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Found 8 results

  1. Sugar, worse than we thought

    Sugar addiction is the problem of 21st century. People consume more and more sugar and get obesity, diabetes and other illnesses. Let's have a comprehensive review of this problem on the whatishealthy, though still in layman terms. It is important that people understand from what products we get  the biggest doses of sugar, what foods should be cut down to most. And what are the health consequences of sugar over-consumption, i.e. what else health problems one can develop except for obesity and diabetes
  2. 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.
  3. In the last decade diets low in carbohydrates and high in protein have become very popular with athletes and those wishing to lose weight.[1] [2] Perhaps the most famous of these high protein, low carbohydrate diets is the Atkins diet.[1] [3]  In normal diets, carbohydrates contained in food are converted into glucose (sugar), which is then transported around the body where it is used as a source of energy. Glucose is particularly important in  fueling the brain, and tight regulation of glucose metabolism is crucial for brain function.[4] If there is very little carbohydrate in the diet, the liver ‘makes up’ for this lack of energy by converting fats from the diet, or stored within the body, into fatty acids and ketone bodies.[5] Ketone bodies pass into the brain and replace glucose as an energy source.[5] Elevated levels of these ketone bodies in the blood is known as ketosis,[6] which has been shown to reduce the frequency of epileptic seizures, and “ketogenic” low carbohydrate diets are therefore used to treat epilepsy in children.[7]  As low carbohydrate diets force the body to burn fats rather than carbohydrates by inducing a ketogenic metabolism, this can lead to rapid weight loss[1] and improvements in cholesterol and lipid levels.[8] This is thought to also be related to the appetite suppressing action of the diet, as the high protein-content maintains feelings of ‘fullness’, reducing spontaneous food intake and decreasing overall energy intake. However ketosis can also have negative side effects, including nausea, fatigue and weakness, headache, irritability, bad or sweet-smelling breath and dehydration.[9] Diets low in carbohydrate have also been shown to impair athletic performance and endurance, despite their popularity in athletes.[10]  The Atkins program is broken down into four phases (detailed on the diet’s website[11]): Induction: Food choices are limited, focusing on protein, fat, and vegetables that are low in carbohydrates and not ‘starchy’. Protein and fat can be consumed as desired, but no more than 20g of carbohydrate can be consumed per day. Ongoing weight loss: Carbohydrate intake is gradually increased, as is food variety. Monitoring of weight and ‘carbohydrate tolerance’ is used to determine a target amount of carbohydrates to be included in the diet moving forwards. Pre-maintenance: To be started when the dieter is approximately 10lb above target weight. The carbohydrate component of the diet is gradually increased, by 10g per week. Maintenance: Once the optimum carbohydrate intake has been determined, the diet is continued indefinitely, Compared with a standard low-calorie, low-fat diet, people on the Atkins diet lose more weight in the short term (6 months) and also show improved cholesterol levels.[1] At 12 months, however,  both diets show comparable results.[1] In addition to rapid weight loss, research also suggests that people on an “Eco-Atkins” diet, which contains foods rich in vegetable fat and protein, will benefit from reduced risk factors for cardiovascular and metabolic diseases, compared to those whose diets are rich in animal fat and protein.[12] [13]  The Atkins diet has been controversial during its 40-year life span, and it is still unclear how the high amounts of animal protein and fat in the Atkins diet affect long-term health. So if you’re considering a low carbohydrate diet, perhaps you should wonder why in four decades, the Atkins diet is yet to reveal clear benefits, and perhaps consider simply reducing calorie intake and increasing your levels of exercise.   [1] Astrup, A, Meinert Larsen, T, Harper, A. (2004) Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss? Lancet. 364(9437). 897-9. [2] Cook, CM, Haub, MD. (2007). Low-carbohydrate diets and performance. Curr Sports Med Rep. 6(4). 225-9. [3] Rollo, I. (2003) Understanding the implications of adopting the Atkin’s diet. Nurs Times. 99(43). 20-1. [4] Mergenthaler, P, Lindauer, U, Dienel, GA, Meisel, A. (2013) Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 36(10). 587-97. [5] Manninen, AH. (2004) Metabolic effects of the very-low-carbohydrate diets: misunderstood “villains” of human metabolism. J Int Soc Sports Nutr. 1(2). 7-11. [6] Kesl, SL, Poff, AM, Ward, NP, Fiorelli, TN, Ari, C, van Putten, AJ, Sherwood, JW, Arnold, P, D’Agostino, DP. (2016) Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and lipoprotein levels in Sprague–Dawley rats. Nutr Metab. 13(9). [epub] doi: 10.1186/s12986-016-0069-y [7] Kossoff, EH, McGrogan, JR, Bluml, RM, Pillas, DJ, Rubenstein, JE, Vining, EP. (2006) A modified Atkins diet is effective for the treatment of intractable pediatric epilepsy. Epilepsia. 47(2). 421-4. [8] Westman, EC, Mavropoulos, J, Yancy, WS, Volek, JS. (2003) A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rev. 5(6). 476-83. [9] The Ohio State University (2008) High protein/ Low carbohydrate diets. Retrieved May 2016 from, https://patienteducation.osumc.edu/Documents/high-pro.pdf [10] Pendergast, DR, Leddy, JJ, Venkatraman, JT. (2000) A perspective on fat intake in athletes. J Am Coll Nutr. 19(3). 345-50. [11] The Atkins Diet (2016) The new atkins diet. Retrieved May 2016 from, http://uk.atkins.com/new-atkins/ [12] Jenkins, DJ, Wong, JM, Kendall, CW, Esfahani, A, Ng, VW, Leong, TC, Faulkner, DA, Vidgen, E, Greaves, KA, Paul, G, Singer, W. (2009) The effect of a plant-based low-carbohydrate ("Eco-Atkins") diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med. 169(11). 1046-54. [13] Jenkins, DJ, Wong, JM, Kendall, CW, Esfahani, A, Ng, VW, Leong, TC, Faulkner, DA, Vidgen, E, Paul, G, Mukherjea, R, Krul, ES,Singer, W. (2014) Effect of a 6-month vegan low-carbohydrate ('Eco-Atkins') diet on cardiovascular risk factors and body weight in hyperlipidaemic adults: a randomised controlled trial. BMJ Open. 4(2). e003505.  
  4. Logic would suggest that consuming fewer calories should result in weight loss, or at the very least, prevent weight gain. However, in the case of artificial sweeteners, which are lower in calories than sugar,  there is a paradox in that it has been shown that they can actually cause weight gain. Therefore, diet drinks are potentially far from the ‘healthier’ calorie-free alternative to regular drinks that they claim to be. As the artificial sweeteners present in diet drinks are now thought to contribute to the development of obesity,[1] they could in fact actually be quite unhealthy. Artificial sweeteners such as sucralose and aspartame have zero calories yet are intensely ‘sweet’ tasting, but the brain is not as easily fooled as the tongue. Artificial sweeteners provide less actual ‘sweetness’ satisfaction, and furthermore reduce the satisfaction obtained when ‘real’ sugar is consumed.[2] This can actually lead to increased carbohydrate cravings, boosting the inclination to overindulge.[2] [3] The first hints at the potential risks of artificial sweeteners arose over two decades ago when studies began revealing that they can stimulate the appetite,[4] with further investigations linking them to increased carbohydrate cravings,[3] the stimulation of fat storage[5] and weight gain.[1] One recent study that followed 474 diet soda drinkers for nearly 10 years, found that they had a staggering 400% greater increase in waist size during the 10 year study period than those who did not drink diet sodas.[6] This increased waist size is not just an aesthetic issue, it is a powerful indicator of the accumulation of visceral fat. This is a dangerous type of fat that gathers around the internal organs, and is strongly linked with type 2 diabetes and heart disease.[7] [8] In fact waist size is now considered a more powerful predictor of cardiovascular risks than body mass index (BMI).[9] However increased body weight is not the only controversial potential side effect of diet drinks. Early studies showed that some artificial sweeteners caused bladder cancer in laboratory animals, [10] although further studies failed to provide clear evidence of an association with cancer in humans, leaving the results inconclusive.[11] Reports also suggest an association between the consumption of aspartame, a widely used artificial sweetener, and neurological and behavioural reactions.[12] Aspartame has been shown to have the potential to induce serious adverse reactions, including seizures.[13]  So if you’re trying to lose weight, so-called ‘diet’ drinks may not be the healthy alternative that they claim to be. They have the potential for major metabolic, cardiovascular and neurological side effects and can actually contribute to weight gain. That being said, sugary drinks are also potentially damaging to health, so care should also be taken with their consumption. Why not opt for safe and simple water, the benefits of which are well known.   [1] Pepino, MY. (2015) Metabolic effects of non-nutritive sweeteners. Physiol Behav. 152(Pt B). 450-5. [2] Rudenga, KJ, Small. DM. (2012) Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Appetite. 58(2). 504-7. [3] Yang, Q. (2010) Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings. Yale J Biol Med. 83(2). 101-8. [4] Rogers, PJ, Blundell, JE. (1989) Separating the actions of sweetness and calories: Effects of saccharin and carbohydrates on hunger and food intake in human subjects. Physiol Behav. 45(6). 1093-9. [5] Maersk, M, Belza, A, Stødkilde-Jørgensen, H, Ringgaard, S, Chabanova, E, Thomsen, H, Pedersen, SB, Astrup, A, Richelsen, B. (2012) Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fatdepot: a 6-mo randomized intervention study. Am J Clin Nutr. 95(2). 283-9. [6] Fowler, RP, Williams, K, Hazuda, HP. (2015) Diet soda intake is associated with long-term increases in waist circumference in a biethnic cohort of older adults: the San Antonio Longitudinal Study of Aging. J Am Geriatr Soc. 63(4). 708-15 [7] Abraham, TM, Pedley, A, Massaro, JM, Hoffmann, U, Fox, CS. (2015) Association between visceral and subcutaneous adipose depots and incident cardiovascular disease risk factors. Circulation. 132(17). 1639-47.  [8] Han, TS, Lean, ME. (2016) A clinical perspective of obesity, metabolic syndrome and cardiovascular disease. JRSM Cardiovasc Dis. [epub ahead of print] doi: 10.1177/2048004016633371. [9] Bastien, M, Poirier, P, Lemieux, I,  Després, JP. (2014) Overview of epidemiology and contribution of obesity to cardiovascular disease. Prog Cardiovasc Dis. 56(4). 369-81. [10] Takayama, S, Sieber, SM, Adamson, RH, Thorgeirsson, UP, Dalgard, DW, Arnold, LL, Cano, M, Eklund, S, Cohen, SM. (1998) Long-term feeding of sodium saccharin to nonhuman primates: implications for urinary tract cancer. J Natl Cancer Inst. 90(1). 19-25. [11] Kessler, II, Clark, P. (1978) Saccharin, cyclamate and human bladder cancer. No evidence of an association. JAMA. 240(4). 349-55.  [12] Lindseth, GN, Coolahan, SE, Petros,TV, Lindseth, PD. (2014) Neurobehavioural effects of aspartame consumption. Res Nurs Health. 37(3). 185-93. [13] Maher, TJ, Wurtman, RJ. (1987) Possible neurologic effects of aspartame, a widely used food additive. Environ Health Perspect. 75. 53-7.
  5. Sugar vs salt: equal evils?

    Sugar is added to a wide variety of foods. Frozen vegetables and meat products such as sausages often contain added sugar to improve their flavour. Added sugar contains no essential nutrients and can have adverse effects on the body such as weight gain, tooth decay and cavities. High sugar intake is indeed one of the main causes of obesity in both children and adults.[1] Its high calorific value promotes increased levels of insulin which can contribute to insulin resistance and ultimately metabolic syndrome and type 2 diabetes.[1]  Added sugar is high in fructose which, compared with glucose, favours lipogenesis (the metabolic formation of fat). This in turn can contribute to hyperlipidaemia (high levels of fat in the blood) and obesity.[2] [3] Overloading the liver with fructose can also lead to non-alcohol related fatty liver disease.[4] High sugar intake is not only damaging, it can also be addictive, as demonstrated by studies performed in rats, where animals given high large amounts of sugar exhibited behavioural patterns and parallel brain changes similar to addictive drugs.[5] Thus high levels of sugar intake can promote a vicious cycle of further intake and further damage. And it’s not just a sweet tooth that can land you in trouble; excess salt is also detrimental to health. It is generally accepted that salt intake is related to ‘water retention’, however research suggests that high intake of sodium (the main constituent of salt) does not actually increase water storage, but instead induces other changes that contribute to increased blood pressure.[6] These increases can, in the long term, lead to heart disease or stroke.[7] Indeed, modest reductions in salt intake do have a significant lowering effect on blood pressure. As a result of reducing salt intake, deaths caused by stroke could be expected to decrease by approximately 14%, and coronary deaths by approximately 9% in patients with high blood pressure.[8]  There is also a correlation between high salt intake and the risk of stomach cancer,[9] although studies of other ill effects of salt have reached contradictory conclusions. Some studies show potential links to insulin resistance and metabolic syndrome,[10] but others oppose this claim.[11] It has also been suggested that high salt intake causing an elevation of urinary calcium excretion is a risk factor for osteoporosis, as any adaptive compensatory increases in calcium absorption are unlikely to be complete if diet is low in calcium.[12] However, yet again the evidence is somewhat unclear, as another study concluded that high salt intake is not an important risk factor for osteoporosis.[13] From the stated evidence, it is seemingly obvious that both sugar and salt can adversely impact on our health. We should therefore try to moderate our intake by trying to avoid processed foods that are likely to have a high content of these substances, and to reduce our use of both in our home cooking.    [1] Gross, LS, Li, L, Ford, ES, Liu, S. (2004) Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecological assessment. Am J Clin Nutr. 79(5). 774-9. [2] Havel, PJ. (2005) Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev. 63(5). 133-57. [3] Elliott, SS, Keim, NL, Stern, JS, Teff, K, Havel, PJ. (2002) Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr. 76(5). 911-22. [4] Ouyang, X, Cirillo, P, Sautin, Y, McCall, S, Bruchette, JL, Diehl, AM, Johnson, RJ, Abdelmalek, MF. (2008) Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepat. 48(6). 993-9. [5] Avena, NM, Rada, P, Hoebel, BG. (2008) Evidence for sugar addiction: behavioural and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Res. 32(1). 20-39. [6] Gavras I. & Gavras H. (2012) ‘Volume-expanded’ hypertension: the effect of fluid overload and the role of sympathetic nervous system in salt-dependent hypertension. J Hypertens. 30(4). 655–9. [7] Meneton, P, Jeunemaitre, X, de Wardener, HE, MacGregor, GA. (2005) Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. Physiol Rev. 85(2). 679-715. [8] He, FJ, MacGregor, GA. (2002) Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. J Hum Hypertens. 16(11). 761-70. [9] Wang, xq, Terry, PD, Yan, H. (2009) Review of salt consumption and stomach cancer risk: epidemiological and biological evidence. World J Gastroenterol. 15(18). 2204-13. [10] Baudrand R, et al. (2014) High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clin Endocrinol. 80(5). 677-684 [11] Garg, R, Williams, GH, Hurwitz, S, Brown, NJ, Hopkins, PN, Adler, GK. (2011) Low-salt diet increased insulin resistance in healthy subjects. Metabolism. 60(7). 965-8. [12] Heaney, RR. (2006) Role of dietary sodium in osteoporosis. J Am Coll Nutr. 25(S3). 271S-276S [13] Cohen, AJ, Roe, FJC. (2000) Review of risk factors for osteoporosis with particular reference to a possible aetiological role of dietary salt. Food and Chem Toxicol. 38(2-3). 237-53.
  6. Sweet drinks lead to soured health

    Sweet-tasting “soft” drinks are any beverage to which sugar or other low calorie sweeteners have been added. These include: Sodas Colas Fruit punch Lemonade and other fruit-flavoured carbonated drinks Sports drinks Energy drinks Sweetened, powdered drinks Fruit or veg juice  It is widely accepted that soft drinks are a major contributor to the current obesity epidemic. Levels of obesity are increasing in tandem with consumption of calorie- laden drinks, which has increased five-fold since 1950.[1] In addition to the other  negative aspects related to weight gain, increased sugar consumption may also be associated with metabolic syndrome.[2] Metabolic syndrome is the term for a cluster of risk factors including obesity, high blood pressure, elevated fasting plasma glucose, high serum triglycerides and low high-density lipoprotein.[3] This syndrome is dangerous to health, as it is linked with the development cardiovascular disease and diabetes.[4]  The calorific value of an average can of soda, cola or fruit punch is 150 calories. Most of these calories are derived from sugar, usually high-fructose corn syrup.[5] This is the equivalent of 10 teaspoons of table sugar, which, when consumed regularly, can contribute to weight gain.[5] Drinking just one can of a sugary drink per day can potentially result in a weight gain of 5 pounds in a year, assuming other calorie intake is not reduced.[5] And it isn’t just the effects on weight and metabolism that are concerning, the inherent acids and sugars in soft drinks result in dental caries and potential enamel erosion if consumed regularly.[6]  Furthermore, drinking sugary beverages does not satisfy the appetite or reduce solid food consumption, despite their high calorific value.[7] This is because fluids do not give the same satisfaction or feeling of “fullness” as solid food and the body doesn’t “register” liquid calories as it does those from solid food.[7] It is also possible that sweet-tasting drinks (whether sweetened with sugar or a low calorie substitute) actually stimulate the appetite for sweet, high carbohydrate foods. A 2014 study highlighted that consumers of sweetened drinks, even if low calorie, tended to have a generally poor diet, with increased consumption of high carbohydrate foods.[8]  Surprisingly, replacing sugary drinks with natural fruit juice is not necessarily a healthy option as although fruit juice is more nutritious, it can contains just as many calories as sugary drinks in the form of naturally occurring fruit sugars, such as fructose. Studies in both adults and children have shown that reducing sugary drink intake (including fruit juice) can lead to better weight control among those who are initially overweight,[9] and that simply replacing sugary drinks or fruit juice with water is also associated with lower long term weight gain, as a result of reduced calorie intake.[2] As well as weight control, a reduction of sugary drink intake can also result in metabolic improvements.[9]  Substituting sugary drinks for diet versions may also not be as beneficial as might be expected. Non- nutritive sweeteners (very low or zero calorie substances) used in diet versions of soft drinks are associated with numerous health risks. They are, surprisingly, known to be linked to metabolic changes and obesity,[10] and it has previously been speculated that they may increase the risk of certain types of cancer, although this theory has been discredited.[11]  Studies have shown that people who drink 1 or more ‘diet’ drinks per day are 67% more likely to develop diabetes than those who don’t drink any.[10] The established links between soft drinks and obesity, poor dental health and metabolic syndrome make a definite case for reducing intake, which could result in an improvement of overall health. The healthiest option of all? Stick to pure water instead of sweetened drinks to avoid souring your health. [1] Bray, GA, Popkin, BM. (2014) Dietary sugar and body weight: have we reached a crisis in the epidemic of obesity and diabetes?: health be damned! Pour on the sugar. Diabetes Care. 37(4). 950-6. [2] Vartanian, LR, Schwartz, MB, Brownell, KD. (2007) Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health. 97(4). 667-75. [3] Grundy, SM, Brewer, B, Cleeman, JI, Smith, SC, Lenfant, C. (2004) NHLBI/AHA Conference Proceedings. Definition of the metabolic syndrome. Circulation. 109. 433-8 [4] Grundy, SM. (2015) Metabolic syndrome update. Trends Cardiovasc Med. [Epub ahead of print] pii: S1050-1738(15)00249-2 [5] Harvard T.H. Chan School of Public Health. (2015) Sugary drinks. Retrieved April 2016, from http://www.hsph.harvard.edu/nutritionsource/healthy-drinks/sugary-drinks/  [6] Moynihan, P, Petersen, PE. (2004) Diet, nutrition and the prevention of dental diseases. Public Health Nutr. 7(1A). 201-26 [7] Pan, A, Hu, FB. (2011) Effects of carbohydrates on satiety: differences between liquid and solid food. Curr Opin Clin Nutr Metab Care. 14(4). 385-90. [8] Piernas, C, Mendez, MA, Ng, SW, Gordon-Larsen, P, Popkin, BM. (2014) Low-calorie and calorie-sweetened beverages: diet quality, food intake, and purchase patterns of US household consumers. Am J Clin Nutr. 99(3). 567-77. [9] Pan, A, Malik, VS, Hao, T, Willett, WC, Mozaffarian, D, Hu, FB. (2013) Changes in water and beverage intake and long-term weight changes: results from three prospective cohort studies. Int J Obes (Lond). 37(10). 1378-85. [10] Nettleton JA, et al. (2009) Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 32(4). 688-94. [11] Weihrauch, MR, Diehl, V. (2004) Artificial sweeteners - do they bear a carcinogen risk? Ann Oncol. 15(10). 1460-5.
  7. What is healthy artificial sweetener “Artificial sweetener” is term used for any sugar substitute used to replace sucrose (table sugar). These sugar substitutes may be synthetically manufactured or derived from chemicals that occur naturally in sources including herbs and sucrose itself. They differ from sucrose in two main respects; firstly they are known as “intense” sugars, as they are many times sweeter than traditional sugar and secondly, their calorific value is much lower, sometimes reaching zero. The fact that the quantity required for the same level of sweetness is a fraction of that of regular sugar makes sweeteners an attractive sugar substitute, both in terms of the potential for weight loss and their use by diabetics, who normally have to avoid sugar.[1] Therefore, sweeteners are widely used in processed foods including baked goods, soft drinks, canned food and dairy products, as well as being available for home use, and in cooking.    Some artificial sweeteners are considered as ‘food additives’, and are officially as such regulated by government bodies such as the European Food Safety Authority (EFSA) or the Food and Drug Administration (FDA) in the US, requiring review and approval before use. The EFSA and FDA declare a substance “generally recognised as safe” if there are sufficient scientific safety data available. However in certain cases substances may be declared safe on the basis of a long history of common use in food. Upon approval, the food safety agency establishes an acceptable daily intake (ADI) for each substance which is intended to be a lot less than the smallest amount that may result in health concerns.[2] Scrutiny of artificial sweeteners has been intense for decades. Critics believe that they cause a variety of health problems, including cancer in the case of one sweetener, saccharin, EFSA approved food additive by code E954. These concerns are mainly derived from studies performed in the 1970s which linked saccharin to bladder cancer in laboratory rats.[3] These data resulted in saccharin carrying a health warning for some time.[4] However since these initial studies, The National Cancer Institute and other health agencies have been unable to find sound scientific evidence of a link between this approved artificial sweetener and cancer,[5] [6] and the warning label on saccharin was therefore subsequently lifted in 2001.[7] Sucralose, EFSA approved food additive by code E955, an artificial sweetener marketed as Splenda®, is found in a wide variety of low calorie foods including ‘diet’ carbonated drinks, chewing gum, table top sweeteners, breakfast cereals and salad dressings. As it is intensely sweet (up to 650 times sweeter than sugar) sucralose is often mixed with other, less sweet ingredients that are not calorie free, such as dextrose or maltodextrin, to dilute its sweetness. Splenda® gained FDA approval as a table-top sweetener in 1998 and for more general use in 1999.[8] However recent studies in rats indicated that administration of Splenda®  for 12 weeks exerted numerous adverse effects, including a reduction in beneficial faecal microflora, increased faecal pH and enhanced expression of key components of the pre-systemic detoxification system involved in first class drug metabolism, known to limit the bioavailability of orally administered drugs.[9] [10]   Another artificial sweetener, aspartame, EFSA approved food additive by code E951, has also been shown to have the potential to be harmful to health. Excessive intake can lead to cell death within the brain, caused by a buildup of its key components such as aspartate in the brain, which can lead to a process called excitotoxicity.[11] Indeed, aspartame has been shown to have numerous adverse effects, a large proportion of which are serious, including seizures and death.[12] It has also been suggested that artificial sweeteners may actually increase the risk of becoming obese, and may be associated with type 2 diabetes when consumed regularly over a long period. Indeed studies have shown that people who drink 1 or more ‘diet’ drinks per day are 67% more likely to develop diabetes than those who don’t drink any.[13]  It is thought that effects such as these may be due to increased carbohydrate cravings and an inclination to overindulge.[14] [15] This is because, despite the fact that artificial sweeteners trigger more communication with the brain’s pleasure centre than sugar, artificial sweeteners provide less actual ‘sweetness’ satisfaction.[14] There are numerous adverse health effects associated with artificial sweetener intake, and seemingly minimal benefits. It may therefore be wise to avoid them and to decrease calorie intake by opting for healthier, natural alternatives.   [1] Qurrat-ul-Ain. & Khan, SA. (2015) Artificial sweeteners: safe or unsafe? J Pak Med Assoc. 65(2). 225-7. [2] EFSA (date unknown) Food Additives. Retrieved October 2016 from, https://www.efsa.europa.eu/en/topics/topic/additives   [3] Price, JM. et al. (1970) Bladder tumors in rats fed cyclohexylamin or high doses of a mixture of cyclamate and saccharin. Science. 167(3921). 1131-2. [4] NIH (2009) Artificial sweeteners and cancer. Retrieved October 2016 from, https://www.cancer.gov/about-cancer/causes-prevention/risk/diet/artificial-sweeteners-fact-sheet [5] Mishra, A. et al. (2015) Systematic review of the relationship between artificial sweetener consumption and cancer in humans: analysis of 599,741 participants. Int J Clin Pract. 69(12). 1418-26. [6] Kamenickova, A. et al. (2013) Effects of artificial sweeteners on the AhR- and GR-dependent CYP1A1 expression in primary human hepatocytes and human cancer cells. Toxicology in Vitro. 27(8). 2283-88. [7] DUJS (2008) Artificial Sweeteners: The Truth About Diet Soda. Retrieved October 2016 from, http://dujs.dartmouth.edu/2008/04/artificial-sweeteners-the-truths-and-lies-behind-diet-soda/#.WANcWOArK00 [8] Stipanuk MH. & Caudill MA. (2012) Biochemical, Physiological and Molecular Aspects of Human Nutrition. 3rd edtn. Saunders, United States [9] 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 A. 71(21). 1415-29. [10] Schiffman, SS. & Rother, KI. (2013) Sucralose, a synthetic organochlorine sweetener: overview of biological issues. J Toxicol Environ Health B Crit Rev. 16(7). 399-451. [11] Arundine, M. & Tymianski, M. (2003) Molecular mechanisms of calcium-dependent neurodegeneration in excitotoxicity. Cell Calcium. 34(4-5). 325-37. [12] Humphries, P. et al. (2008) Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. 62(4). 451-62. [13] Nettleton JA, et al. (2009) Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 32(4). 688-94. [14] Rudenga, KJ. & Small. DM. (2012) Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Appetite. 58(2). 504-7. [15] Yang, Q. (2010) Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings. Yale J Biol Med. 83(2). 101-8.          
  8. Risks and benefits of Honey vs. Sugar

    What is healthy sugar Granulated sugar, which is the most common type of sugar used for sweetening our cups of tea and coffee, consists of a mixture of 50% glucose and 50% fructose (the sugar naturally found in fruit). The pure sugar content of a 100g of granulated sugar is 99.8g, which has a calorific value of 387kcal. 100g of honey, however, has a smaller pure sugar content of 82.1g, and a lower calorific value of 304kcal. This is not the only difference, as honey is only about 30% glucose, and less than 40% fructose.[1] In addition, honey is more complex than granulated sugar, as it contains many other sugars, as well as proteins and amino acids.[2] Honey also may contain small quantities of minerals (e.g. selenium and zinc), trace elements and some vitamins.[2] This varies depending on the region from which the honey was sourced and from what plants the bees gathered nectar etc. One of the roles of our digestive system is to convert carbohydrates to glucose, for use as energy. The components of granulated sugar are broken down very easily, providing a surge in blood glucose levels.  Any excess glucose not immediately required is converted in fat and stored in the body. Many of the sugars contained in honey are more complex than those in granulated sugar, meaning that the amount of energy required to break them down into glucose is greater.[3] This can mean that the amount of calories you absorb are actually less than those from an equivalent calorific value of granulated sugar. The nutritional value of honey over and above calorific content is totally dependent on its source. It can range from being just a sugar substitute (with a slightly lower calorific value) to actually being quite nutritious. As stated above, honey contains traces of numerous vitamins and minerals,{2} which can have beneficial effects on the body. Honey has also been found to have anti-inflammatory and antiseptic properties, and to assist in the process of wound healing.[4] In fact honey is now included in some proprietary dressings. Furthermore, honey does not ‘go off’ or  deteriorate in quality over time and so has no requirement for any preservatives or any other food additives, which can themselves have adverse effects on health.[6][7][8] Whilst its relatively high sugar content means that the consumption of large quantities of honey should be avoided, its healthier composition than granulated sugar means that, as a sugar substitute, honey could be a healthier option. Furthermore, honey can have many beneficial components such as antioxidants with anticancer actions,[9] found in particularly high levels in good quality honey purchased from a reliable, genuinely organic source.   [1] USDA (2016) Full Report (All Nutrients): 19296, Honey. Retrieved April 2016, https://ndb.nal.usda.gov/ndb/foods/show/6287?fg=&man=&lfacet=&count=&max=35&sort=&qlookup=honey&offset=&format=Full&new=&measureby= [2] Bristol University (2001) Chemical composition of honey. Retrieved April 2016, from http://www.chm.bris.ac.uk/webprojects2001/loveridge/index-page3.html [3] Elia, M. & Cummings, JH. (2007) Physiological aspects of energy metabolism and gastrointestinal effects of carbohydrates. Eur J Clin Nutr. 61 Suppl 1. S40-74. [4] Postmes, TJ. et al. (1997) Speeding up the healing of burns with honey: An experimental study with histological assessment of wound biopsies In bee products. Springer, US. [5] Lay-flurrie, K. (2008) Honey in wound care: effects, clinical application and patient benefit. Br J Nurs. 17(11). S32-6. [6] Yim, E. et al.(2014) Contact dermatitis caused by preservatives. Dermatitis. 25(5). 215-31. [7] Konikowska, K. et al. (2012) The influence of components of diet on the symptoms of ADHD in children. Rocz Panstw Zakl Hig. 63(2). 127-34. [8] Vally, H. et al. (2009) Clinical effects of sulphite additives. Clin Exp Allergy. 39(11). 1643-51. [9] Ahmed, S. & Othman, NH. (2013) Honey as a potential natural anticancer agent: a review of its mechanisms. Evid Based Complement Alternat Med. [epub] doi: 10.1155/2013/829070