Wednesday, November 12, 2025

Diet, lifestyle hacks to say goodbye to acid reflux and protect yourself from oesophageal cancer

Doctor shares diet tips and lifestyle tweaks to manage acid reflux and prevent oesophageal cancer, along with treatment and medications to avoid complications.

 Acid reflux might seem harmless, but chronic gastroesophageal reflux disease (GERD) can have life-altering consequences, including the development of oesophageal cancer. In an interview with HT Lifestyle, Dr Aparna Govil Bhasker (Consultant Bariatric and Laparoscopic Surgeon at MetaHeal - Laparoscopy and Bariatric Surgery Center in Mumbai and Saifee and Apollo and Namaha Hospitals in Mumbai) highlighted that certain factors make some people more susceptible to oesophageal cancer, including:

 Chronic GERD (acid reflux lasting for years)

Barrett’s oesophagus

Obesity (which increases pressure on the stomach, worsening reflux)

Smoking and excessive alcohol use

A diet

If you experience any of these symptoms or have multiple risk factors, do not ignore them. Seeking medical attention early can improve outcomes.

How to reduce the risk:

1. Managing acid reflux to prevent cancer

One of the ways to lower the risk of oesophageal cancer is by controlling acid reflux effectively. As per Dr Aparna Govil Bhasker, here’s how that can be done: 

  • Maintain a healthy weight – Excess weight increases abdominal pressure, pushing acid into the esophagus.
  • Eat smaller meals – Overeating increases acid production and worsens reflux.
  • Avoid trigger foods – Limit spicy, fatty and acidic foods, as they weaken the LES.
  • Quit smoking and reduce alcohol consumption – Both can damage the esophageal lining and weaken the LES.
  • Do not lie down immediately after eating – Wait at least 2–3 hours before lying down to prevent acid reflux.
  • Elevate your head while sleeping – Sleeping with an elevated head can reduce nighttime reflux.

 

2. Medical treatment options

Dr Aparna Govil Bhasker revealed that doctors may prescribe medications to help manage GERD and prevent complications:

  • Antacids – Neutralise stomach acid for temporary relief.
  • H2 Blockers – Reduce acid production (e.g., ranitidine, famotidine).
  • Proton Pump Inhibitors (PPIs) – Stronger acid reducers (e.g., omeprazole, pantoprazole).

When is surgery needed?

For severe GERD that does not respond to medications, Dr Aparna Govil Bhasker recommended that surgical options like fundoplication may be considered as this procedure tightens the LES, preventing acid reflux. If diagnosed with Barrett’s oesophagus, Dr Aparna Govil Bhasker suggested that regular endoscopic monitoring is essential to detect early signs of cancer.

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Thursday, February 28, 2019

Newly identified drug targets could open door for oesophageal cancer therapeutics

A new research has found that blocking two molecular pathways that send signals inside cancer cells could stave off oesophageal adenocarcinoma (EAC), the most common oesophageal malignancy in the United States.

Researchers identified the pathways using advanced computational and genetic analyses of tumour biopsies from EAC patients. They found 80 percent of tumours had unusually active genes related to two specific pathways, and that exposing the cells to pathway inhibitors stymied EAC tumour growth in mice.

The results of the study, published in a journal point to two signaling pathways (controlled by JNK and TGF-beta proteins, respectively) as contributing to EAC tumours.

The pathways represent molecular chain reactions that were overactive in patient tumour cells, but not in biopsies from patients with non-cancerous oesophageal conditions, including Barrett’s Oesophagus.

Harmful effects of these pathways could be reduced by turning down JNK or TGF-beta activity. “These findings suggest a rationale for testing JNK/TGF-beta-targeted therapies as a new treatment approach in this increasingly prevalent and lethal cancer,” said the senior author.

National Cancer Institute estimates, only 20 per cent of patients diagnosed with EAC survive five years. Patients struggle to swallow as tumours and cancer cells narrow their oesophagus. Some require nasogastric feeding tubes in end stages of disease. Limited available treatments to shrink tumours include surgery, radiation, or chemotherapy, but the majority of EAC tumours are resistant.

“Targeted therapies are virtually non-existent,” he said, adding, “Treatment advancements are also slowed because we don’t know exactly what molecular signals drive EAC pathogenesis.”

In the new study, researchers collected 397 biopsy specimens to find common mechanisms that underlie EAC tumour progression. They integrated computational and genetic analyses to identify signaling pathways highly active in EAC. They compared EAC biopsies to those collected from patients with conditions that often precede EAC, but who did not develop the cancer.

After finding JNK and TGF-beta pathways to be overactive only in EAC biopsies, they then incubated EAC tumour cells with therapeutic small molecules designed to block the pathways.

Exposure to JNK or TGF-beta inhibitors reduced the ability of EAC cells to proliferate, migrate, or form tumours when transplanted into mice. Several mice had near total regression of tumour growth following treatment.

Combining JNK and TGF-beta pathway inhibitor treatments further prevented cancer cell growth, but more studies are needed to understand synergy between the pathways during EAC progression.

EAC tumour cells’ reliance on the TGF-beta pathway was unexpected given its widely recognised role as a cancer suppressor, said  co-senior author on the study. The difference, he said, potentially lies in different roles for TGF-beta in different stages of EAC development.

He added, “In normal esophageal cells, TGF-beta acts as a gatekeeper by inhibiting uncontrolled cell growth.”

“As EAC develops, TGF-beta switches from a growth suppressor to a growth promoter. This is unlike its function in other cancers such as those arising in the colon.” he said, adding, “Our unique application of advanced mathematical modelling that we developed allowed us to tease out these intricate mechanisms, which would have otherwise been missed.”


The results open a new targeted therapeutic avenue for EAC, and lay the foundation for studies in humans.

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