Phosphates are compounds containing phosphorus and other minerals. Naturally occurring phosphate (organic phosphate) is organically bound and only 40-60% is absorbed in the gastrointestinal (GI) tract. The phosphates used as food additives (inorganic phosphates) are not organically bound and are efficiently absorbed by the GI tract. They are often used in processed meats, canned fish, soft drinks and baked goods.

In 1991 COMA set the UK a Reference Nutrient Intake (RNI) of 550 mg/day of phosphorus for males and females aged 19-50 years. An increment of 440 mg/day was derived for women during lactation, giving a total of 990 mg/day. The UK RNI for infants and children ranges from 400 to 775 mg/day (COMA 1991). In 1992 the European Commission’s Scientific Committee on Food also set the population reference intake for phosphorus at 550mg (SCF, 1993).

Phosphates and kidney disease

Chronic kidney disease (CKD) inhibits the ability to excrete phosphorous and high serum phosphorous levels (hyperphosphataemia) are associated with increased morbidity and mortality in those with CKD. The National Institute of Clinical Excellence recommends that CKD patients with hyperphosphataemia are provided with individual advice on dietary phosphate management by a specialist dietitian (NICE 2013).


Phosphates and cardiovascular disease (CVD)


In 2012, a scientific article was published suggesting an association between inorganic phosphates and increased risk of cardiovascular disease in the general population (Ritz et al 2012).  This review cited three main studies suggesting a link between high  serum phosphorus levels and coronary calcification in young men (Foley et al 2009), increased mortality in those with cardiovascular disease (Tonelli et al. 2005) and CVD (Dhingra et al. 2007).

To support the hypothesis that normal serum phosphorus serum levels are associated with coronary calcification, the review referred to is a US prospective study (n=3015) which reported a relationship between high phosphorus serum levels and increased calcification in young men (Foley et al 2009). However, PTH and vitamin D were not recorded and only 9.5% of the sample had coronary calcification at the follow up, reducing the strength of the findings.

The review also reported findings from a post-hoc study using participants from the Cholesterol and Recurrent Events randomised control trial (Tonelli et al. 2005).  All the participants (n=4159) had previously suffered from a myocardial infarction so although this may suggest a relationship between high serum phosphorus levels and increased mortality, this is not representative of the general population. Additionally, the number of subjects defined within the ‘high’ phosphorus group was small (8% of participants).

Finally, the review refers to a community based cohort from The Framingham Offspring Study (n=3368), aiming to investigate whether high serum phosphorus levels were associated with CVD in healthy individuals. This study found serum phosphorus to be positively associated with CVD risk in a continuous fashion. It should be noted that this study did not measure parathyroid hormone, Vitamin D, exercise or other dietary factors associated with CVD. There were also methodological limitations of the review itself. Although the search terms were provided, it did not define the inclusion/exclusion criteria for studies and the studies included were non-interventional in design. Following the publication of this review, EFSA produced a statement on the health risks associated with phosphate additives in food. This highlighted the fact that the review by Ritz et al. had omitted several studies, many of which reported contradictory findings to those included in this review (EFSA 2012).

EFSA’s assessment concluded that the lack of intervention studies in this area prevents any cause inference from being made between high serum phosphate and CVD risk. Also, it is not clear whether the increased cardiovascular risk observed in the observational studies is attributable to differences in dietary phosphorus intake or intake of phosphate additives.

Phosphates for use as food additives will be re-evaluated by EFSA with high priority by 31 December 2018. In conclusion, there is some evidence to suggest a relationship between high serum phosphorus levels and increased risk of cardiovascular disease but a cause and effect relationship has not been demonstrated.  Although a number of mechanisms have been proposed for the increase in CVD risk, such as premature ageing, endothelial dysfunction, vascular calcification and cardiac hypertrophy, in the absence of intervention-based research, as the possibility of confounding from dietary, lifestyle or genetic factors cannot be excluded.

The EFSA opinion of the review by Ritz is available here:


COMA (Committee on Medical Aspects of Food and Nutrition Policy) 1991 Dietary Reference Values for Food Energy and Nutrients for the United Kingdom. London:HMSO

Dhingra, Sullivan, Fox et al (2007) Relations of serum phosphorus and calcium levels to the incidence of cardiovascular disease in the community. Archives of Internal Medicine 167: 879–85.

EFSA (European Food Safety Authority) (2012) Assessment of one published review on health risks associated with phosphate additives in food. EFSA Journal 11: 3444

Foley, Collins, Herzog et al. (2009) Serum phosphorus levels associate with coronary atherosclerosis in young adults.  Journal of the American Society of Nephrology 20: 397–404.

NICE (2013) Hyperphosphataemia in chronic kidney disease Available at: Accessed 12/2/14

Ritz, Hahn, Ketteler et al. (2012). Phosphate Additives in Food-a Health Risk. Deutsches Arzteblatt International, 109: 4955.

Tonelli M, Sacks, Pfeffer et al. (2005) Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation 112: 2627–33.  SCF (Scientific Committee for Food) (1993). Nutrient and energy intakes for the European Community. (Opinion expressed on 11 December 1992). Available online: Accessed 12/2/14