New Delhi: Love to binge on packaged baked goods and snacks, fizzy drinks, sugary cereals, and ready-to-eat or heat foods? Beware, it can cut short your lifespan and raise the risk of early death, according to a 30-year-long study published in the journal The BMJ on Thursday. The risk is because ultra-processed foods often contain colours, emulsifiers, flavours, and other additives and are typically high in energy, added sugar, saturated fat, and salt, but lack vitamins and fibre -- leading to poor health, and raising the risk of obesity, diabetes, and hypertension, which can further raise the risk of cardiovascular diseases and cancer.
For the study, an international team of researchers including from the US, Brazil, and China, tracked the long-term health of 74,563 female registered nurses from 11 US states between 1984 and 2018; and 39,501 male health professionals from all 50 US states from 1986 to 2018 with no history of cancer, cardiovascular diseases, or diabetes.
The results revealed that eating an average of 7 servings per day of ultra-processed foods caused a 4 per cent higher risk of total deaths and a 9 per cent higher risk of other deaths, including an 8 per cent higher risk of neurodegenerative deaths.
The rate of death from any cause among participants in this group was 1,536 per 100,000 person-years.
Further, eating meat, poultry, and seafood-based ready-to-eat products showed the strongest risk of early death, followed by sugar-sweetened and artificially sweetened beverages, dairy-based desserts, and ultra-processed breakfast food.
Even though this is an observational study, so no firm conclusions can be drawn about cause and effect, “the findings provide support for limiting consumption of certain types of ultra-processed food for long-term health,” said the researchers.
“Future studies are warranted to improve the classification of ultra-processed foods and confirm our findings in other populations,” they added. (IANS) mine protection against liver inflammation: The number and duration of fasting cycles play a role, as does the start of the fasting phase. A 5:2 dietary pattern works better than 6:1; 24-hour fasting phases better than 12-hour ones. A particularly unhealthy diet requires more frequent dieting cycles.
Heikenwalder’s team now wanted to find out the molecular background of the response to fasting. To this end, the researchers compared protein composition, metabolic pathways and gene activity in the liver of fasting and non-fasting mice. Two main players responsible for the protective fasting response emerged: the transcription factor PPARa and the enzyme PCK1. The two molecular players work together to increase the breakdown of fatty acids and gluconeogenesis and inhibit the build-up of fats.
“The fasting cycles lead to profound metabolic changes, which together act as beneficial detoxification mechanisms and help to combat MASH,” says Heikenwalder, summarizing the molecular details.
The fact that these correlations are not just a mouse phenomenon was shown when tissue samples from MASH patients were examined: Here, too, the researchers found the same molecular pattern with reduced PPAR a and PCK1. Are PPAR a and PCK1 actually responsible for the beneficial effects of fasting? When both proteins were genetically switched off simultaneously in the liver cells of the mice, intermittent fasting was unable to prevent either chronic inflammation or fibrosis.
The drug pemafibrate mimics the effects of PPARa in the cell. Can the substance also mimic the protective effect of fasting? The researchers investigated this question in mice. Pemafibrate induced some of the favorable metabolic changes that were observed with 5:2 fasting. However, it was only able to partially mimic the protective effects of fasting. “This is hardly surprising, as we can only influence one of the two key players with pemafibrate. Unfortunately, a drug that mimics the effects of PCK1 is not yet available,” explains Mathias Heikenwalder.
While Heikenwalder and his team initially focused on the effects of intermittent fasting on the prevention of MASH, they then investigated whether the 5:2 diet could also alleviate existing chronic liver inflammation.
To this end, the team examined mice that had developed MASH after months of being fed a high-sugar, high-fat diet. After a further four months of 5:2 intermittent fasting (on the same diet), these animals were compared with the non-fasting control group. The fasting mice had better blood values, less fatty liver and liver inflammation and above all: they developed less liver cancer and had fewer cancer foci in the liver.
“This shows us that 5:2 intermittent fasting has great potential - both in the prevention of MASH and liver cancer, as well as in the treatment of established chronic liver inflammation,” summarizes principal investigator Heikenwalder. “The promising results justify studies in patients to find out whether intermittent fasting protects against chronic liver inflammation as well as in the mouse model.”
The 5:2 fasting regimen is popular. It is considered comparatively easy to integrate into everyday life, as the fasting days can be tailored to personal needs and no specific foods are prohibited. “Nevertheless, there will always be people who can’t stick to a strict diet in the long term,” says Heikenwalder. “That’s why we want to continue to investigate which combinations of drugs we can use to fully mimic the protective effects of fasting.” (ANI)
Also Read: Ultra-processed foods may up mouth, throat & oesophagus cancer risk (sentinelassam.com)
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