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Phosphorus is an essential dietary element and may be either organic or inorganic. They are required for bone and teeth formation, involved in the utilisation of carbohydrate and fats, and are critical for the maintenance, repair and growth of all cells and tissues. Naturally occurring organic phosphorous compounds are not completely absorbed by the body and do not pose any known risks for health. In fact reducing intake of these natural phosphates may even result in protein malnutrition. However inorganic food-grade phosphates, usually in the form of either sodium or potassium salts, are readily absorbed and may present a risk to health. Inorganic phosphates are used as additives in many meat and poultry products such as sausages, hams and salami, but are not used in fresh meat. They serve many purposes including pH stabilisation, increasing water retention capacity, shelf life extension and the improvement of texture, colour, juiciness and flavour. There is also a suggestion that these added phosphates are beneficial in that they provide an additional supply of essential phosphorous to the diet.  However another, more worrying view is that the impact of phosphate additives on general public health has been underestimated, as high phosphorus intake may be associated with a increased risk of mortality.  Indeed several studies verify the harmful effects of these food additives, which include an increased risk of cardiovascular disease and the progression of vascular calcification and plaque development within the arteries.      Elevated phosphorous levels have also been shown to promote bone loss and disordered mineral metabolism.  In patients with chronic kidney disease (CKD) or on dialysis, an excess of phosphorous can be dangerous   and contribute to renal impairment.   In fact one study showed that 12% of deaths in patients with advanced CKD (who have an annual mortality rate of 20%) were attributable to elevated serum phosphate. Lower socioeconomic groups may be more susceptible to these damaging effects, as they consume more “fast” and processed foods, known to have high phosphate content. Between 1987 and 2007 average phosphorus consumption in the USA increased by 10–15%, and as a result of recent concerns regarding health impact on the population, research is being carried out to find natural organic alternatives. The role of phosphate additives in meat products is largely commercial, enhancing visual ‘quality’, extending shelf life and enabling more water to be injected into the product. However these commercial benefits come with significant health risks. To avoid excessive phosphate intake, it is advisable to eat fresh meat instead of processed and avoid products containing phosphate additives whenever possible.  Long, N. et al. (2011) Use of phosphates in meat products. African Journal of Biotechnology, 10(86), 19874-19882.  Ritz, E. et al. (2012) Phosphate additives in food - a health risk. Deutsches Arzteblatt International, 109(4), 49-55.  Carrigan, A. et al. (2014) Contribution of Food Additives to Sodium and Phosphorus Content of Diets Rich in Processed Foods. Journal of Renal Nutrition, 24(1), 13-19.  Chang, A. et al. (2014) High dietary phosphorus intake is associated with all-cause mortality: results from NHANES III. The American Journal of Clinical Nutrition, 99(2), 320-327.  Sullivan, C. (2007) Phosphorous Containing Food Additives and the Accuracy of Nutrient Databases: Implications for Renal Patients. Journal of Renal Nutrition, 17(5), 350-354.  Kuro-o, M. (2011) A phosphate-centric paradigm for pathophysiology and therapy of chronic kidney disease. Kidney International Supplements, 3(5), 420-426.  Calvo, M. et al. (2014) Assessing the Health Impact of Phosphorus in the Food Supply: Issues and Considerations. Advances in Nutrition, 5(1), 104-113.  Calvo, M. (2013) Public health impact of dietary phosphorus excess on bone and cardiovascular health in the general population. The American Journal of Clinical Nutrition, 98(1), 6-15.  Giachelli, C. (2009) The Emerging Role of Phosphate in Vascular Calcification. Kidney International, 75(9), 890-897.  Takeda, E. et al. (2014) Increasing Dietary Phosphorus Intake from Food Additives: Potential for Negative Impact on Bone Health. Advances in Nutrition, 5(1), 92-97.  Noya, C. (2008). Evaluation of a High PH Solution as an Alternative for Phosphate Meat. (1st ed.). USA: ProQuest.
It was previously approved for use in 1974, but its approval was put on hold due to objections filed by neuroscientist Aspartame is a compound consisting of 3 chemicals: methanol, and the amino acids aspartic acid and phenylalanine. It is a non-nutritional food additive (European Food Safety Authority [EFSA] additive code E951), which means that it has no nutritional value and is regulated by EFSA. Aspartame was approved by the Federal Drug Agency (FDA) for use in dry goods in 1981 and in carbonated beverages in 1983.Dr John W. Olney (who found aspartame caused holes in the brains of mice) and consumer attorney James Turner (who believed aspartame could cause brain damage), and investigations into the research practices of G.D. Searle, who did not inform the FDA of one study in which an infant monkey died after 300 days’ consumption of milk sweetened with aspartame.  Following aspartame’s approval in the US, it quickly also gained approval in the UK in 1982, after a review of its safety by the UK's Committee on Toxicity, Consumer Products and the Environment. This then led to European-wide approval of aspartame with the universal adoption of the EU Sweetener Regulations (94/35/EC) in 1994. Today aspartame is widely used as a non-nutritive sweetener, as a replacement for sugar. As excessive sugar is linked to numerous health conditions including diabetes, obesity and metabolic syndrome, substituting with an artificial sweetener would seem to be beneficial for health. However this may not necessarily be the case. Aspartic acid (also known as aspartate), one of the components of aspartame, acts as neurotransmitter in the brain, facilitating the transmission of information from neuron to neuron. The excess of aspartate in the blood shortly after ingesting aspartame could therefore lead to a high level of these neurotransmitters in certain areas of the brain. This surplus of neurotransmitters in the brain can kill neurons by allowing an influx of too much calcium into the cells. This influx triggers the production of excessive amounts of free radicals, which destroy the cells. These chemicals are known as “excitotoxins” because they “excite” or stimulate the cell to death. Disorders, such as attention deficit hyperactivity disorder (ADHD). The behaviourFurthermore, exposure to non-nutritional food additives during the critical developmental window during childhood has been implicated in the induction and severity of blood brain barrier (BBB), which protects the brain from excess glutamate (a breakdown product of aspartate), aspartate and other toxins, is not completely developed until after birth. The brains of unborn and young children are therefore not fully protected from toxin exposure, such as that caused by excessive aspartame ingestion. In adults the efficacy of the BBB can also be reduced as a consequence of chronic and acute conditions. However, even when intact, the BBB permits seepage of excess aspartate and glutamate into the brain, which slowly destroys neurons through excitotoxicity as described above.  Whilst the quantities of non-nutritional food additives in single servings may be considered “safe”, the cumulative effect of several ingested together is, at the very least, questionable. Aspartame is known to have the potential to cause adverse effects, which can be serious, including seizures. The severity of these reactions can be the result of unnoticed cell death within the brain, which is highly plastic in its ability to cope with widespread cell death. In the light of what evidence is available, it is therefore perhaps advisable to limit aspartame intake.  Nill, A (2000) The History of Aspartame. Retrieved October 2016 from, https://dash.harvard.edu/bitstream/handle/1/8846759/Nill,_Ashley_-_The_History_of_Aspartame.pdf?sequence=3  FDA (2003) Docket #02P-0317 Recall aspartame as a neurotoxic drug: file #7: aspartame history. Retrieved April 2016 from, http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012203/02P-0317_emc-000202.txt  FSA (2016) Aspartame. Retrieved April 2016 from, https://www.food.gov.uk/science/additives/aspartame  Ashurst, PR. (2008) Chemistry and Technology of Soft Drinks and Fruit Juices. Retrieved April 2016 from, https://goo.gl/NVEN1M  Kudo, Y, Ogura, A. (1986) Glutamate-induced increase in intracellular Ca2+ concentration in isolated hippocampal neurones. Br J Pharmacol. 89(1). 191-8.  Arundine, M, Tymianski, M. (2003) Molecular mechanisms of calcium-dependent neurodegeneration in excitotoxicity. Cell Calcium. 34(4-5). 325-37.  Olney, JW. (1994) Excitotoxins in foods. Neurotoxicology. 15(3). 535-44.  Marc, T. (2013) Brain development and the immune system: an introduction to inflammatory and infectious diseases of the child’s brain. Handb Clin Neurol. 112. 1087-9.  Yang, Y, Rosenberg, GA. (2011) Blood-brain barrier breakdown in acute and chronic cerebrovascular disease. Stroke. 42(11). 3323-8.  Choi, DW, Koh, JY, Peters, S. (1988) Pharmacology of glutamate neurotoxicity in cortical cell culture attenuation by NMDA antagonists. J Neurosci. 8(1). 185-96.  Lau, K, McLean, WG, Williams, DP, Howard, CV. (2006) Synergistic interactions between commonly used food additives in a developmental neurotoxicity test. Toxicol Sci. 90(1). 178-87.  Humphries, P, Pretorius, E, Naude, H. (2008) Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. 62(4). 451-62.  Wieloch, T, Nikolich, K. (2006) Mechanisms of neural plasticity following brain injury. Curr Opin Neurobiol. 16(3). 258-64.