“Drinking too much pop can speed up the ageing process,” the_ Daily Mail_ reported. It said research has found that phosphate, a chemical that gives many drinks their tangy taste, can accelerate ageing.
This study was in mice that were genetically engineered to age prematurely. Although animal studies can provide information on how biological processes work, these findings may or may not be relevant to the human body. It is a big leap from these findings to the suggestion that fizzy drinks containing phosphates could cause premature ageing.
The effect of excess phosphate on health is important enough to justify further research. However, it is unclear if the levels of phosphate in fizzy drinks are high enough to affect health. At present, the high sugar and calorie content of these drinks would seem to be a more compelling reason for limiting their intake.
This research was carried out by Mutsuko Ohnishi and M Shawkat Razzaque from the Harvard School of Dental Medicine, USA, and Nagasaki University Graduate School of Biomedical Sciences, Japan. The study was funded by the National Institute of Diabetes and Digestive and Kidney Disease. The work was published in the peer-reviewed scientific journal Federation of American Societies for Experimental Biology (FASEB).
This animal study investigated factors potentially involved in the ageing process and aimed to identify possible therapeutic targets for slowing down this process. Of particular interest was the breakdown of phosphate in the body. Phosphate is widely distributed throughout the body and is involved in many cellular processes. The researchers say that problems with phosphate breakdown have been noted in several heart, kidney and skeletal diseases. However, whether or not phosphate has a role in the ageing process has never been firmly established.
The researchers used genetically engineered “klotho-knockout” mice. These mice have a short lifespan and show many biochemical and physical signs that are consistent with premature ageing. These include curvature of the spine and brittle bones, uncoordinated movement, muscle wasting, lung complaints and generalised weakness of several body tissues and organs.
Phosphate absorption in the body is mainly controlled through sodium-phosphate transporter (NaPi2a) channels. These are found in the large intestine, where they absorb phosphate from the gut, and in the kidney, where they reabsorb phosphate and prevent it from being lost in urine. In klotho-knockout mice, the activity of the sodium-phosphate transporter (NaPi2a) channels in the kidney is increased, resulting in their bodies having a lifelong high level of phosphate.
The researchers adapted these mice further, creating a mouse that lacked this transporter (klotho-knockout/NaPi2a-knockout mice). In theory, this mouse would retain its properties of premature ageing, but would also have reduced phosphate levels in the body.
The researchers fed one group of klotho-knockout mice and klotho-knockout/NaPi2a-knockout mice a normal diet. Another group of the two types of genetically engineered mice was fed a high-phosphate diet.
The researchers found that, on the normal diet, the klotho-knockout/NaPi2a-knockout mice showed less evidence of premature ageing than the klotho-knockout mice. The mice regained reproductive ability and had improved body weight, reduced wasting and weakness of body organs, and overall prolonged survival. Conversely, in klotho-knockout/NaPi2a-knockout mice that were fed a high-phosphate diet, the signs of premature ageing reappeared.
The researchers concluded that high phosphate levels are the main cause of ageing in mice that are genetically engineered to age prematurely.
This animal study investigated the possible role that levels of phosphate in the body play in the ageing process. Problems with phosphate breakdown have previously been noted in several heart, kidney and skeletal diseases.
The study looked at a group of mice genetically engineered to age prematurely, and assessed the effect of removing a phosphate transporter in the kidney (by further genetic alteration). As expected, these mice had reduced phosphate levels in the body and were free of the signs of premature ageing that the other mice had (for example, they retained fertility and had less skeletal and muscle wasting). Giving these mice a high-phosphate diet raised their phosphate levels, resulting in changes associated with ageing.
While animal studies can provide information on how biological processes work, these findings in mice, which were genetically engineered to prematurely age, may or may not be relevant to the human body. It is a big leap from these findings to the suggestion that fizzy drinks containing phosphates can cause premature ageing.
The effect of excess phosphate on health is important enough to justify further research. However, it is unclear whether the levels of phosphate in fizzy drinks are enough to affect health. At present, the high sugar and calorie content of these drinks would seem to be a more compelling reason for limiting their intake.