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  2. Common acidic foods include vinegar, lemon juice, tomatoes, fruit juices, milk, cola and other fizzy drinks. Food that is acidic can react with materials such as plastic containers and packaging, which may contain toxic components such as bisphenol A (BPA), bisphenol S (BPS), bisphenol F (BPF), lead and antimony, to list just a few amongst potentially thousands. When acidic food is stored in plastic containers, or comes in contact with epoxy resins found in food packaging, leaching of these toxic compounds can occur. One study has shown that, when in contact with acidic foods, there is increased leaching of toxins from plastic or plastic-lined baby bottles. Another study found that darker coloured bottles leach more toxins than light or clear ones when in contact with acidic foods, and that leaching actually increases over the lifespan of a product.[1], [2] While it may seem simple to avoid ‘acidic’ foods and drinks, it may be surprising that milk, a common beverage served in plastic baby bottles, is in fact an acidic liquid.[3]  Some studies have shown that the levels of toxic substances leaching from plastic containers when in contact with acidic food are not above the levels deemed ‘safe’ by the European Commission in Regulation 10/2011, thus suggesting that this leaching should not be a concern for health.[4] However other studies suggest that even doses below the accepted ‘safe’ limit of BPA, for example, can be harmful.[5] BPA is a recognised endocrine disruptor, meaning it interferes with hormonal systems in mammals.[6] It has also been demonstrated that exposure during gestation and in the first few weeks following birth may be associated with male and female infertility, an increased predisposition to breast and prostate cancer and behavioural abnormalities.[7] Concerns over the impact of the endocrine disruptor BPA on health have resulted in its removal from many consumer products, especially baby bottles, which are therefore named “BPA Free”. In many cases, however, the BPA in these products has been replaced with alternative toxic substances, such as bisphenol S (BPS) or bisphenol F (BPF), which have been shown to have similar, or potentially worse endocrine disrupting properties to BPA, with the unfortunate added potential for other adverse effects.[8], [9] Given that milk is an acidic liquid, which have been shown to increase the leaching of these substances, BPA-free bottles may not be the ‘safe’ alternative they are claimed to be. Whilst it could be argued that the levels of leached toxins safely reside within the recommended limits, these limits often do not take into account multiple exposure routes or the volume or frequency of exposure. These regulations do not account for what may seem obvious: the vast difference in exposure to these toxins between consumers, for example those who drink no cola as opposed to those who drink five bottles. Given the increased rate of toxic chemical leaching when plastic is in contact with acidic food, a much safer option is to use glass containers for these products, but caution should still be taken, as glass containers often have plastic lid seals. [1]  Sanchez-Martinez, M. et al. (2013) Migration of antimony from PET containers into regulated EU food simulants. Food Chem. 141(2). 816-22 [2] Kubwabo, C. et al. (2009). Migration of bisphenol A from plastic baby bottles, baby bottle liners and reusable polycarbonate drinking bottles. Food Additives & Contaminants. 26(6). 928-937 [3] FDA (2007) Approximate pH of foods and food products. Retrieved October 2016 from, http://www.foodscience.caes.uga.edu/extension/documents/FDAapproximatepHoffoodslacf-phs.pdf  [4] Reimann, C. et al. (2007). Bottled drinking water: Water contamination from bottle materials (glass, hard PET, soft PET), the influence of colour and acidification. Applied Geochemistry. 25(7). 1030-1046 [5] Richter, C.A. et al. (2007). In vivo effects of bisphenol A in laboratory rodent studies. Reproductive Toxicology. 24(2). 199-224   [6] James, A.  et al. (2013). Review: Endocrine disrupting chemicals and immune responses: A focus on bisphenol-A and its potential mechanisms. Molecular Immunology. 53(4). 421-430 [7] Maffini, M.B. et al. (2006). Endocrine disruptors and reproductive health: the case of bisphenol-A. Molecular and Cellular Endocrinology. (25). 179-186 [8] Rochester, J.R. et al. (2015). Bisphenol S and F: A Systematic Review and Comparison of the Hormonal Activity of Bisphenol A Substitutes. Environmental Health Perspectives. 123(7). 643-650 [9] Eladak, S. et al. (2015). A new chapter in the bisphenol A story: bisphenol S and bisphenol F are not safe alternatives to this compound. Fertility and Sterility. 103(1). 11-21
  3. According to the World Health Organisation (WHO), dietary factors are thought to account for as much as 35% of all cancers.[1] The most noticeable correlation between diet and cancer is the fact that people who do not eat meat are much less likely to develop the disease.[2]  As shown by large studies, vegetarians are approximately 40% less likely to develop cancer than subjects who eat meat.[3] Another study investigated the link between meat consumption and cancer by observing cancer incidence in Seventh–Day Adventists, a religious group whose members avoid alcohol and tobacco. Approximately half of the population are vegetarian and half still eat meat, allowing for observations regarding the effects of meat-eating, separate from other lifestyle factors. Results indeed demonstrated that there was a significantly lower colorectal cancer risk in the vegetarian subpopulation than in the meat-eaters.[4]  A number of hypotheses have been suggested to explain the connection between meat consumption and cancer risk. Meat is devoid of fibre, and other nutrients, that have a protective effect against cancer. It is also high in animal protein and saturated fat, which form carcinogenic compounds such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) during processing and/or cooking.[5], [6] The major classes of HCAs include amino-imidazo-quinolines and amino-imidazo-quinoxalines (collectively called IQ-type compounds) and amino-imidazo-pyridines such as 2-amino-1-methyl-6- phenylimidazo(4, 5-b)pyridine (PhIP). IQ-type compounds and PhIP are formed from creatine or creatinine (found in all meats), specific amino acids and sugars.[7] These HCAs are formed as meat (including chicken and fish) is cooked, even under normal grilling, frying or roasting conditions, and their formation increases with higher temperatures, and longer cooking times.[8], [9], [10], [11] One study that included 952 subjects with rectal cancer and 1,205 control subjects found that men and women with the highest consumption of processed or well-cooked meat had an increased risk of rectal cancer.[12] Other research has shown that the high fat content of meat (and other animal products) can increase hormone production within the body, thus increasing the risk of hormone-related cancers, such as breast and prostate cancer.[13] One study found that consumption of a Western diet (especially large amounts of chicken, eggs and meat) increased the serum concentrations of estradiol, a hormone implicated in breast cancer.[14] The American Institute for Cancer Research (AICR) published a review in 2007 of the major studies on food, nutrition and cancer prevention.[15] For cancers of the oesophagus, lung, pancreas, stomach, endometrium, and prostate, it was determined that red meat (beef, pork, or lamb) and processed meat consumption possibly increased cancer risk. For colorectal cancer, a review of the literature determined that there is convincing scientific evidence that red meat, processed meat, saturated/animal fat, and heavily cooked meat all increase cancer risk.[15]  The evidence is therefore clear that eating meat, particularly if processed or well cooked, increases the risk of developing cancer. The best option for cancer prevention through diet, therefore, is perhaps to become vegetarian, but this is not acceptable to many people. In which case a decrease in meat consumption (especially processed meats), and a reduction in meat cooking times are more viable options for reducing the risk of cancer development.   [1] Anand, P. et al. (2008) Cancer is a Preventable Disease that requires major lifestyle changes. Pharm Res. 25(9). 2097-116. [2] Lanou, AJ. & Svenson, B. (2010) Reduced cancer risk in vegetarians: an analysis of recent reports. Cancer Manag Res. 3. 1-8. [3] Sinha, R. et al. (2009)  Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 169(6). 562-71. [4] Orlich, MJ. et al. (2015) Vegetarian dietary patterns and the risk of colorectal cancers. JAMA Intern Med.  175(5). 767-76. [5] European Commission. (2011) Polycyclic aromatic hydrocarbons - Factsheet. Retrieved November 2016 from, https://ec.europa.eu/jrc/sites/jrcsh/files/Factsheet%20PAH_0.pdf  [6] Knize, MG. et al. (2002) Factors affecting human heterocyclic amine intake and the metabolism of PhIP. Mutat Res. 506-607. 153-62. [7] Schuirmann, E. & Eichner, K. (1991) [Formation of IQ-compounds in meat and meat products]. Z Ernahrungswiss. 30(1). 56-64. [8] Skog, KI. et al. (1998) Carcinogenic heterocyclic amines in model systems and cooked foods: a review on formation, occurrence and intake.Food Chem Toxicol. 36(9-10). 879-96. [9] Thiebaud, HP. et al. (1995) Airborne mutagens produced by frying beef, pork and soy-based food. Food Chem Toxicol. 33(10). 821-8. [10] Sinha, R. et al. (1995) High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo- [4,5-b]pyridine (PhIP) occur in chicken but are dependent on the cooking method. Cancer Res. 55(20). 4516-9. [11] Murkovic, M. (2004) Formation of heterocyclic aromatic amines in model systems.J Chromatogr B Analyt Technol Biomed Life Sci. 802(1). 3-10. [12] Murtaugh, MA. et al. (2004) Meat consumption patterns and preparation, genetic variants of metabolic enzymes, and their association with rectal cancer in men and Women. J Nutr. 134(4). 776-784. [13] Henderson, BE. & Feigelson, HS. (2000) Hormonal carcinogenesis. Carcinogenesis. 21(3). 427-433. [14] Sanchez-Zamorano, LM. et al. (2016) The Western dietary pattern is associated with increased serum concentrations of free estradiol in postmenopausal women: implications for breast cancer prevention. Nutr Res. 36(8). 845-54. [15] AICR.(2007) Food, nutrition, physical activity and the prevention of cancer: a global perspective. Retrieved April 2016 from, http://www.aicr.org/assets/docs/pdf/reports/Second_Expert_Report.pdf 
  4. What makes a healthy diet?

    The foundation of a healthy diet is balance, variety and moderation. The maintenance of a healthy body requires the intake of carbohydrate (sugar, starch or fibre), fat, protein, vitamins and minerals. The World Health Organisation states that a healthy adult diet should therefore ideally contain a balance of fruit, vegetables, legumes (e.g. lentils and beans), nuts and whole grains (e.g. unprocessed cereals or brown rice), with a minimum of five portions (400g) of fruit and vegetables to be consumed daily.[1] To achieve the optimum level of nutrition, a healthy diet should consist of:  Approximately one third starchy foods such as bread, rice or pasta (preferably whole grain varieties, as the increased fibre content is beneficial to the intestine)[2], [3]  Some protein rich foods such as meat, fish or lentils Some milk or other dairy products Limited amounts of fat, salt and sugar Fats should make up less than a third of daily caloric intake, and the unsaturated fats found in fish, avocado, nuts, sunflower and olive oils are preferable to the saturated fats found in fatty meats, coconut oil, cream, cheese and lard. This is because unsaturated fats can provide beneficial fatty acids such as omegas 3 and 6, that are known to help decrease cholesterol levels.[4] Indeed studies have shown that a diet containing a maximum of 10% of daily caloric intake from saturated fat significantly decreases the risk of heart disease.[5], [6]  Studies have also shown that coronary heart disease (CHD) risk is reduced by 10-15% for each 5% of energy intake that is exchanged from saturated to polyunsaturated (but not monounsaturated) fats. Exchanging saturated fat with carbohydrates increases CHD risk, by 7% for each 5% exchanged.[7] Trans fats commonly found in processed or ‘fast’ foods such as pizza, pies and margarines should also be avoided, as they can also increase the risk of raised cholesterol, type 2 diabetes and stroke.[8]  Meat is a good source of protein which also contains vitamins and minerals including iron, zinc and B group vitamins, making it one of the main dietary sources of vitamin B12.[9] Opting for lean meat and skinless poultry can help to reduce the fat intake associated with eating meat. However, certain meat-cooking processes, such as BBQing, have recently been shown to be carcinogenic,[10] and some meat products can contain endocrine-disrupting chemicals,[11] so care should be taken when choosing and preparing meat for consumption. Fish is an alternative significant source of protein which also contains numerous vitamins and minerals. Oily fish is also rich in omega-3 fatty acids which, as stated above, are considered beneficial for health via the prevention of heart disease and reduction of cholesterol levels.[4] However, as with meat, many of the high-temperature cooking processes used on fish can lead to the formation of carcinogenic compounds, such as polyaromatic hydrocarbons. Dairy products such as milk, cheese and yoghurt are also good sources of protein and are rich in calcium, essential for healthy bones. There has previously been controversy over the effect of dairy products in the diet, as some can be quite high in fat. However, observational studies have shown that dairy fat does not necessarily contributes to obesity.[12]  Fruit and vegetables are an essential source of dietary vitamins and minerals, and there is increasing evidence that eating at least five portions a day reduces the risks of heart disease, stroke and some cancers. Studies have demonstrated the efficacy of a Mediterranean style diet, which includes lots of fruits and vegetables, in reducing both cancers and cardiovascular disease [13], [14],[15], [16], [17] However it is important to note that not all fruits and vegetables are equal. For example, a fresh piece of fruit is inherently more healthy than its fried equivalent, a glass of sugar-loaded, low fibre fruit juice or a processed alternative. Care should be taken to always wash and peel fruits and vegetables though, as they are commonly contaminated with pesticide residues, even when organic options are chosen, due to the widespread contamination of our environment.[18], [19]  Sugar should ideally contribute less than 10% of daily caloric intake, or ideally less than 5% for additional health benefits.[20] This is about 50g, or 12 teaspoons, for a person consuming the recommended 2000 calories a day. Sugar is routinely added to numerous foods and drinks by manufacturers, cooks and consumers, but it also occurs naturally in honey, syrups and fruit juices and so monitoring intake can prove difficult.[21], [22], [23] Salt intake should also be limited to 5g (one teaspoon) per day, although iodised salt can be beneficial, as it provides the essential mineral iodine. Reduction in overall salt intake helps prevent high blood pressure and reduces the risk of heart disease. In fact it has been shown that reducing sodium intake to <2 g/day can lower systolic blood pressure by 3.47 mmHg, and diastolic blood pressure by 1.81 mmHg.[24], [25] Consuming more calories than are required by the body will ultimately result in weight gain. When monitoring dietary calorie intake, drinks are often forgotten, yet sugary drinks, beer and alcohol all have a high calorific value.[26] Fats and sugars are good sources of energy, but excessive consumption can also result in obesity and the increased risk of type 2 diabetes, some cancers, heart disease and stroke.[27], [28], [29], [30] Dairy products can also have a high caloric value and should be consumed as part of a balanced diet, choosing low fat options when possible. However it is important to remember that children under two years should not be given skimmed milk, as it lacks essential fatty acids and fat soluble vitamins, which are important for development.  Many eating habits are learned in childhood, so it is important that parents and educators explain the importance of a balanced diet and healthy eating choices early in life. By eating a healthy diet ourselves, and by instilling good eating habits in children we may be able to tackle some of the problems facing the modern world today, such as the increased prevalences of obesity and cancer. [1] Lichtenstein, A et al. (2006). Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee.American Heart Association Nutrition Committee, 114(1), 82-96.  [2] Schatzkin, A et al. (2008). Prospective Study of Dietary Fiber, Whole Grain Foods,   and Small Intestinal Cancer. Gastroenterology, 135(4), 1163-1167.  [3] Jenkins , D et al. (1987). Starchy foods and fiber: reduced rate of digestion and improved carbohydrate metabolism , Journal of Gastroenterology.Scandinavian Journal of Gastroenterology, 22(129), 132-141.  [4] Covington, M. (2004). Omega 3 Fatty Acids. American Family Physician, 70(1), 133-140.  [5] Perk, J. et al. (2012). European Guidelines on cardiovascular disease prevention in clinical practice . European Heart Journal, 33(13), 1635-1701. [6] Piepole, M. et al. (2016). 2016 European Guidelines on cardiovascular disease prevention in clinical practice. European Heart Journal, 37(1), 2315 - 2381. [7] Go, AS. et al. (2016). Heart disease and stroke statistics - a 2014 update: a report from the American Heart Association. Circulation, 139(3), e28-292 [8] Mozaffarian, D. (2009). Health effects of trans-fatty acids: experimental and observational evidence. European Journal of Clinical Nutrition, 63(2). [9] Williams, P. (2007). Nutritional composition of red meat. Journal of the Dieticians Association of Australia, 64(S4), 113-119. [10] European Commission. (2002) Polycyclic aromatic hydrocarbons - occurrence in foods, dietary exposure and health effects. Retrieved April 2016 from, http://ec.europa.eu/food/fs/sc/scf/out154_en.pdf  [11] Sanchez-Zamorano LM, et al. (2016) The Western dietary pattern is associated with increased serum concentrations of free estradiol in postmenopausal women: implications for breast cancer prevention. Nutr Res, 36(8), 845-54. [12] Kraytz, M. et al. (2013). The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease Kratz M1, Baars T, Guyenet S.European Journal of Nutrition, 52(1), 1-24. [13] Liu, S. et al. (2000). Fruit and vegetable intake and risk of cardiovascular disease: the Women's Health Study. The American Journal of Clinical Nutrition, 72(4), 922-928.   [14] Report of the joint who/fao expert consultation. (2002). Diet, nutrition and the prevention of chronic diseases. WHO Technical Report Series, 916,  [15] Aune, D. et al. (2012). Fruits, vegetables and breast cancer risk: a systematic review and meta-analysis of prospective studies. Breast Cancer Research and Treatment, 134(2), 479-493.  [16] Williams, M. et al. (2005). The role of dietary factors in cancer prevention: beyond fruits and vegetables. Nutrition in Clinical Practice, 20(4), 451-459.   [17] Slavin, J.L. & Lloyd, B. (2012). Health benefits of fruits and vegetables. Advances in Nutrition, 3(4), 506-516.  [18] European Commission (2008) Annex II: pesticides - plant protection products referred to in Article 5(1). Retrieved October 2016 from, http://ec.europa.eu/agriculture/organic/eu-policy/expert-advice/documents/final-reports/final_report_egtop_on_plant_protection_products_en.pdf  [19] The Expert Committee on Pesticide Residues in Food. (2015) Report on the Pesticide Residues Monitoring Programme for Quarter 1 2015. Retrieved October 2016 from, http://webarchive.nationalarchives.gov.uk/20151023155227/http://www.pesticides.gov.uk/Resources/CRD/PRiF/Documents/Results%20and%20Reports/2015/Q1%202015%20FINAL.pdf [20] World health organisation. (2003). Global Strategy on Diet, Physical Activity and Health. WHO Technical Report Series, 916.  [21] World health organisation. (2015). Sugars intake for adults and children. Guideline.  Retrieved October 2016 from, http://apps.who.int/iris/bitstream/10665/149782/1/9789241549028_eng.pdf [22] Malik, V.S et al. (2010). Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. US National Library of Medicine, 121(11),1356-1364.   [23] Meneton, P et al. (2005). Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases. Physiological Reviews, 85(2), 679-715.  [24] World health organisation. (2012). Sodium intake for adults and children. Guideline. Retrieved October 2016 from, http://apps.who.int/iris/bitstream/10665/77985/1/9789241504836_eng.pdf  [25] Steinberger, J & Daniels, S.R. (2003). Obesity, Insulin Resistance, Diabetes, and Cardiovascular Risk in Children. American Heart Association , 107(1), 1448-1453. [26] Vartanian, LR. et al. (2007) Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health. 97(4). 667-75. [27] Azeem, S. et al. (2015). Diet and Colorectal Cancer Risk in Asia - a Systematic Review. Asian Pacific Journal of Cancer Prevention, 16(13), 5389-5396. [28] Ley, S. et al. (2014). Prevention and management of type 2 diabetes: dietary components and nutritional strategies. Lancet, 383(9933), 1999-2007. [29] De souza, R. et al. (2015). Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ, 351(H3978), . [30] Richelsen, B. (2013). Sugar-sweetened beverages and cardio-metabolic disease risks. Current Opinion in Clinical Nutrition and Metabolic Care, 16(4), 478-484
  5. Good fats vs bad fats

    Fats in our diet are a valuable source of energy (1 g is equivalent to 9 kcal), and they are essential in a healthy balanced diet. While some fats are beneficial, others, if consumed in excessive amounts, have detrimental effects on health. Fats are classified by their chemical structure, falling into several groups including saturated fats, mono-/polyunsaturated fats and trans fats. The fatty acid chains in saturated fats consist of only single bonds, indicating that there are no bonds available for further binding.[1] Foods that contain high levels of saturated fat include whole milk, butter, cheese, lard, palm oil, coconut oil, “fatty” meat and meat products, fried food, and some cakes, biscuits and pastries. All of the above should be eaten in small amounts as saturated fats have a proven association with increased cholesterol levels, which can progress to clogged arteries and increased risk of heart disease and stroke.[2] There have been numerous studies confirming the benefits of reducing saturated fats in our diets. For example, replacing saturated fats with unsaturated fats reduces cholesterol levels, thus decreasing the risks of heart disease and stroke.[2], [3] Both epidemiological and randomised clinical trials have consistently evidenced that replacing saturated fat with unsaturated fat, is beneficial in coronary heart disease.[4]    The fatty acid chains in unsaturated fats contain either one double bond (monounsaturated fat) or more than one double bond (polyunsaturated fat).[1] Foods rich in these types of fats include vegetable oils such as olive, rapeseed or sunflower oils, avocados, nuts and seeds. It has been demonstrated these fats help decrease the risk of heart disease.[5], [6] Omega-3 fatty acids are a group of polyunsaturated fats found mainly in oily fish such as mackerel, salmon or sardines. Omega-3 fatty acids have many health benefits, and are associated with good heart health as they reduce the risk of blood clots and assist in the regulation of heart rhythm.[7], [8] They are also important during pregnancy and breastfeeding, supporting infant development.[7], [8] Trans-fats are the most harmful to our bodies. This group of fats are manufactured by partially hydrogenating vegetable oils, resulting in a firmer, better tasting fat with an increased shelf life. They are found in most processed and ‘fast’ foods, that are already very high in saturated fats.[9] Manufactured trans-fats have been shown to have an even more adverse impact on cholesterol levels than saturated fats, which in turn is associated with diabetes and cardiovascular disease.[10], [11]   Whilst knowing which fats are more healthy than others can certainly help in reducing the risks associated with fat consumption, some fats can actually become more harmful during cooking, depending on the processes involved. Vegetable oil, for example can accumulate by-products known to pose a significant risk of cardiovascular disease when heated repeatedly.[12] Cooking can also change the ratio of healthier unsaturated fatty acids to unhealthy saturated fats and trans fats.[13] Reducing fat in the diet is advisable to prevent obesity and its related complications, such as type 2 diabetes. Even beneficial mono-/polyunsaturated fats should be consumed in moderation, as they still have a high calorific value. In fact studies on mice have shown that a high fat diet induces greater weight gain than a low fat diet, even if their calorific intake is the same.[14]   A reduction of saturated and trans-fats in the diet can be achieved by avoiding processed and ‘fast’ foods as much as possible and choosing food prepared at home from fresh, low fat ingredients. Lean sources of protein, low fat dairy foods, legumes, fresh fruit and vegetables are a healthier choice than foods high in fat, although beneficial oils such as olive, canola and sunflower oil can be used for cooking and salad dressings. [1] Nelson, D & Cox, M. (2008). Lehninger principles of biochemistry. (5 ed.) [2] Jakopsen, M.U. (2009). Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. The American Journal of Clinical Nutrition. 85(5). 1425-1432 [3] Mozaffarian, D. et al. (2010). Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLos Med. 7(3). e1000252 [4] Siri-tarino, P.W. et al. (2010). Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Current atherosclerosis reports. 12(6). 384-390 [5] Covas, M.I. (2007). Olive oil and the cardiovascular system. Nutritional Pharmacology. 55(3). 175-186 [6] Gillingham, L.G. et al. (2011). Dietary monounsaturated fatty acids are protective against metabolic syndrome and cardiovascular disease risk factors. Lipids. 46(3). 209-228 [7] Swanson, D. et al. (2012). Omega-3 fatty acids EPA and DHA: health benefits throughout life. Advances in Nutrition. 3(1). 1-7 [8] Calder, P.C. et al. (2009). Omega-3 polyunsaturated fatty acids and human health outcomes. BioFactors. 35(3). 266-272 [9] Stender, S. et al. (2006). A trans world journey. Atherosclerosis Supplements, 7(2), 47-52. [10] Micha, R. et al. (2009). Trans fatty acids: effects on metabolic syndrome, heart disease and diabetes. Nature Reviews: Endocrinology. 5(6). 335-344 [11] Bhardwaj, S. et al. (2011). Overview of trans fatty acids: Biochemistry and health effects. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 5(3). 161-164 [12] Ng, CY. et al. (2014) Heated vegetable oils and cardiovascular disease risk factors. Vascul Pharmacol. 61(1). 1-9 [13] Bhardwaj, S. et al. (2016) Effect of heating/reheating of fats/oils, as used by Asian Indians, on trans fatty acid formation. Food Chem. 212. 663-70 [14] Petro, A.E. et al. (2004). Fat, carbohydrate, and calories in the development of diabetes and obesity in the C57BL/6J mouse. Metabolism: clinical and experimental. 53(4). 454-457
  6. Yeast is an anaerobic organism that can be beneficial, but some yeast species can have an adverse impact on our health. Candida albicans is the most common “harmful” yeast, which is normally a commensal organism, i.e. it lives within the body but does not cause any harm. However, when opportunities arise, such as if the immune system is compromised or debilitated in some way, it can become an opportunist pathogen which results in infection.[1] Infection with Candida albicans, also known as candidiasis, can occur in humans in the vagina, mouth, oesophagus, digestive and vascular systems, and the skin.[2] Candidiasis is indeed more common when the immune system is compromised, e.g. in patients with uncontrolled diabetes or AIDS,[3], [4] however people who are not immunodeficient may also be present with candidiasis.[5]  Antibiotics and oral contraceptives are also known to increase the risk of candidiasis, as is a diet high in sugars.[6], [7], [8], [9], [10] As a type of yeast, Candida Albicans is a single cell microorganism which will thrive on the abundance of sugar derived from modern diets. Processed food, consumed in high quantities today, are often high in sugar and other carbohydrates.[11] One study has shown that dietary glucose intake is in fact a fundamental factor in the growth of Candida Albicans in the gastrointestinal tract. The effects of candidiasis are varied and can be more serious than well-known side effects such as itching and foul-smelling discharge. One human study found an association between candidiasis and chronic fatigue syndrome,[12] while another small study of short children found that candidiasis may lead to stunted growth.[13] The study suggested that, according to the mimicry theory, antigens present in the yeast cells that are highly similar to peptide hormones that regulate appetite and growth might trigger the generation of antibodies that would cross react with these hormones, blocking their effect. Essentially, this means that the body attacks and neutralises the hormones needed to stimulate growth, thinking that they are harmful yeast particles. However these assumptions are far from conclusive and further study is required.[14], [15], [16] In order to reduce the risk of harmful opportunistic yeast infections, a lifestyle consisting of a healthy diet and adequate physical activity should be maintained. The diet should minimise intake of processed foods, sugars, and refined carbohydrates such as white rice and white bread and increase the intake of vegetables, which will help reduce blood sugar levels and subsequently the likelihood of yeast infections. Exercise, apart from helping to maintain a healthy weight also reduces blood sugar levels.  [1] Kim, J. (2011) Candida albicans, a major human fungal pathogen. Journal of Microbiology, 49(2), 1064-1067. [2] Calderone, RA. et al. (2001) Virulence factors of Candida albicans. Trends in Microbiology, 9(7), 327-335. [3] Bartholomew, G. et al. (1987) Oral Candidiasis in Patients With Diabetes Mellitus: A Thorough Analysis. Diabetes Care, 10(5), 607 -612. [4] Kaspar, L.et al. (1998) Some Opportunistic Parasitic Infections in AIDS: Candidiasis, Pneumocystosis, Cryptosporidiosis, Toxoplasmosis . Trends in Parasitology, 14(4), 150-156. [5] Salvatori, O. et al. (2016) Innate Immunity and Saliva in Candida albicans-mediated Oral Diseases. Journal of Dental Research, 95(4), 365-371. [6] Sano, T. et al (2012) Antimicrobial Agent, Tetracycline, Enhanced Upper Alimentary Tract Candida albicans Infection and Its Related Mucosal Proliferation in Alloxan-induced Diabetic Rats. Toxicologic Pathology, 40(7), 1014 - 1019. [7] Helstrom, P. et al. (1979) Effect of oral tetracycline, the microbial flora, and the athymic state on gastrointestinal colonization and infection of BALB/c mice with Candida albicans. Infection and Immunity, 23(3), 764 - 774. [8] Yuthika, H. et al. (2001) Experimental Oral Candidiasis in Animal Models. Clinical Microbiology Reviews, 14(2), 398 -429. [9] Spinillo, A. et al. (1995) The impact of oral contraception on vulvovaginal candidiasis. Contraception, 51(5), 293-297. [10] Horowitz, BJ. et al. (1984) Sugar chromatography studies in recurrent Candida vulvovaginitis. The Journal of Reproductive Medicine, 29(7), 441-443. [11] Vargas, SL. et al. (1993) Modulating effect of dietary carbohydrate supplementation on Candida albicans colonization and invasion in a neutropenic mouse model. Infectious Immunology, 61(2), 619-626. [12] Cater, R. (1995) Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome. Medical Hypotheses, 44(6), 507-515. [13] Stawerska, R. et al. (2015) Prevalence of autoantibodies against some selected growth and appetite-regulating neuropeptides in serum of short children exposed to Candida albicans colonization and/or Helicobacter pylori infection: the molecular mimicry phenomenon diet for chronic fatigue caused by Candida albicans?. Neuro endocrinology letters, 36(5), 458-464. [14] Fetissov, SO. et al. (2008) Autoantibodies against appetite regulating peptide hormones and neuropeptides: putative modulation by gut microflora. Nutrition, 24, 348–359. [15] Fetissov, SO. et al. (2008) Emerging role of autoantibodies against appetite-regulating neuropeptides in eating disorders. Nutrition, 24, 854–859.  
  7. What is cholesterol?

    Cholesterols are types of fat found in the blood. The liver produces sufficient cholesterol for the body’s requirements, but it can also be acquired from foods, particularly animal products, such as meat, egg yolks, butter, cheese and milk. Cholesterol is necessary for the body to function properly, as it is involved in the production of hormones and vitamin D, and in the digestive process.[1]  Cholesterol is not soluble in the blood and has to be transported through the bloodstream by carriers called lipoproteins (complexes of fatty acids and proteins).[1] There are two types of proteins that transport cholesterol to and from cells, high-density lipoproteins (HDL), and low-density lipoproteins (LDL). The levels of cholesterol bound to these lipoproteins in the bloodstream can be an important indicator of the risk of heart disease. A blood test commonly used by doctors to determine your ‘cholesterol level’ calculates the overall cholesterol level by adding HDL and LDL to 20% of the amount of triglyceride (another fat present in the blood). [2] LDL is commonly known as ‘bad’ cholesterol. This is because it contributes to the formation of plaques within blood vessels, which are thick hard deposits that can clog arteries and decrease their flexibility, resulting in atherosclerosis. [3] If a blood clot forms in one of these narrowed arteries, it can result in a heart attack or a stroke.[1] Excess LDL can also contribute to peripheral artery disease, which is the result of plaque narrowing an artery that supplies blood to the extremities, such as the legs.[1] HDL is known as ‘good’ cholesterol as it assists in the removal of LDL by acting as a scavenger, carrying LDL back to the liver where it is broken down and excreted.[4] 20% to 30% of cholesterol is carried by HDL.[4], [5]  However, despite its beneficial actions, studies have shown that the level of HDL in the plasma may not reliably indicate the degree of reduction of LDL and so research into this area is continuing.[6] A satisfactory level of HDL can, however, decrease the risk of heart attack and stroke and, conversely, a level that is too low increases the risk.[7]  Triglycerides are another type of fat also present in the blood. They are also produced by the liver and are additionally found in oils, meat and dairy products. Their purpose is to provide energy to the body’s cells and tissues. When excess calories are ingested they are converted to triglycerides and stored as body fat and as fatty deposits within organs and tissues.[8] Like LDL, high levels of triglycerides are also associated with atherosclerosis,[9] and many people with diabetes or heart disease have high triglyceride levels within their blood. It is also common for people with high triglyceride levels to have a high ‘overall’ cholesterol level (i.e. a high LDL level and a low HDL level). One study has shown that a healthy lipid profile (i.e. low LDL, high HDL and low triglycerides), can reduce the risk of chronic heart disease by 71%.[10] Some common causes of elevated triglyceride levels include obesity, high alcohol consumption, cigarette smoking and a diet high in saturated fats.[11] Underlying diseases, e.g. poorly controlled diabetes, an underactive thyroid (hypothyroidism), kidney disease, and alcoholism,[11] and genetic disorders such as familial hypertriglyceridemia[12] can also cause increased levels of triglycerides. The best way to maintain healthy cholesterol levels is by leading a healthy lifestyle: a varied and balanced diet, low in saturated fat and plenty of pesticide-free fruit and vegetables, in addition to sustaining a healthy weight. Exercise is another key factor in reducing or maintaining healthy cholesterol levels, although the exact mechanism for this is not yet clear.[13] Exercise is also beneficial in controlling weight. Smoking should be avoided and alcohol consumed in moderation; as well as increasing cholesterol levels, the adverse effects on health of both smoking and excess alcohol are well documented. [1] NIH (2016) What is cholesterol? Retrieved May 2016 from, http://www.nhlbi.nih.gov/health/health-topics/topics/hbc  [2] Barter, P. et al. (2007) HDL Cholesterol, Very Low Levels of LDL Cholesterol, and Cardiovascular Events. The New England Journal of Medicine. 57. 1301-1310. [3] Kyle, D. (2004) Understanding lipoproteins as transporters of cholesterol and other lipids. Advances in Physiology Education. 28(3). 105-106. [4] Lee-Rueckert, M. et al. (2016) HDL functionality in reverse cholesterol transport - Challenges in translating data emerging from mouse models to human disease. Biochim Biophys Acta. 1861(7). 566-83. [5] Schwartz, CC. et al. (2004) Lipoprotein cholesteryl ester production, transfer, and output in vivo in humans. J Lipid Res. 45(9). 1594-1607. [6] Rothblat, G.H. et al. (2010) High-density lipoprotein heterogeneity and function in reverse cholesterol transport. Current Opinion in Lipidology, 21(3), 229-238. [7] University of Pennsylvania. (2016) Fat and ketoacids, cholesterol, repair. Retrieved June, 2016, from https://www.med.upenn.edu/biocbiop/faculty/vanderkooi/chap7-9.pdf  [8] Toth, P. (2005) The “Good Cholesterol”. Circulation. 111(5). 89-91. [9] Borge, G. et al. (2007) Nonfasting Triglycerides and Risk of Myocardial Infarction, Ischemic Heart Disease, and Death in Men and Women. Journal of the American Medical Association. 298(3). 299-308. [10] Manninen, V. (1992) Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for treatment. Circulation. 85(1). 37-45. [11] University of Colorado, Denver (2016) Cholesterol and Triglycerides Retrieved August, 2016, from http://www.ucdenver.edu/academics/colleges/medicalschool/departments/medicine/EndocrinologyMetabolismDiabetes/clinical/Documents/Lipid_Brochure.pdf  [12] NIH (2016) Familial hypertriglyceridemia.  Retrieved June, 2016, from https://www.nlm.nih.gov/medlineplus/ency/article/000397.htm [13] Meissner, M. et al. (2010) Exercise enhances whole-body cholesterol turnover in mice. Med Sci in Sports Exercise. 42.1460-1468.
  8. A crucial part of a healthy lifestyle is generally considered to be the inclusion of plenty (5-7 portions per day) of fruit and vegetables in our diets. However current farming practices include the use of pesticides, antibiotics and hormones to treat crops in order to increase output via higher crop production and faster plant growth. Furthermore, by limiting pest damage, the use of pesticides can also enhance the looks of produce. These chemicals can remain on the surface of fruits and vegetables, even on organic varieties,[1] contaminating them and leading to pesticide ingestion by consumers. Unfortunately, the drugs, hormones, and pesticides currently in use can be hazardous to humans if consumed in a quantity large enough. By definition, pesticides are designed to kill, and the majority are toxic to humans at some level.[2] Organophosphates (OPs) are a group of organic compounds containing phosphates that are frequently used in pesticides and are known to be toxic to humans.[3], [4], [5]  Studies into the effects of OPs have mainly been carried out in subjects that are exposed to OPs through their occupation, for example, farm workers or crop sprayers. These studies have found the symptoms of OP poisoning to include nausea, abdominal cramps, diarrhoea, dizziness anxiety, and confusion.[6] Fortunately, as severe as the symptoms may be, they are frequently reversible.[6] There have not been as many studies in people who have not been occupationally exposed to pesticides, but those undertaken have found that exposure to a low dose over a long period of time may be associated with neurodegenerative conditions such as Parkinson’s disease.[7], [8] Furthermore, prenatal exposure may result in long term irreversible changes in the brain structure of the unborn child, resulting in a lower IQ and a poorer memory.[9], [10], [11]  One of the larger studies, examining a nationally representative sample of children exposed to a chronic low dose of pesticides, found an increased chance of attention deficit hyperactivity disorder (ADHD) in children aged 8-15 years old.[12] Increased quantities of OPs were also found in their urine, indicating systemic exposure.[12] The degree of damage that pesticides such as OPs can inflict is directly proportional to the amount of substance ingested. It is not disputed that pesticide residues are present on fruit and vegetables, which unfortunately means that, in the quest to remain healthy by eating high proportions of fruits and vegetables in their daily diet, many consumers may also potentially be ingesting high levels of toxins. Could it be that the ‘healthier’ the diet based on a higher fruit and vegetable content, the higher the risk of toxicity? Test data obtained in 2014 from the US Department of Agriculture and the Federal Drug Agency found that as little as 1.7% of tomatoes, 2.2% of cherries, 1.7% of strawberries and 2.5% of peaches were pesticide free, meaning that over 97% of these products were contaminated with these chemicals.[13] The average potato had more pesticide residue by weight than any other produce tested,[13] which is of particular concern as many people eat potatoes most days.[14] The UK’s 2014 Pesticides Residues Committee Annual Report stated that, of 3,615 samples tested, 56.2% had no pesticides, 41.9% contained pesticides below the ‘safe’ limit and 1.9% above the limits.[1]  Whilst these tests mean that the vast majority of pesticide residues were well below the maximum residue limit (MRL) and are therefore unlikely to be toxic, some products did exceed the MRL. Nevertheless, the health benefits of eating plenty of fruit and vegetables remain clear and rather than omitting them from the diet whatsoever, it is advisable to wash fruits and vegetables well. Some studies suggest that washing with salt water is an effective way of removing pesticides.[15], [16] Indeed one study using chinese cabbage found that washing with soda-salt water removed as much as 60% of pesticides.[17] An even better approach is to peel them when possible, to remove the potentially harmful wax that is applied during processing.[18]  Furthermore, whilst organic produce generally contains less pesticide residues than non-organic produce, even these fruits and vegetables are not guaranteed pesticide-free.[19] Tests performed in the EU identified pesticide residues in a wide range of organic food products, even finding traces of the highly toxic dichlorodiphenyltrichloroethane (DDT)[20] Organic regulations stipulate that pesticides can be used in organic production, as long as the chemicals are ‘natural’. However one such ‘natural’ pesticide, rotenone, has been linked to the development of Parkinson’s disease in humans,[21] with such a strong effect that it is now used to create animal models of Parkinson’s disease.[22] With the help of more robust regulations governing organic production, organic fruits and vegetables should one day be the exception to the pesticide--contamination rule. However until then, care should also be taken to wash and peel organic produce. [1] National Archives. (2016)  Retrieved September, 2016, from http://webarchive.nationalarchives.gov.uk/20151023160002/http://pesticides.gov.uk/Resources/CRD/PRiF/Documents/Results and Reports/2014/PRIF Annual Report 2014 FINAL.pdf  [2] Damalas, C. et al. (2011) Pesticide Exposure, Safety Issues, and Risk Assessment Indicators. Int J Environ Res Public Health, 8(5), 1402 - 1419. [3] Costa, L. (2006) Current issues in organophosphate toxicology. Clinica Chimica Acta, 366(1-2), 1-13. [4] Kerami-mohajeri, S. et al. (2011) Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates.Hum and Experiment Toxicology, 30(9), 1119-1140. [5] Kamanyire, R. (2004). Organophosphate toxicity and occupational exposure. Occupational Medicine, 54(2), 69-75. [6] Peter, JV. et al (2014) Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med, 18(11), 735-45. [7] Slotkin, T. et al. (2011) Developmental exposure to organophosphates triggers transcriptional changes in genes associated with Parkinson's disease in vitro and in vivo. Brain Res Bull, 86(5-6), 340-347. [8] Berry, C. et al. (2010) Paraquat and Parkinson's disease. Cell Death and Different, 17(7), 1115 - 1125. [9] Ruah, V. et al. (2012) Brain anomalies in children exposed prenatally to a common organophosphate pesticide. PNAS, 109(20), 7871-7876. [10] Cecchi, A. et al. (2012) Environmental exposure to organophosphate pesticides: Assessment of endocrine disruption and hepatotoxicity in pregnant women. Ecotoxicol and Environ Safety, 80(1), 280 -287. [11] Columbia University (2016). Prenatal Exposure to Insecticide Chlorpyrifos Linked to Alterations in Brain Structure and Cognition. Retrieved September, 2016, from https://www.mailman.columbia.edu/public-health-now/news/prenatal-exposure-insecticide-chlorpyrifos-linked-alterations-brain-structure  [12] Bouchard, M. et al. (2010) Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics, 125(6), 1270-1277. [13] USDA (2016) Retrieved September, 2016, from https://www.ams.usda.gov/sites/default/files/media/2014%20PDP%20Annual%20Summary.pdf          [14] King, JC. & Slavin, JL. (2013). White potatoes, human health, and dietary guidance. Adv Nutr, 4(3), 393S-401S. [15] Aktar, W. et al. (2009) Risk assessment and decontamination of Quinalphos under different culinary processes in/on cabbage. Environ Monit Assess, 163(1), 369-377. [16] Vemuri, SB. et al. (2014) Methods for removal of pesticide residues in tomatoes. Food Sci Technol, 2(5), 64-68. [17] Zhang, Y-S. et al. (2013) Study on universal cleaning solution in removing blended pesticide residues in Chinese cabbage. J Environ Chem Ecotoxicol, 5(8), 202-207 [18] Ministry of Fisheries, Crops and Livestock (2004) Retrieved October 2016 from, http://pdf.usaid.gov/pdf_docs/Pnacy849.pdf  [19] European Commission (2008) Annex II: pesticides - plant protection products referred to in Article 5(1). Retrieved October 2016 from, https://members.wto.org/crnattachments/2016/TBT/EEC/16_0337_01_e.pdf  [20] The Expert Committee on Pesticide Residues in Food. (2015) Report on the Pesticide Residues Monitoring Programme for Quarter 1 2015. Retrieved October 2016 from, http://webarchive.nationalarchives.gov.uk/20151023155227/http://www.pesticides.gov.uk/Resources/CRD/PRiF/Documents/Results%20and%20Reports/2015/Q1%202015%20FINAL.pdf  [21] Nandipati, S. & Litvan, I. (2016) Environmental exposures and Parkinson’s Disease. Int J Environ Res Public Health, 13(9), doi: 10.3390/ijerph13090881 [epub ahead of print] [22] Johnson, ME. & Bobrovskaya, L. (2015) An update on the rotenone models of Parkinson's disease: their ability to reproduce the features of clinical disease and model gene-environment interactions. Neurotoxicity, 46, 101-16.
  9. ‘Fast’ or ‘junk’ food is very popular with young children and adolescents, but frequent consumption of this type of food is associated with negative impacts on nutrition and health. Fast food meals are usually high in calories and fat, with higher proportions of carbohydrates and added sugar and salt than regular meals. Children who regularly eat fattening fast food are generally less likely to consume healthy dietary components such as fibre, milk, fruit and vegetables than children who do not regularly eat fast food.[1] Regular fast food consumption may also prove to be addictive.[2], [3] As many of the foundations for lifelong eating habits are laid down during childhood and adolescence, this can mean that excessive fast food consumption can be particularly hazardous to children’s long term health and development.[4] Studies have shown that fast food consumption is linked with many dangerous precursors for obesity and other metabolic conditions. Genetics, individual behaviour, and environment all play a role in the development of obesity, but high levels of fast food consumption can have a dramatic impact. Regular consumption of fast food by children can result in weight gains of several pounds per year.[5] This is coupled with increased rates of chronic illnesses such as asthma,[6] diabetes, high blood pressure and stroke.[5], [7]  The effect of unhealthy weight gain resulting from frequent consumption of fast food can not only impact the physical development of the child, but can have implications for children's’ mental health. As a result of stigmatisation, children who are overweight or obese are more prone to suffer from low self-esteem and low self-confidence,[8] both of which are considered important to a child’s personal development. Low self-esteem can be the precursor to depression, which can have an adverse impact on almost every aspect of the child’s life and development.[9] It has also been suggested that diet can significantly impact children’s concentration and academic performance.[10], [11], [12] High energy levels and the ability to concentrate are essential attributes for success in school children that can be affected positively or negatively by diet. High sugar foods can ultimately deplete energy levels and reduce the ability to concentrate for extended periods of time compared with lower-sugar alternatives.[13] Studies now also suggest that attention deficit hyperactivity disorder (ADHD) is associated with high sugar intake.[2] The increasing prevalence of ADHD, which now affects 5-11% of children in the USA,[14] may therefore be the result of increasingly poor diets. These damaging effects of excessive fast food consumption are varied and far reaching, and can include obesity, chronic or critical illness, low self-esteem and depression. Diet can affect both a child’s mental and physical health, as well as their performance, both at school and in extracurricular activities. To stay healthy in both body and mind, sticking to healthier, non-processed food options can go a long way.   [1] Bowman, SA, Gortmaker, SL, Ebbeling, CB, Pereira, MA, Ludwig, DS. (2004) Effects of fast-food consumption on energy intake and diet quality among children in a national household survey. Pediatrics. 113(1). 112-8. [2] Gearhardt, AN, Grilo, CM, DiLeone, RJ, Brownell, KD, Potenza, MN. (2011) Can food be addictive? Public health and policy implications. Addiction. 106(7). 1208-12. [3] Garber, AK, Lustig, RH. (2011) Is fast food addictive? Curr Drug Abuse Rev. 4(3). 146-62. [4] Johnson, RJ, Gold, MS, Johnson, DR, Ishimoto, T, Lanaspa, MA, Zahniser, NR, Avena, NM. (2011) Attention-Deficit/Hyperactivity Disorder: Is it Time to Reappraise the Role of Sugar Consumption? Postgrad Med. 123(5). 39-49. [5] Pereira, MA, Kartashov, AI, Ebbeling, CB, Van Horn, L, Slattery, ML, Jacobs, DR, Ludwig, DS. (2005) Fat-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet. 365(9453). 36-42. [6] Wickens, K, Barry, D, Friezema, A, Rhodius, R, Bone, N, Purdie, G, Crane, J. (2005) Fast foods - are they a risk factor for asthma? Allergy. 60(12). 1537-41.  [7]  Alter, DA, Eny, K. (2005) The relationship between the supply of fast-food chains and cardiovascular outcomes. Canadian J Public Health. 96(3). 173-7. [8] Puhl, RM, King, KM (2013) Weight discrimination and bullying. Best Pract Res Clin Endocrinol Metab. 27(2). 117-27. [9] Simon, GE, Von Korff, M, Saunders, K, Miglioretti, DL, Crane, PK, van Belle, G, Kessler, RC. (2006) Association between obesity and psychiatric disorders in the US adult population. JAMA Psychiatry. 63(7). 824-30. [10] Martin, A, Saunders, DH, Shenkin, SD, Sproule, J. (2014) Lifestyle intervention for improving school achievement in overweight or obese children and adolescents. Cochrane Database Syst Rev. [epub] doi: 10.1002/14651858.CD009728.pub2. [11] Benton, D. (2010) The influence of dietary status on the cognitive performance of children. Mol Nutr Food Res. 54(4). 457-70. [12] Stevenson, J. (2006) Dietary influences on cognitive development and behaviour in children. Proc Nutr Soc. 65(4). 361-5. [13] Cooper, SB, Bandelow, S, Nute, M, Morris, JG, Nevill, ME. (2012) Breakfast glycaemic index and cognitive function in adolescent school children. Br J Nutr. 107(12). 1823-32. [14] Hamed, AM, Kauer, AJ, Stevens, HE. (2015) Why the diagnosis of attention deficit hyperactivity disorder matters. Front Psychiatry. [ecollection] doi: 10.3389/fpsyt.2015.00168  
  10. The fibres used to make textile products can be synthetic (such as acrylic, nylon and lycra) or natural (such as cellulose or protein). To achieve certain desirable fibre properties, various additives are used during manufacture, such as heat or light stabilizers, flame retardants and delustrants (used to reduce shininess). Additionally,  pigments and dyes are also used to colour the fibers. All of these chemicals are regularly added to both synthetic and natural fibres.  Some of the toxic chemicals contained within clothing include:[1]  Perfluorinated compounds Phthalates Heavy metals Flame retardants Isocyanates Formaldehyde Azo dyes Urea Various glycols Aliphatic hydrocarbons  Many of these substances have been linked to numerous health concerns. Formaldehyde and azo dyes, for example, have been linked to increases in certain cancers in humans, [2] [3] whereas phthalate exposure during pregnancy has been shown to have lifelong effects on offspring hormone levels in animal models.[4] The mutagenic effects of azo dyes are so well documented that the EU has banned the use of 22 dyes of this type in textile manufacture.[5]  When present in textiles, heavy metals can pose a potential danger to human health. One study found that there were high levels of chromium in polyamide-based dark clothes, high antimony concentrations in polyester-based clothes, and high levels of copper in certain green cotton fabrics.[6] Although most of the levels were still below what is deemed “safe and acceptable” according to international standards, antimony was present at levels 10% higher than the specified safety level for dermal contact with clothes.[6] Heavy metals like these have been linked to numerous health issues. Chromium, for example, is a carcinogen that is also found in leather articles such as bags and shoes.[7] In 2014, concerns regarding chromium exposure from clothing items led the EU to introduce a limit of 3 mg/kg in all leather items.[8] Some clothes also contain bactericidal silver nanoparticles, which can be released from textiles during washing, abrasion and even just everyday usage, potentially contaminating not just us, but the environment too.[9], [10], [11] One study found this use of silver nanoparticles unnecessary, as similar results could be achieved with other silver formulations.[11]  One of the major health problems related to textile additive exposure is contact dermatitis and skin irritation.[12], [13] One study in 2014 detailed the epidemiological features of textile dermatitis, finding that it was most common in 40-50 year old females and in atopic dermatitis patients. Most cases were located on the hands in textile workers, and on the torso and legs in non-occupational cases. Just three specific dyes (Disperse Blue 124, Disperse Blue 106, and Disperse Yellow 3) were responsible for nearly 80% of cases.[14]  A 2013 report by the Swedish Chemicals Agency highlighted the lack of regulation surrounding textile manufacturing, stating that “today there is no unified legislation at the EU level covering the wide range of hazardous chemicals that may be present in textile products”.[1] Furthermore, it was also suggested that there is a need for EU-level regulation in order to obtain a more cohesive handling of chemical use in textile manufacture.[1]  So how can you limit your exposure to these toxic compounds? One way is by washing and airing new garments before wearing them. This is because many of these toxic compounds, such as formaldehyde, are water soluble and washing the clothing after purchasing it will remove much of the contamination.[13] But change needs to come from the manufacturers too, who should take advantage of new methods that reduce the need for harmful chemicals.[15]  [1] Swedish Chemicals Agency. (2013) Hazardous chemicals in textiles – report of a government assignment. Retrieved May 2016 from, https://www.kemi.se/global/rapporter/2013/rapport-3-13-textiles.pdf  [2] Committee to Review the Formaldehyde Assessment in the National Toxicology Program 12th Report on Carcinogens; Board on Environmental Studies and Toxicology; Division on Earth and Life Sciences;National Research Council. (2014) Review of the Formaldehyde Assessment in the National Toxicology Program 12th Report on Carcinogens. National Academies Press. [3] Golka, K, Kopps, S, Myslak, ZW. (2004) Carcinogenicity of azo colorants: influence of solubility and bioavailability. Toxicol Lett. 151(1). 203-10. [4] Martinez-Arquelles, DB, Papadopoulos, V. (2016) Prenatal phthalate exposure: epigenetic changes leading to lifelong impact on steroid formation. Andrology. [epub] doi: 10.1111/andr.12175  [5] European Commission (2002) Directive 2002/61/EC Retrieved May 2016 from, http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2002:243:0015:0018:en:PDF  [6] Rovira, J, Nadal M, Schuhmacher, M, Domingo, JL. (2015) Human exposure to trace elements through the skin by direct contact with clothing: risk assessment. Environ Res. 140. 308-316. [7] Salnikow, K, Zhitkovich, A. (2008) Genetic and Epigenetic Mechanisms in Metal Carcinogenesis and Cocarcinogenesis: Nickel, Arsenic and Chromium. Chem Res Toxicol. 21(1). 28-44. [8] European Commission (2014)  Regulation (EU) No 301/2014. Retrieved May 2016 from, http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX%3A32014R0301  [9] Geranio, L, Heuberger, M, Nowack, B. (2009) The behaviour of silver nanotextiles during washing. Environ Sci Technol. 43(21). 8113-8. [10] Benn, TM, Westerhoff, P. (2008) Nanoparticle Silver Released into Water from Commercially Available Sock Fabrics. Environ Sci Technol. 42(11). 4133-9. [11] Emam, HE, Manian, AP, Siroka, B, Duelli, H, Redl, Pipal, A, Bechtold, T. (2013) Treatments to impart antimicrobial activity to clothing and household cellulosic-textiles – why “Nano”-silver? J Clean Prod. 39. 17-23. [12] Brookstein, DS. (2009) Factors associated with textile pattern dermatitis caused by contact allergy to dyes, finishes, foams, and preservatives. Dermatol Clin. 27(3). 309-22 [13] Australian Government Department of Health. (2013) Formaldehyde in clothing and textiles FactSheet. Retrieved May 2016 from, https://www.nicnas.gov.au/communications/publications/information-sheets/existing-chemical-info-sheets/formaldehyde-in-clothing-and-textiles-factsheet  [14] Lisi, P, Stingeni, L, Cristaudo, A, Foti, C, Pigatto, P, Gola, M, Schena, D, Corazza, M, Bianchi, L. (2014) Clinical and epidemiological features of textile contact dermatitis:an Italian multicentre study. Contact Dermatitis. 70(6). 344-50. [15] Yu, M, Li, W, Wang, Z, Zhang, B, Ma, H, Li, L, Li, J. (2016) Covalent immobilization of metal-organic frameworks onto the surface of nylon-a new approach to the functionalization and coloration of textiles. Sci Rep. 6. 22796.
  11. Vitamins, dietary minerals and trace elements are essential to the healthy function of the human body. Vitamins are organic compounds that are vital to, but not always produced by, the body and so have to be obtained through the diet. Similarly, dietary minerals (e.g. calcium and phosphorous) and trace elements, of which even smaller amounts are required (e.g. zinc and selenium), are acquired through food. For the majority of people, a balanced, nutritious diet satisfies the body’s vitamin and mineral requirements.[1] There are two types of vitamins; fat soluble and water soluble. Fat soluble vitamins are found mainly in fatty foods and animal products, such as oils, butter, eggs, liver and oily fish. Whilst the body requires a constant supply of these vitamins, the tiny quantities needed coupled with their storage in the liver and fatty tissue for use when required mean that it is not vital to consume them every day. In fact large doses of fat soluble vitamins can be harmful. For example, the risk of lung and stomach cancers is increased in those who consume 20-30mg/day of B-carotene.[2] However many of the side effects seen with excess vitamin intake are not likely to happen as a result of dietary intake, but rather by exceeding the recommended dose with supplementation.[3], [4], [5]  Water soluble vitamins such as vitamin C, folic acid and niacin are found in a wide range of foods including vegetables, fruit, potatoes, grains and dairy food.[6] These water soluble vitamins are less stable than fat soluble vitamins. They are often destroyed by heat or air, meaning that they cannot be stored by the body and excesses are excreted in urine. The consumption of foods containing water soluble vitamins is therefore needed more often, to maintain the body’s supply. As they are excreted in the urine, water soluble vitamins are generally less harmful than fat soluble vitamins, although very high doses may have an adverse effect on the body.[7] For example, large doses vitamin C can cause diarrhoea,[8] while excess folic acid can have effects that range from abdominal cramps and nausea to confusion and increased seizure frequency.[9] Dietary minerals and trace elements have many functions including building strong bones and teeth, regulating the composition of the fluid inside and surrounding cells, and converting food to energy.[10] However high doses taken over a long period can be harmful, as demonstrated by the doubling of hospital admissions for gastrointestinal problems, 17% increase in kidney stones and 20-40% increase in the risk of a heart attack in those taking calcium supplements.[11] Despite the fact that a varied, healthy diet will provide adequate amounts of all essential vitamins, minerals and trace elements for most people, the use of dietary supplementation is increasing. There is no real evidence, that taking synthesised vitamins and mineral supplements has any real benefit to health. Furthermore, in addition to a lack of proven efficacy, the manufacture of dietary supplements is not regulated as stringently as that of medicines. This is because they are not classified as a food or a drug, and as such, they are not technically permitted to make any health claims. More worryingly, no clinical trials are required prior to their production and sale. Many supplements are manufactured by synthetic methods and contain additives such as sweeteners, which may be harmful to health, and they can interact with prescribed medications with serious and even life-threatening results.[12] In conclusion, naturally occurring vitamins and microelements are an important part of our diet. Whilst many synthetic supplements are available that contain high doses of these essential nutrients, it is often the case that our dietary intake is sufficient, except in cases of diseases or conditions that result in a vitamin deficiency. The potential for damaging effects seen with high intake of certain man made vitamins, coupled with the possibility for drug interactions means that you could be doing more harm than good by taking these ‘healthy’ supplements.   [1]  FAO/WHO (2001) Human vitamin and mineral requirements. Retrieved April 2016 from, http://www.fao.org/3/a-y2809e.pdf [2]  Druesne-Pecollo N, et al. (2010) Beta-carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials.Int J Cancer. 127(1). 172-84. [3] Schwalfenberg, GK. & Genius, SJ. (2015) Vitamin D, Essential Minerals, and Toxic Elements: Exploring Interactions between Nutrients and Toxicants in Clinical Medicine.ScientificWorldJournal. 318595. [4]  Brown, AC. (2016) An overview of Herb and dietary supplement efficacy, safety and government regulations in the United States with suggested improvements. Part 1 of 5 series. Food Chem Toxicol. [epub ahead of print] doi: 10.1016/j.fct.2016.11.001. [5] Brown, AC. (2016) Liver toxicity related to herbs and dietary supplements: Online table of case reports. Part 3 of 6. Food Chem Toxicol. [epub ahead of print] doi: 10.1016/j.fct.2016.07.001. [6] CSU (2012) Water-soluble vitamins: B-complex and vitamin C. Retrieved November 2016 from, http://extension.colostate.edu/docs/pubs/foodnut/09312.pdf [7]  CSU (2012) Fat-soluble vitamins: A, D, E, and KB-complex and vitamin C. Retrieved November 2016 from, http://extension.colostate.edu/docs/pubs/foodnut/09315.pdf [8] Mulholland, CA, Benford, DJ. (2007) What is known about the safety of multivitamin-multimineral supplements for the generally healthy population? Theoretical basis for harm. Am J Clin Nutr. 85(1). 318S-322S [9] Rogovik, AL, Vohra, S, Goldman, RD. (2010) Safety considerations and potential interactions of vitamins: should vitamins be considered drugs? Ann Pharmacother. 44(2). 311-24. [10] Shenkin, A. (2006) Micronutrients in health and disease. Postgrad Med J. 82(971). 559-567. [11] Reid, IR, Bristow, SM, Bolland, MJ. (2015) Calcium supplements: benefits and risks. J Intern Med. 278(4). 354-68. [12] Williamson, EM. (2003) Drug-interactions between herbal and prescription medicines. Drug Saf. 26(15). 1075-92.  
  12. Chewing gum: hidden harms

    There are a variety of reasons why people chew gums; to freshen their breath, to clean their mouth and even to reduce food cravings, theoretically helping them to avoid eating unhealthy foods. However, while some research has shown that chewing gum can indeed decrease the appetite and the motivation to eat,[1] [2] it has also highlighted the fact that gum chewers' meals can actually end up being less nutritious than those chosen by non-gum-chewers.[3] One study showed, for example, that people who chewed gum were less likely to eat fruit and instead were more motivated to eat junk food.[3] This is likely due to a minty flavor in the gum making fruits and vegetables taste sour or bitter. Regardless of the reason for gum chewing, it can have numerous ill effects on health. This is especially true for people with pre-existing jaw conditions like the painful chronic condition temporomandibular joint disorder (TMJ or TMD).[4] However, even in healthy people, excessive gum chewing can aggravate the cartilage and surrounding joints in the mouth through extra wear and tear.[5] The strain placed on the jaw and surrounding muscles can also increase the incidence of chronic headaches.[6] Chewing gum also causes you to swallow excess air,[7] which can contribute to abdominal pain and bloating seen with irritable bowel syndrome (IBS).[8] Furthermore, chewing gum sends physical signals to the body indicating that food is about to be ingested, resulting in increased production of stomach acid in preparation.[9] Excess stomach acid can have a wide range of negative effects on the digestive system, including ulceration.[10]  Sugar free chewing gums often contain artificial sweeteners, such as aspartame or sucralose. Aspartame has been linked to numerous deleterious effects on health, including headaches, insomnia and seizures,[11] as well as changes in metabolism and weight gain.[12] Sucralose consumption can also have numerous ill effects. Animal studies showed that 12 weeks sucralose administration reduced beneficial gut bacteria, increased fecal pH, and altered the expression of enzymes involved in drug metabolism.[13] So next time you chew gum, remember that you may be doing more to your body than just freshening your breath. Gum chewing has been linked to effects on metabolism and appetite, as well as potentially causing harm to the jaw and digestive system. Chewing gum should therefore ideally be kept to a minimum where possible.   [1] Park, E, et al. (2016) Short-term effects of chewing gum on satiety and afternoon snack intake in healthy weight and obese women. Physiol Behav. 159. 64-71. [2] Hetherington, MM & Boyland, E. (2007) Short-term effects of chewing gum on snack intake and appetite. Appetite. 48(3). 397-401. [3] Swoboda, C & Temple, JL. (2013) Acute and chronic effects of gum chewing on food reinforcement and energy intake. Eating Behaviours. 14(2). 149-56. [4] Haggman-Henrikson, B, et al. (2004) Endurance during chewing in whiplash-associated disorders and TMD. J Dent Res. 82(12). 946-50 [5] Blasberg, B & Greenberg, MS. (2003) Temporomandibular disorders In Burket’s Oral Medicine. PMPH, USA [6] Watemberg, N, et al. (2014) The influence of excessive chewing gum use on headache frequency and severity among adolescents. Pediatr Neurol. 50(1). 69-72. [7] Silva, AC, et al. (2015) Effect of gum chewing on air swallowing, saliva swallowing and belching. Arg Gastroenterol. 52(3). 190-4. [8] Friedman, G. (1991) Diet and the irritable bowel syndrome. Gastroenterol Clin North Am. 20(2). 313-24. [9] Helman, CA. (1988( Chewing gum is as effective as food in stimulating cephalic phase gastric secretion. Am J Gastroenterol. 83(6). 640-2/ [10] Hunt, RH, et al. The stomach in health and disease. Gut. 64(10). 1650-1668. [11] Humphries, P, et al. (2008) Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. 62. 451-62.  [12] Feijo Fde, M, et al. (2013) .Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 60(1). 203-7. [13] Abou-Donia, MB, et al. (2008) Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. J Toxicol Environ Health. 71(21). 1415-29.
  13. Genetically modified organisms, also known as “GM” organisms or “GMO”, are organisms whose genetic material (DNA) has been manipulated artificially. Whilst this may sound futuristic, a version of genetic modification has been going on for centuries, through traditional farming practices such as tree splicing and selective breeding.  However, the term “GM food” today generally refers to cases where the genetic material of an organism (either a plant or animal) has been manipulated in a laboratory, through a process called genetic engineering. This relatively recent science introduces new genes, such as those from viruses or bacteria, into crops or animals in a way that can not occur naturally through traditional farming methods. One example of how this technology can be used is the production of insulin, a medication widely used by diabetics. Here, however, it is an animal gene that is inserted into bacteria and not vice versa. Genetic material coding for insulin production is inserted into the bacterium’s genome, allowing it to make insulin which is harvested and used for therapeutic applications.[1] So why use molecular biology over traditional selective breeding? With selective breeding, plants or animals exchange large amounts of their genetic material, in a relatively unregulated process. This can lead to the offspring inheriting both the desired, and undesirable traits of the parent.[2] This can therefore diminish the benefit that comes from the selective breeding process, and breeders sometimes have to cross many organisms over multiple generations to produce the desired effect. One example of when selective breeding can lead to unwanted effects is the selective breeding of certain potato varieties that inadvertently produced excessive levels of naturally occurring glycoalkoloids.[3] These compounds can lead to many of the circulatory, gastrointestinal, neurological and dermatological symptoms associated with alkaloid poisoning.[4]  With GM foods, however, beneficial genes can be chosen and inserted in isolation into the ‘offspring’ product. This also means that genes from different species can be inserted into offspring, such as genes from bacteria being inserted into plants and vice versa, such as genes that code for pest, or even pesticide, resistance. Pesticides associated GM foods (PAGMF) are engineered to tolerate certain forms of pesticides, allowing them to survive while unwanted plants and weeds are killed.[5] Indeed there are many traits that can be engineered into plants and animals that can enhance their survival, including genes that help the organism to resist certain viruses or to produce certain vitamins.[6] [7] And it isn’t just benefits for the plants that can be ‘added in’ - genetic engineering can also be used to increase the nutritional value or yield of crops, or enable them to grow in areas where they naturally wouldn’t, making them of particular importance in developing countries.[6] However GM foods are not without their controversies, specifically in relation to approaches to risk regulation. The ambiguity and uncertainty of the science behind GM foods, coupled with the lack of specific research mean that the knowledge necessary to design and undertake adequate risk assessments is sadly lacking.[8] More worryingly, these GM foods may have the potential for harmful effects to human health, including the production of novel allergens or carcinogens.[7] More recent studies have also shown the potential for genetic material from GM foods entering the bloodstream and persisting systemically. Traditional paradigms regarding food absorption stated that large macromolecules within food cannot pass directly to the circulatory system from the digestive system.[9] This is because, during digestion, proteins and DNA were thought to be degraded into their constituents (amino acids and nucleic acids), before being absorbed into the circulatory system by a complex, active process and distributed to different regions of the body.[9] However recent data, based on an analysis of over 1000 human samples from 4 independent studies, provided evidence that food-derived DNA fragments large enough to carry complete genes can survive digestion and enter the circulatory system.[9] One sample even contained a higher relative concentration of plant DNA than human DNA.[9] Furthermore there are also a wide range of possible environmental impacts of GM foods, including the accidental creation of new or more pesticide-resistant pests, an increased reliance on herbicides in agriculture and harmful effects on non-target species that may disrupt entire ecosystems.[10] At present, scientists lack the necessary data to accurately predict the consequences of the widespread introduction of GM crops and animals, largely because the technology itself remains so novel.[11] It is clear that there is the potential for great benefits from GM foods, particularly in developing countries where modification can assist with plant growth and increase yield. However this relatively new science is plagued with controversy and numerous ‘unknowns’, meaning that there is much research and technological development needed before we can truly see the unhindered benefits of this technique.   [1] Baeshen, NA, Baeshen, MN, Sheikh, A, Bora, RS, Ahmed, MM, Ramadan, HA, Saini, KS, Redwan EM. (2014) Cell factories for insulin production. Microb Cell Fact. 13. 141. [2] Aroian, R. (2016) Genetically modified organisms (GMO). Retrieved May 2016 from, http://www.bt.ucsd.edu/gmo.html [3] National Research Council and Institute of Medicine. (2004) Safety of Genetically Engineered Foods: Approaches to Assessing Unintended Health Effects. Retrieved May 2016 from, http://www.nap.edu/read/10977/chapter/5 [4] Tice, R. (1998) a-Chaconine [20562-03-2] and a-Solanine [20562-02-1] Review of Toxicological Literature. Retrieved May 2016 from, http://ntp.niehs.nih.gov/ntp/htdocs/chem_background/exsumpdf/chaconinesolanine_508.pdf [5] Aris, A, Leblanc, S. (2011) Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada. Reprod Toxicol. 31(4). 528-33. [6] Basu, SK, Dutta, M, Goyal, A, Bhowmik, PK, Kumar, J, Nandy, S, Scagliusi, SM, Prasad, R. (2010) Is genetically modified crop the answer for the next green revolution? GM Crops. 1(2). 68-79. [7] Bakshi, A. (2003) Potential adverse health effects of genetically modified crops. J Toxicol Environ Health B Crit Rev. 6(3). 211-25. [8] Myhr, AI, Traavik, T. (2002) The Precautionary Principle: Scientific Uncertainty and Omitted Research in the Context of GMO Use and Release. J Agricult Environ Ethics. 15(1). 73-86. [9] Spisak, S, Solymosi, N, Ittzes, P, Bodor, A, Kondor, D, Vattay, G, Bartak, BK, Sipos, F, Galamb, O, Tulassay, Z,Szallasi, Z, Rasmussen, S, Sicheritz-Ponten, T, Brunak, S, Molnar, B, Csabai, I. (2013) Complete genes may pass from food to human blood. PLoS One. 8(7). E69805. [10] National Research Council (US) Committee on Genetically Modified Pest-Protected Plants. (2000) Potential Environmental and Human Health Implications of Pest-Protected Plants In Genetically Modified Pest-Protected Plants: Science and Regulation. Washington. National Academic Press. [11] Marvier, M. (2001) Ecology of Transgenic Crops. American Scientist. 89(2). 160
  14. The smoking process for meat, fish and cheese has been used for centuries in some countries. Its original purpose was for preservation, brought about by drying the food and introducing anti-microbiological constituents, such as a chemical called phenol, into the food from the smoke. Currently, the main purpose of smoking food is the achievement of a characteristic taste and appearance. Today four methods of smoking are used:  Smoking with freshly generated wood smoke (the traditional method) Smoking with smoke regenerated from smoke condensates Flavouring with smoke flavour produced from smoke condensates Flavouring with chemically derived smoke flavours Traditionally-smoked food gives rise to health concerns, particularly due to the process leading to the possible production of nitrosamines and/or polycyclic aromatic hydrocarbon (PAHs). Nitrosamines are carcinogenic compounds produced by the reaction of nitrogen oxides and amines or amides (components of protein) contained in food.[1] The risk of nitrosamine consumption is compounded by the fact that the foods that are traditionally smoked are also those highest in proteins; meat and fish. PAHs, which are also known to be carcinogenic,[2] are formed when organic matter is burned, particularly at high temperatures.[3]  Food products smoked at high temperatures may therefore contain a high level of PAHs, predominantly on the surface. However foods smoked at lower temperatures also carry inherent risks, such as an increased risk of Listeriosis, a disease caused by a gram-positive bacterium called Listeria monocytogenes.[4] [5]  Smoke condensates, used as flavourings, are made by condensing smoke, which may then be further fractionated, concentrated or purified. These additional processes are employed to either enhance the smoke’s aroma, or to reduce the concentration of undesirable by-products. Smoke condensates are used to flavour food in two ways; either by being directly added to food as a liquid flavouring, or by being added to a system being used for traditional smoking,to intensify the flavour.[6]  Smoke flavour blends are mixes of known substances in specific quantities that are added directly to food to instill a ‘smoked’ flavour. Liquid smoke (now readily available at supermarkets for home use) is produced by the destructive distillation of wood.[7] The basic substance, pyroligneous acid, contains methanol, acetic acid, acetone, furfural  and also tars and associated substances.[8] Water, tar and acids are removed by alkali washing. The process is completed by re-acidification and the extraction of solvent.  The European Food Safety Authority is still undecided regarding the safety of these smoke flavourings.[9] Despite there being several means available to reduce the harmful effects of the smoking process (e.g. reducing temperature or indirect smoking) and the availability of smoke flavourings that have well-known, safe compositions, traditional smoking methods are still used today. As current regulations are not strict enough to eliminate the risk of toxicity, the limitation, or even complete avoidance, of “smoked” products certainly seems one way to protect against these cancer risks.    [1] Douglass, ML, Kabacoff, BL, Anderson, GA, Cheng, MC. (1978) The chemistry of nitrosamine formation inhibition and destruction. J Soc Cosmet Chem. 29. 581-606. [2] Baird, WM, Hooven, LA, Mahadevan, B. (2005) Carcinogenic polycyclic aromatic hydrocarbon-DNA adducts and mechanism of action. Environ Mol Mutagen. 45(2-3). 106-114. [3] Phillips, DH. (1999) Polycyclic aromatic hydrocarbons in the diet. Mutat Res. 443(1-2). 139-47. [4] Norton, DM, McCarney, MA, Gall, KL, Scarlett, JM, Boor, KJ, Wiedmann, M. (2001) Molecular studies on the ecology of Listeria monocytogenes in the smoked fish processing industry. Appl Environ Microbiol. 67(1). 198-205. [5] Heinitz, M, Johnson, JM. (1998) The incidence of Listeria spp., Salmonella spp., Clostridium botulinum in smoked fish and shellfish. J Food Protect. 3. 265-367. [6] Council of Europe. (1992) Health aspects of using smoke flavours as food ingredients. Retrieved April 2016 from, https://books.google.co.uk/books/about/Health_Aspects_of_Using_Smoke_Flavours_A.html?id=zlMWAAAAYAAJ&redir_esc=y [7] Lingbeck, JM, Cordero, P, O’Bryan, CA, Johnson, MG, Ricke, SC, Crandall, PG. (2014) Functionality of liquid smoke as an al all natural antimicrobial in food preservation. Meat Sci. 97(2). 197-206. [8] Hawley, LF. (1944) Wood Chemistry. Retrieved April 2016 from, http://14.139.56.90/bitstream/1/2057495/1/ANAND-91.pdf#page=667 [9] European Food Safety Authority. (2010) Statement on the safety evaluation of smoke flavourings primary products: interpretation of the margin of safety. Retrieved April 2016 from, http://www.efsa.europa.eu/en/efsajournal/pub/1325   
  15. Aspartame: a daily toxin

    It was previously approved for use in 1974, but its approval was put on hold due to objections filed by neuroscientist [1]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.[1] [2] 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.[3] This then led to European-wide approval of aspartame with the universal adoption of the EU Sweetener Regulations (94/35/EC) in 1994.[4] 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.[5] This surplus of neurotransmitters in the brain can kill neurons by allowing an influx of too much calcium into the cells.[6] 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.[7] 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.[8] 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.[9] 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. [10] 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.[11] Aspartame is known to have the potential to cause adverse effects, which can be serious, including seizures.[12] 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.[13] In the light of what evidence is available, it is therefore perhaps advisable to limit aspartame intake.   [1] 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 [2] 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 [3] FSA (2016) Aspartame. Retrieved April 2016 from, https://www.food.gov.uk/science/additives/aspartame [4] Ashurst, PR. (2008) Chemistry and Technology of Soft Drinks and Fruit Juices. Retrieved April 2016 from, https://goo.gl/NVEN1M [5] Kudo, Y, Ogura, A. (1986) Glutamate-induced increase in intracellular Ca2+ concentration in isolated hippocampal neurones. Br J Pharmacol. 89(1). 191-8. [6] Arundine, M, Tymianski, M. (2003) Molecular mechanisms of calcium-dependent neurodegeneration in excitotoxicity. Cell Calcium. 34(4-5). 325-37. [7] Olney, JW. (1994) Excitotoxins in foods. Neurotoxicology. 15(3). 535-44. [8] 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. [9] Yang, Y, Rosenberg, GA. (2011) Blood-brain barrier breakdown in acute and chronic cerebrovascular disease. Stroke. 42(11). 3323-8. [10] 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. [11] 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. [12] 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. [13] Wieloch, T, Nikolich, K. (2006) Mechanisms of neural plasticity following brain injury. Curr Opin Neurobiol. 16(3). 258-64.
  16. Artificial sweeteners: low in calories, high in harm

    Aspartame is also linked to anxiety and depression, there are a lot of articles about that. Aspartame contains phenylalanine which being consumed in too big amounts can reduce the level of happiness hormone - serotonin. And I suppose there are even worse things linked to aspartame
  17. Gain weight by going 'diet'

    Counting calories helps as well as burning them in the gym. But diet drinks lost its sense long ago for me, science facts speak for themselves. I've heard this news a year or two ago, but world does not change that fast, money and media rules - diet drinks are still on the supermarket shelves and it means there is a demand for it.
  18. It's just one more way to fool people to part with their money, nothing new. Health always has been a subject of manipulation and remains so tody. I believe that eventually dietary supplements will be banned or restricted, but I am also sure that by the moment it happens, there will be many more other means to manipulate people with. Unfortunately, it's human nature, we will never reach full truth and fairness in this world, though we still can make it a bit better.
  19. The risks and benefits of eating farmed vs. wild salmon

    Agree with you, both wild and farmed salmon can contain contaminants, but the fact that farmed salmon has selective diets (i.e. fed with food high in EFAs) is still a fact which does not depend on year or season. If farmers can choose the feed - it can be close to natural or not. So quality of fish must be controled on constant basis and controlled to well defined regulations if to aim to deliver the healthier option to the wild salmon. Until that comes I will rather trust nature than humankind. 
  20. The risks and benefits of eating farmed vs. wild salmon

    Judging by article, wild salmon is not much more healthier, it is only a little bit better, but the difference is not so considerable. It can be that other studies will show that farmed is healthier than wild - it depends on a lot of factors (season, weather, amount of pollutants in water, etc.) which vary from year to year. So, it may be that one year wild is better and another - farmed is better. 
  21. lugerber, you are absolutely right. Another thing about fluorinated water is that different people consume different amounts of water, e.g. people having diabetes will consume much more fluoride than others. And I fully agree that world is moving to total removal of water fluoridation, so hope for the better
  22. Generally it is not so bad, many counties have already refused fluoridation of water. It's just a question of time, I am sure that in several years 99% of countries will make tap water fluoride-free. It's a bit strange that in modern world dietary supplements are supplied in such way, literally one has no choice but consume artificially added chemicals/drugs without being aware of it. Everyone has the right to decide what to eat/drink/consume, and if one thinks "I need to add some fluoride to my diet", then he may go to supermarket and buy fluorinated water or green tea or whatever just for himself but one ones has been given the right or privilage to enforce ones subjective ideas onto whole public. It seems today if you want to fight off water fluoridation it is possible, see here http://www.bbc.co.uk/news/uk-england-hampshire-29803864
  23. Artificial sweeteners: low in calories, high in harm

    gespalding, that is true, it's extremely difficult to avoid sweeteners, but it's possible. At least we can cut its amount as much as possible. And we should do it. If producers don't care about customers health, we must look after ourselves.
  24. Artificial sweeteners: low in calories, high in harm

    Can't believe that organisations such as FDA and EFSA, who are actualy responsible for our health, put at risk human health so easily. And what for? For money! This world is screwed up!
  25. Health benefits and risks of processed supermarket milk

    Homogenisation and pasteurisation are only a part of "improvements" made to raw milk. Did you know that cows are treated in such a way that they produce much more milk than they would in natural conditions? It makes them less healthy and farmers feed their cows with antibiotics, which apperently will get into milk. Beside that, milk may contain many additives, such as vitamins, sweeteners and preservatives. Homogenisation and pasteurisation are the most inoffensive.
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