Imagine this. A young teenager, 17, years old, who is fully developed. Now imagine this, the same teenager has a fully developed extra set of limbs and a pelvis. That extra set of pair is attached with chest artery. But, how can this happen?

While it is extremely rare, and has a chance of less than one case occurring per 100,000 births. Such things do happen. This is called parasitic twin.

What Is A Parasitic Twin?

It is an extremely rare type of cojoined twin where a baby is born with an underdeveloped twin attached to its body. This condition is also known as vestigial twins. The condition is very closely related to conjoined twins, where babies are connected at birth and share organs. However, the main difference is that in conjoined twins, there are two developed babies, whereas in parasitic twins, only one is fully developed, other one is underdeveloped and non functional.

In such a case, the twin who is developed is medically known as the autositic or the dominant twin. The dominant twin is healthy in most aspect but may have extra tissue, organs, or limbs from the parasitic twin.

The parasitic twin may be attached with the dominant twin through several places. The common joints are at the head, torso, chest, pelvis, buttocks, or back. In these cases, the parasitic twin is not alive and they die either in the womb or during the childbirth.

Doctors Remove Parasitic Twin

Now, let's go back to the case we referred to, where a young teenager had an extra pair of limbs attached to chest. The teenager who has not been named is from Uttar Pradesh's Unnao neighbourhood, and was treated in AIIMS, Delhi. The team of doctors successfully removed the extra set of limbs from his body.

Dr Asuri Krishna, who led the team of specialist who surgically removed the extra limbs told the BBC that only 40 to 50 cases of parasitic twins have been documented in world medical literature, and in those cases, the surgery had been attempted on children. The doctor said that without much medical literature to guide them, the team of doctors depended on "intuition, skill and knowledge".

The doctor shared that the child had two fully formed legs, buttocks and external genitalia, which weighed around 15kg "protruding from his abdomen".

How Was The Surgery Performed?

The doctor shared that first they identified how interconnected the parasitic and host twins were. The doctors took scans and found that parasitic twin was attached to the teen's breastbone. The blood was being supplied from a vessel in his chest. However, "there wasn't much connection with other main organs like the liver or kidneys," said Dr Krishna. The team also found a large cyst in the teen's abdomen.

Then the surgery was performed in two stages. In the first stage, the parasitic twin was removed. Then the cystic mass was extracted from the surrounded area. The entire surgery was completed in two and a half hours and the team of doctors included radiologists, anaesthetists, and plastic surgeons.

The biggest challenge was when the teen's blood pressure dropped as 30 to 40% of his blood flowed to the parasitic twin, however, the doctors were prepared for it and they stabilized him.

A recent study has found proof that an autoimmune reaction is triggering certain neurological symptoms seen in some long COVID patients. The study, conducted in healthy mice, found that the mice exhibited symptoms mirroring those of affected patients to some extent.

What is Long COVID?

While it has been a long time since the end of the COVID pandemic, its effects continue to linger even today. Several patients who contracted COVID continue to suffer.

Autoantibodies Behind Long COVID Symptoms?

A US NIH-funded research group, directed by Drs. Akiko Iwasaki and Tamas L. Horvath of the Yale University School of Medicine and Dr. David Putrino of the Icahn School of Medicine at Mount Sinai recently found that autoantibodies could be triggering these neurological symptoms in some long COVID patients.

Antibodies, in a healthy person, help fight infections. In patients with autoimmune diseases, these antibodies target the body’s own tissues. They are called autoantibodies.

The study also discovered that patients who had these autoantibodies are more likely to experience similar symptoms. For example, people with autoantibodies are more likely to face symptoms like loss of taste and smell. They are also more likely to experience nausea and joint pain.

The Mouse Experiment

The researchers conducted the study by transferring purified antibodies from long COVID patients into healthy mice. It was discovered that the mice developed the following changes that resembled the donors' symptoms:

• Antibodies from patients with chronic pain caused increased pain sensitivity

• Antibodies from patients with dizziness caused balance problems

• Antibodies from fatigued patients reduced treadmill endurance

The recent breakthrough in long COVID research has brought the healthcare industry one step closer to personalizing care for those affected.

Dr. Putrino says, “Our study now shows that if you are in a subgroup of Long COVID patients who have autoantibodies circulating in your body, this is a quantifiable sign that you may be a good candidate for these drugs.”

Long COVID Patients More Likely To Develop Heart Diseases

The study finds that cardiovascular diseases were more common among long COVID patients. It concluded that 11.9% of those with long COVID have CVD compared to 6.8% without this condition.

Specifically, it further revealed that long COVID was associated with a higher risk of chest pain and heart attack, but not coronary heart disease and stroke.

There is a growing belief that ‘sugar feeds cancer.’ Because of this, many people think that stopping sugar and carbohydrates completely can starve cancer cells and help defeat the disease. However, the trend may have side effects. This half-truth is becoming dangerous for many patients. This trend is making it even more difficult for patients to cope with the side effects of chemotherapy.

This fact is not entirely unscientific, but it is incomplete. In 1924, the German scientist Otto Warburg found that cancer cells consume more glucose than normal cells. This phenomenon is known as the Warburg Effect.

This finding has subsequently been validated in numerous studies. This is also the reason why cancer cells appear clearly in PET-CT scans. They absorb glucose-like substances more aggressively than normal cells. But this does not mean cancer can be “starved” by reducing sugar in food.

Why The Body Still Needs Glucose?

Glucose is an essential fuel for the human body. The brain, heart, red blood cells, and immune system all depend on it.

If a person completely stops eating carbohydrates, the body starts producing glucose on its own. It breaks down muscles and proteins to make energy. This process is known as gluconeogenesis. This means the cancer cells still receive fuel, but the patient’s body becomes weaker day by day. This condition is described as ‘cancer cachexia.’

In this condition, body weight and muscle mass reduce rapidly. Such patients often cannot tolerate chemotherapy and surgery properly. In some cases, their protein levels and white blood cell counts had dropped too much.

As a result, doctors had to delay treatment, reduce medicine doses, or even stop some treatment cycles. Irony is painful. In trying to starve cancer, patients sometimes end up weakening their own bodies so much that proper treatment becomes difficult.

In my clinic, I see it almost every week. In such a case, a cancer patient walks in visibly frail. She almost had lost several kilograms over the past month. When I asked about her diet, her IT professional son said that she has cut out sugar entirely. The reason behind this was the same reel-based knowledge about sugar and cancer cells. His son strictly follows this half-truth. Due to her weakness, we had to push back her treatment for a few weeks.

What Cancer Patients Should Eat

We simply suggest avoiding foods that rapidly increase blood sugar levels. These include refined sugar, sweets, soft drinks, maida, and highly processed foods. We advise cancer patients to eat complex carbohydrates, whole grains, pulses, vegetables, healthy fats, and enough protein. The best way is not to cut sugar entirely, but to lower the glycemic load.

Will Fasting help?

Some animal studies have shown the benefits of fasting during cancer treatment. However, there is still not enough evidence in humans. For patients who are already weak or losing weight rapidly, long fasting can become harmful.

The Goal Is to Stay Strong During Treatment

Cancer cells use more glucose, but starving the body cannot stop cancer. If you want to help your body, then avoid refined sugar and junk food, but continue eating balanced meals. Because sufficient protein and calories are extremely important. Practising long fasting without medical advice is harmful. The goal should be to keep the body stable and strong, not weak.

The purpose of cancer nutrition is to nourish the patient, not to starve them. Proper nutrition helps the body tolerate treatment and fight disease more effectively. What is needed is to reduce the intake of refined sugar and foods with a high glycemic index, not to declare every carbohydrate an enemy. After all, one cannot win the battle against disease by weakening the body.

A new oral weight-loss drug is showing promising results for people living with obesity or who are overweight. In a phase II clinical trial published in Nature Medicine, participants taking the experimental medication aleniglipron lost up to 12% of their body weight over 36 weeks.

The study included contributions from Robert Kushner, MD, professor emeritus of medicine at Northwestern University and a longtime expert in obesity treatment.

Aleniglipron belongs to the GLP-1 family of drugs, the same class as popular medications such as Ozempic and Wegovy. These treatments help people lose weight by mimicking a natural hormone that reduces appetite, increases feelings of fullness, and helps regulate blood sugar levels.

What makes aleniglipron different is that it comes in pill form. Most currently available GLP-1 medications require injections and often need special storage, which can make them less convenient and more difficult for some patients to access.

Researchers believe an oral option could make treatment easier for many people. Because aleniglipron is a small-molecule drug—meaning it is chemically manufactured rather than peptide-based—it can be produced more efficiently and potentially at a lower cost.

“Aleniglipron is different because it’s a small molecule that can be taken with or without food,” Kushner said. “Most medicines people take every day, from aspirin to blood pressure drugs, are small molecules. That also creates opportunities to combine it with other treatments in the future.”

If further studies confirm its safety and effectiveness, aleniglipron could offer a more convenient alternative to injectable GLP-1 medications and help expand access to obesity treatment.

Why Is GLP-1 Drug A Medical Breakthrough?

Dr Shubham Vatsya explains that it took 20 years of research for scientists to come up with these medicines. This drug underwent proper lengthy trials, and have been approved by the US Food and Drug Administration (FDA), "which is not obtained by giving any bribe".

He also noted that when a person is not able to lose weight, Ozempic and drugs alike give a "head start" to them, along with a hope.

Talking about side effects, he says that every drug has its side effects, this is where a doctor's role comes in.

"Now, the person who is not able to lose weight, if you tell him 'you hit 100 kg bench press', he will break his shoulder. He needs a kickstart somewhere. This is what weight loss drugs allow," he says.

He also points out that the scientists who made GLP-1 agonists got a Nobel Prize, which "cannot be a scam". This is what makes weight loss drugs truly different.

Also Read: Raising Sons Linked to Faster Cognitive Decline in Later Life, Study Find

What Are GLP-1 Drugs?

GLP-1 Drugs stand for Glucagon-like peptide 1, a naturally occurring hormones that helps regulate blood sugar and appetite after eating. It was first identified almost 50 years ago and scientists have since uncovered its role in type 2 diabetes.