Junk food's immediate impact on your cells

Junk food's immediate impact on your cells: State-of-the-art scans reveal burgers and greasy fries cause instant stiffening that lead to heart issues A University of Illinois team analyzed how much exposure to junk food is needed before cells see an impact They used state-of-the-art scanning techniques to look at the impact on human cells  Junk food caused the cell membrane to immediately stiffen and thicken compared to those not given lipoproteins

By Dailymail.com Reporter

Published: 14:32 GMT, 1 March 2019 | Updated: 14:32 GMT, 1 March 2019

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Slipping out of your diet into a junk food rut has a near-immediate impact on blood vessels at the cellular level, alarming new research found.

Eating burgers, pizzas and sausage rolls over a short period can trigger hardening of the arteries - by rapidly changing their structure, warn scientists.

The condition, known as atherosclerosis, is the main cause of heart attacks and strokes.

It suggests processed products are more harmful to health than feared.

State-of-the-art scanning techniques of human cells by the University of Illinois team showed junk food caused the cell membrane to stiffen and thicken compared to those not given lipoproteins

State-of-the-art scanning techniques of human cells by the University of Illinois team showed junk food caused the cell membrane to stiffen and thicken compared to those not given lipoproteins

Experiments on mice and lab grown human cells found two types of 'bad' cholesterol were the culprits.

These are LDL (low density lipoprotein) and the less commonly known oxidised LDL - a form produced by damaging chemicals called free radicals.

The rodents were fed either a normal well balanced diet or a 'western' alternative mirroring levels of fat, protein and carbohydrate found on a typical fast food menu.

Those consuming the latter quickly developed stiffer arteries - down to the layer of endothelial cells in the outer wall of the blood vessels.

In the first study of its kind the US team measured the LDLs and oxidised LDLs - and then applied the same concentrations to the cultured human endothelial cells.

State-of-the-art scanning techniques showed physiological levels of both caused the

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