We love experimenting with our hair, but that comes with its fair share of hair damage and brittleness. Does that mean we just let our hair be their normal self? Actually no, to enhance your looks and bring out your personality it is important to keep changing your hair but it is also important to take goo care of your hair.

And for those who think hair care can cost a bomb, then follow the below mentioned DIY recipes and you can thank us forever.

Rice Water and Fenugreek Hair Mask

• Soak two tablespoons of fenugreek seeds in rice water overnight.
• Blend the soaked seeds with rice water to form a paste.
• Apply it to your scalp and hair, leaving it on for 45 minutes before washing.

Avocado & Olive Oil Hair Mask

• Scoop out the pulp from the avocado and mash it. Now add olive oil to the pulp and mix properly.
• Apply the mixture to your scalp and strands. Leave it on for about an hour before washing your hair.
• Use this mask once a week.

Banana and Olive Oil Hair Mask

• Use one ripe banana and one tablespoon of olive oil.
• Blend or mash the banana until it reaches a lump-free puree. Add the olive oil and continue blending.
• While in the shower, apply the mask throughout the hair and scalp with fingers. Leave on for 10 to 15 minutes before rinsing.

Lemon and Yogurt Hair Mask

• Take 1 bowl of yogurt and add 3-4 drops of lemon juice to it.
• Mix it thoroughly and apply it evenly onto your hair.
• Keep it on for 20 minutes and then rinse it off and remember to use a conditioner after.

Shea Butter Homemade Hair Mask

• Melt shea butter and add some coconut oil to it. You can also add argan oil instead of coconut oil.
• Apply it to your scalp and strands. Give it one to two hours to work its magic. After a few hours, wash and condition as usual.
• Use it twice a week.

Schizophrenia is a severe, chronic brain disorder that can lead psychosis, hallucinations, delusions, disorganized thinking and reduced emotional expression. It can affect how a person thinks, feels and behaves, making it hard to distinguish reality.

The chronic neurological condition affects less than one percent of the global population and typically emerges in late teens to early thirties, requiring lifelong treatment.

However, Canadian researchers have now pointed towards the placenta as a possible source of early indicators of schizophrenia risk.

According to the scientists, the placenta can "record" what happens during pregnancy and can reflect both healthy and unhealthy conditions for the baby, a phenomenon known as the placenta-brain axis.

The theory suggests that when the placenta is negatively affected, brain development may also be harmed in both the short and long term and increase the baby's risk of developing the lifelong condition.

Multiple large-scale studies have found that in pregnancies where babies are born with low birth weight, certain genetic markers in the placenta are altered. These changes are strongly linked to a higher risk of schizophrenia and other developmental problems, such as autism and learning difficulties.

There is also strong evidence that using cannabis during pregnancy can harm a baby’s brain development and increase the risk of schizophrenia.

However, while cannabis use during pregnancy is known to be linked to low birth weight, it is still unclear whether cannabis exposure affects the same placental genetic markers associated with schizophrenia.

How Is Brain Impacted During Schizophrenia?

In schizophrenia, the brain experiences structural and chemical changes that disrupt normal thinking, emotions, and behaviour. Research shows that people with schizophrenia often have reduced grey matter volume, particularly in areas involved in memory, emotion, and decision-making, like the hippocampus and prefrontal cortex.

Abnormalities in neurotransmitters, especially dopamine and glutamate, also play a key role, leading to symptoms such as hallucinations, delusions, and cognitive difficulties. Connectivity between different brain regions may become impaired, affecting the brain's ability to process information smoothly.

These changes typically emerge gradually, often beginning in late adolescence or early adulthood, and vary significantly from person to person.

How To Identify Schizophrenia?

According to the DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th Edition), schizophrenia is diagnosed based on a set of specific symptoms. Here's the list of core symptoms:

• Delusions – strong false beliefs not based in reality (e.g., believing you are being persecuted or have special powers).
• Hallucinations – hearing, seeing, or sensing things that aren't actually there (most commonly auditory hallucinations).
• Disorganised speech – frequent derailment, incoherence, or illogical conversation.
• Grossly disorganised or catatonic behavior – unpredictable agitation, inappropriate behaviour, or lack of movement/responsiveness.
• Negative symptoms – diminished emotional expression, reduced motivation (avolition), reduced speech (alogia), social withdrawal, or inability to experience pleasure (anhedonia).

Researchers at the National University of Singapore (NUS Medicine) have found a key protein in the brain which can help to regenerate neural stem cells and improve aging-associated memory decline.

Known as cyclin D-binding myb-like transcription factor 1 or DMTF1, the scientists found that this protein's levels are repressed in the “aged” neural stem cells and that restoring it is sufficient to restore the regeneration capabilities of such neural stem cells.

Assistant Professor Ong Sek Tong Derrick explained: "Impaired neural stem cell regeneration has long been associated with neurological ageing. Inadequate neural stem cell regeneration inhibits the formation of new cells needed to support learning and memory functions.

"While studies have found that defective neural stem cell regeneration can be partially restored, its underlying mechanisms remain poorly understood. Understanding the mechanisms for neural stem cell regeneration provides a stronger foundation for studying age-related cognitive decline."

How Does DMTF1 Protect Against Memory Decline And Dementia?

But DMTF1 seems to bypass this limit by helping neural stem cells to keep multiplying, even during brain aging. It does this by switching on helper genes that promote cell growth through a process called chromatin remodeling.

Importantly, this process can restore the growth of stem cells that had already been damaged by telomere shortening, showing that the effects of aging may not always be permanent.

The researchers plan to further explore if elevating DMTF1 expression can regenerate neural stem cell numbers as well as improve learning and memory under the conditions of telomere shortening and natural ageing, without increasing the risk of brain tumours.

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.

Dr Ambrish Mithal, endocrinologist in a podcast with Ranveer Allahbadia, highlighted the difference between the popular weight loss drug Ozempic and Mounjaro. Dr Mithal said that a person can lose around 10 kgs in four to six months. When Allahbadia asked Dr Mithal if there is any difference. To this, Dr Mithal said that while Ozempic is a GLP-1 drug, Mounjaro is a combination of GLP-1 and GIP. In simpler language, if one has to compare the two for only weight loss, Mounjaro can outweigh Ozempic by roughly 10 per cent.

What Is The Difference Between Ozempic and Mounjaro?

While both drugs are approved by FDA and requires prescription, and doses increases over time to a maintenance dose, experiences shortages, not FDA-approved for weight loss.

Although several studies suggest that Mounjaro may lead to greater weight loss than Ozempic, it is not currently approved by the U.S. Food and Drug Administration specifically for weight loss. That said, doctors may prescribe both Mounjaro and Ozempic off-label to support weight management in certain patients.

A real-world comparative effectiveness study by Truveta Research examined the active ingredients in both drugs among overweight and obese adults. The findings showed that tirzepatide, the active ingredient in Mounjaro, resulted in greater weight loss within one year of treatment. Individuals taking tirzepatide were more likely to achieve meaningful body weight reduction at three, six, and 12 months compared to those on semaglutide.

According to Eli Lilly, participants in Mounjaro clinical trials lost between 12 and 25 pounds. The trials reported an average weight loss of 21.1 percent after 12 weeks and a total mean weight loss of 26.6 percent over 84 weeks.

In contrast, clinical trials conducted by Novo Nordisk found that Ozempic users lost between 9.3 and 14.1 pounds. On average, participants lost about 15 percent of their body weight after 68 weeks of treatment.

Is Mounjaro More Effective Than Ozempic?

The answer depends on individual health goals and medical needs. Mounjaro is widely recognised for its strong impact on lowering A1C levels and promoting weight loss. Ozempic, meanwhile, not only helps control blood sugar but is also approved to reduce cardiovascular risk in people with Type 2 diabetes.

Head-to-head research suggests that Mounjaro may offer greater reductions in both blood sugar and body weight. In the SURPASS-2 trial, tirzepatide outperformed semaglutide in lowering A1C levels. The 5 mg, 10 mg, and 15 mg doses of tirzepatide reduced A1C by 2.01, 2.24, and 2.30 percentage points respectively, compared to a 1.86-point reduction with the 1 mg dose of semaglutide.

Read: WHO Issues First Guidance On Obesity Drugs — GLP-1 Drugs Get the Green Light

How Do Mounjaro and Ozempic Side Effects Compare?

Both medications share similar side effects, most commonly gastrointestinal issues such as nausea and vomiting. However, some data suggest that side effects with Mounjaro may be slightly more frequent or severe.

The SURPASS-2 trial found that the most common side effects were generally comparable between tirzepatide and semaglutide. However, tirzepatide was associated with a slightly higher rate of serious adverse events.

Mounjaro’s prescribing information includes a warning about severe gastrointestinal disease, a caution not listed in Ozempic’s label. Clinical trials also showed that more patients discontinued Mounjaro due to gastrointestinal side effects. For both drugs, higher doses were linked to an increased likelihood of side effects.

Ultimately, how a person responds to either medication can vary. Each drug works differently in the body, and individual tolerance, medical history, and treatment goals all play a role in determining which option may be more suitable.

Difference Between GLP-1 Drug and GIP Drug

GLP-1 Drugs

GLP-1 drugs mimic the action of the natural hormone GLP-1 to regulate blood sugar and promote weight loss. They work by increasing insulin release in a glucose-dependent manner, decreasing the liver's production of glucagon, and slowing down the emptying of the stomach, which helps lower blood sugar levels after a meal. They also act on the brain to suppress appetite and increase feelings of fullness, leading to reduced calorie intake.

In people with type 2 diabetes, notes Harvard Health, the body's cells are resistant to the effects of insulin and body does not produce enough insulin, or both. This is when GLP-1 agonists stimulate pancreas to release insulin and suppress the release of another hormone called glucagon.

These drugs also act in the brain to reduce hunger and act on the stomach to delay emptying, so you feel full for a longer time. These effects can lead to weight loss, which can be an important part of managing diabetes.

GIP Drugs

As per the American Diabetes Association's published study, Gastric inhibitory peptide (GIP) is best known for its role as an incretin hormone in control of blood glucose concentrations.

GIP is produced from a larger 153–amino acid precursor protein encoded by the GIP gene. In the bloodstream, it circulates as an active 42–amino acid peptide. It is synthesised by K cells located in the lining of the duodenum and jejunum in the small intestine.

Like other endocrine hormones, GIP is released into the bloodstream and travels to target organs through circulation. Its receptors are seven-transmembrane G protein–coupled receptors (GPCRs) found primarily on the beta cells of the pancreas.