenon all over the world, totally conserved in sickness, during famines, during epidemics, even during the times of starvation."

But what are the reasons? These reasons are often more complicated and less established. It is important to note that only because women are outliving men does not mean they are living a better life. In fact, women tend to have shorter health spans, which means the number of healthy years in a person's life is less in women than men, confirmed Bérénice Benayoun, an associate professor at the U.S.C. Leonard Davis School of Gerontology.

As per a 2021 study titled, Sex differences in frailty: Comparisons between humans and preclinical models, found that women are more physically grail than men in old age. They are also more vulnerable, especially after menopause and are at more risk of developing cardiovascular issues and Alzheimer's disease because of age.

The key is in figuring out what makes one sex more resilient or vulnerable.

Genetics

For things which do not find easy explanations, scientists look for their answers in genes. Many research, including a 2020 study titled, The sex with the reduced sex chromosome dies earlier: a comparison across the tree of life, suggests that the XX set of female sex chromosomes may impact longevity. However, there has not been any clarity on how it affects longevity.

Another 2018 study titled, Female XX sex chromosomes increase survival and extend lifespan in aging mice, which was conducted by Dr Dubal's lab, looked at genetically manipulated mice with different combinations of sex chromosomes and reproductive organs. It was found that those with two X chromosomes and ovaries lived longest, followed by mice with two X chromosomes and testes. Mice with XY chromosomes had shorter life spans.

"There was something about the second X chromosome that was protecting the mice from dying earlier in life, even if they had testes. What if there was something on that second X chromosome that was in some ways a sprinkle of the fountain of youth," says Dr Dubal. While scientists have not yet looked at this factor in humans, Dr Dubal suggests that humans have the same hormones and sex chromosomes, and similar reproductive system that could corroborate the similar findings in people.

Hormones

Plenty research has shown that estrogen is responsible for longevity also effect on the immune system. The data also shows that before menopause, the female immune system tends to do better. In fact Dr Benayoun said that males tend to do much worse in response to infection.

Another 2017 study titled, Ages at Menarche and Menopause and Reproductive Lifespan As Predictors of Exceptional Longevity in Women: The Women's Health Initiative, found that women who experienced menopause later in life over the age 50 lived longer than those who experienced it earlier.

Lifestyle and Behavior

There are also disparity in behavioral patterns between men and women. This includes smoking, drinking heavily, which can contribute significantly to mortality. Women also have more "health promoting behavior", believe experts. Women are also more likely to socialize than men and thus it protects them from detrimental effects of social isolation and loneliness. In fact, a 2023 analysis published in Jama Network, titled, Widening Gender Gap in Life Expectancy in the US, 2010-2021, found that women are less likely to die by drug overdose or suicide.

GLP-1 receptor agonist drugs such as Ozempic and Wegovy have shown significant benefits for people with diabetes and obesity. However, not everyone experiences the same results.

Now, a study suggests that this variation may be due to genetic resistance, which means that some people are biologically less responsive to these medications, making these drugs less effective.

The new study by scientists at Stanford University in the US showed that about 10 per cent of the general population carry genetic variants that lead to what the researchers called “GLP-1 resistance”.

The GLP-1- receptor agonist drugs typically work by mimicking the hormone GLP-1 (glucagon-like peptide-1), which naturally helps regulate blood sugar by stimulating insulin release. The process slows the emptying of the stomach and reduces appetite.

However, in individuals with certain genetic variants, the team found that higher levels of GLP-1 did not regulate blood sugar better.

The researchers noted that the findings, published in the journal Genome Medicine, may be key to developing new therapies for people with GLP-1 resistance.

“There are a whole class of medications that are insulin sensitizers, so perhaps we can develop medications that will allow people to be sensitized to GLP-1s or find formulations of GLP-1, like the longer-acting versions, that avoid the GLP-1 resistance,” said Anna Gloyn, professor of pediatrics and of genetics at Stanford Medicine.

The Gene Linked to GLP-1 Resistance

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To zero in on the gene resistant to GLP-1 drugs, the team conducted experiments in humans. They traced this resistance to a PAM variant known as p.S539W.

PAM (peptidyl-glycine alpha-amidating monooxygenase) is an enzyme that is uniquely capable of activating many hormones in the body, including GLP-1.

While the researchers suspected that people with the PAM variant would have lower levels of GLP-1 in their blood, it actually increased levels of GLP-1. Although the exact mechanism is still unclear, experiments in both humans and mice confirmed signs of reduced response to GLP-1.

Analyzing diabetes drug trial data, they found that individuals with these variants were less able to lower their blood sugar levels even after six months of treatment. This suggests that despite having more circulating GLP-1, their bodies are less responsive to it.

“When I treat patients in the diabetes clinic, I see a huge variation in response to these GLP-1-based medications and it is difficult to predict this response clinically,” said Mahesh Umapathysivam, an endocrinologist and clinical researcher at Adelaide University in Australia.

“This is the first step in being able to use someone’s genetic make-up to help us improve that decision-making process,” he added.

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Importantly, participants with the PAM variants did not respond differently to other common diabetes treatments, including sulfonylureas, metformin, and DPP-4i.

The finding may help develop precision medicine, the researchers said. Knowing ahead of time who is likely to respond would help patients get on the right drugs faster, Gloyn said.

Reasons Why Ozempic May Not Help All People Lose Weight

Ozempic is primarily indicated for type 2 diabetes management. But some doctors may prescribe it for weight loss in appropriate patients without diabetes.

Previous research has shown that medical conditions such as sleep apnea, along with certain common medications, such as antidepressants, steroids, and contraceptives, can hamper the process of shedding extra pounds.

Another major reason that can hamper weight loss is the side-effects of these drugs that can prompt a person to halt their prescription mid-way.

Once widely known as non-alcoholic fatty liver disease (NAFLD), the common and dangerous fatty liver condition was rephrased as Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) due to its strong link to metabolic health issues like obesity and diabetes.

MASLD now includes patients with fatty liver disease linked to metabolic risk factors such as obesity, diabetes, and hypertension.

MASLD: So What Prompted The Change?

Globally, it was observed that all patients who have non-alcoholic fatty liver disease also have some associated form of metabolic dysfunction. The patients reported having either obesity, diabetes, metabolic syndrome, hypertension, or cholesterol problems.

And all these problems eventually lead to significant comorbidities later, like some people developed heart disease, while others developed complications of diabetes.

In view of these, a global consensus process in 2023 involving hundreds of experts from different countries adopted MASLD as it better reflected these underlying causes of the condition.

What Does MASLD Mean?

Also read: Lancet Study Shows Metabolic Liver Disease To Rise Over 38% By 2050: What’s Behind The Surge

MASLD is an umbrella term for liver conditions that develop in the presence of 1 or more cardiometabolic risk factors—including high blood sugar, elevated body mass index (BMI), and hypertension—but in the absence of other causes of liver fat accumulation.

The condition can be defined by excess liver fat accumulation (more than 5 per cent of liver weight) in the presence of metabolic dysfunction, independent of alcohol intake.

It encompasses a spectrum from simple steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma.

“Initially, it was thought that having fatty liver disease without alcohol was a benign condition, but now it is recognized that, since it is associated with lots of metabolic comorbidities, it's no longer benign,” Dr. Ashish Kumar, Professor of gastroenterology and hepatology at Sir Ganga Ram Hospital in New Delhi, told HealthandMe.

He stated that whenever a diagnosis of fatty liver is present, "we should actually include other comorbidities, like obesity, dyslipidemia, which means cholesterol problem, diabetes, sugar problem, pre-diabetes, and hypertension. At least 50–70–80 percent of these patients will have one or more of these comorbidities".

Why Alcohol Is Not The Only Culprit For Fatty Liver

Although alcohol has remained the number one risk for liver disease, MASLD seems to be rising globally, including among people who do not drink. Why?

The reasons include:

a sedentary lifestyle,

increased consumption of fast and processed food,

lack of exercise,

lack of sleep,

stressful life.

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The experts noted that food, especially the increasingly accessible junk food or processed food, is a major culprit.

“So even if the person is not drinking alcohol, people are developing addiction to processed food, and this is causing an epidemic level of obesity and diabetes. Consequently, MASLD is also increasing, and now it is becoming the number one cause of liver disease,” Dr Kumar said.

How To Prevent MASLD?

According to Dr. Sanjay Goja, Director, Liver Transplant & HPB Surgery, Narayana Hospital, Gurugram, prevention must focus on following a healthy lifestyle like maintaining a healthy BMI, engaging in regular physical activity, and eating a balanced diet.

Controlling diabetes, cholesterol, and blood pressure is also important to prevent the risk of MASLD.

Dr Siddharth Badola, Manipal Hospital, Ghaziabad, suggested sustainable lifestyle changes such as:

Maintaining an adequate body weight: Even slight weight loss (5–10 percent) has been shown to significantly reduce liver fat and inflammation.

Follow a balanced and nutrient-rich diet: People should focus on consuming whole grains, fresh fruits and vegetables, lean proteins, and healthy fats, while limiting refined carbohydrates and processed foods.

Avoid foods with added sugar: Excess consumption of fructose, commonly found in packaged foods and sugary beverages, is a key contributor to fat accumulation in the liver.

Engage in regular physical activity: At least 150 minutes of moderate-intensity exercise per week is recommended to improve insulin sensitivity and liver health.

Manage associated metabolic conditions: Effective control of diabetes, hypertension, and dyslipidemia is essential in reducing the risk of MASLD progression.

Ensure adequate sleep and stress management: Poor sleep quality and chronic stress can negatively impact metabolic balance and liver function.

Keep your body hydrated with ample water intake and follow structured meal timings.

Although a heart attack is generally considered a disease of the elderly, its incidence in young individuals is unfortunately on the rise. The reasons behind this are multifactorial. A heart attack is a condition where one of the arteries (blood vessels) suddenly becomes partially or completely occluded by a thrombus. Although the thrombus generally occurs suddenly, the underlying reason is a chronic process of lipid deposition in the vessel walls called atherosclerosis. Atherosclerosis can begin even in the first decade of life, but events like heart attacks conventionally occurred beyond 45 years in men and 55 years in women. On average, heart attacks occur in Indians about 10 years earlier than in their Western counterparts.

Dr Shyam Sasidharan, Consultant, Department of Cardiology, KIMSHEALTH Thiruvananthapuram, spoke about the early onset of heart attacks. From a population perspective, the rising number of heart diseases due to coronary artery disease (CAD) is significant not only because of its overall negative impact on the healthy population but also due to the potential for preventive interventions.

Heart attacks among younger people

Acute coronary syndromes, or heart attacks, are on the rise among younger individuals, particularly in our country. Studies of the Asian-Indian migrant population have revealed a probable racial predisposition for premature CAD. However, the majority of the risk can still be attributed to the increased incidence of conventional CAD risk factors in young people, such as obesity, inactivity, diabetes, hypertension, and dyslipidaemia.

Smoking and substance abuse are resulting in more heart disease among the young. Lesser-discussed, unconventional risk factors, such as mental stress, lack of healthy employment practices, environmental pollution, and lack of proper food safety regulations, are in fact contributing significantly to this silent epidemic. COVID-19 infection as well as vaccination were widely attributed as causes of heart attacks in young people, but without adequate scientific evidence.

How to reduce heart disease risk in your 30s?

1. Creating awareness: The most important step towards prevention is creating awareness. Awareness regarding heart disease risk factors, healthy lifestyle choices, early symptoms of heart attack, and the need for timely medical attention is crucial.
2. Diet and physical activity: With rapid urbanisation and industrialisation, a nutritional transition is occurring in India. An increase in refined sugars, fats, and processed foods sets the stage for premature heart disease. Efforts to increase physical activity to at least 30 minutes of moderate activity per day, for five days a week, need to be promoted.
3. Prevention programmes: Programmes targeting the prevention of early development of lifestyle diseases such as diabetes, hypertension, and dyslipidemia need to be extended to younger individuals. Improving access to medical services across all social strata can enhance prevention, early detection, treatment, and reduction in morbidity and mortality from heart diseases.
4. Political will: Efforts to curb pollution, promote a better work culture, and enforce strong legislation for food safety will go a long way in not only preventing early heart disease but also promoting the overall health of the population.
5. Preventive health check-ups: At an individual level, promoting healthy habits and undergoing regular health check-ups can contribute significantly towards early detection of risk factors as well as early diagnosis of heart disease itself.
6. Improving mental health: There should be more discussions and interventions focused on overall mental health, work–life balance, and happiness, as these are known to impact heart health.