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In the last decade diets low in carbohydrates and high in protein have become very popular with athletes and those wishing to lose weight.  Perhaps the most famous of these high protein, low carbohydrate diets is the Atkins diet.  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. 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. Ketone bodies pass into the brain and replace glucose as an energy source. Elevated levels of these ketone bodies in the blood is known as ketosis, which has been shown to reduce the frequency of epileptic seizures, and “ketogenic” low carbohydrate diets are therefore used to treat epilepsy in children. 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 and improvements in cholesterol and lipid levels. 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. Diets low in carbohydrate have also been shown to impair athletic performance and endurance, despite their popularity in athletes. The Atkins program is broken down into four phases (detailed on the diet’s website): 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. At 12 months, however, both diets show comparable results. 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.  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.  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.  Cook, CM, Haub, MD. (2007). Low-carbohydrate diets and performance. Curr Sports Med Rep. 6(4). 225-9.  Rollo, I. (2003) Understanding the implications of adopting the Atkin’s diet. Nurs Times. 99(43). 20-1.  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.  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.  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  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.  Westman, EC, Mavropoulos, J, Yancy, WS, Volek, JS. (2003) A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rev. 5(6). 476-83.  The Ohio State University (2008) High protein/ Low carbohydrate diets. Retrieved May 2016 from, https://patienteducation.osumc.edu/Documents/high-pro.pdf  Pendergast, DR, Leddy, JJ, Venkatraman, JT. (2000) A perspective on fat intake in athletes. J Am Coll Nutr. 19(3). 345-50.  The Atkins Diet (2016) The new atkins diet. Retrieved May 2016 from, http://uk.atkins.com/new-atkins/  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.  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.
What is healthy diet Sweeteners, used as sugar replacements, are compounds that are so intensely sweet that only a little is needed to replace a larger amount of sugar. They are available in two forms: natural sweeteners of plant origin and synthetic, artificial sweeteners. Natural sweeteners include glycyrrhizin, thaumatins, rabaudioside, stevioside, monellin, perillaldehyde and osladin. Another natural product, miraculin, is not actually sweet, but transforms our perception of sour taste into sweet taste. Artificial, or synthesised, sweeteners include aspartame, saccharin, acesulfame K and sucralose. Among all sweeteners, artificial sweeteners are consider the worst for us, as they are thought to impact on our health, despite artificially sweetened products often being advertised as “diet” alternatives thanks to their reduced calorie content. This ‘diet’ label comes from old studies that showed artificially sweetened products can assist in weight loss and weight maintenance. However, although sweeteners provide intense sweetness with minimal or no calories, studies suggest that they may actually increase appetite. This can actually lead to increased carbohydrate cravings, boosting the inclination to overindulge.  Some studies have also showed that artificially sweetened drinks are linked with an increased incidence of Type 2 Diabetes, although no causal link was identified. One study of 3,682 individuals examined the long-term (7-8 year) relationship between ‘diet’ drink consumption and body weight. Even after adjusting for other weight-gain risk factors (such as exercise and diet), results showed that those who regularly consumed ‘diet’ drinks had a 47% higher BMI increase across the follow-up period than those who did not. Another recent study that followed 474 diet soda drinkers for nearly 10 years, found that their waists grew 70% more than the waists of non-diet soda drinkers. In addition, those who drank two or more diet sodas per day had, on average, nearly 4 times the increase in waist size during the 10 year study period compared to non-diet soda drinkers. These effects are thought to potentially stem from the way that artificial sweeteners and sugar affect the brain. By providing sweetness without any calories, it is thought that consumption of artificial sweeteners can cause us to crave other sweet foods and drinks, which can contribute to excess calorie consumption. This is because artificial sweeteners provide less ‘sweetness satisfaction’, and actually reduce the ‘reward’ obtained when going on to consume actual sugar. This means that, not only does the artificial sweetener not fully satisfy sweetness cravings, it also reduces how rewarding actual sugar is, and thus more is ingested. This is further supported by results from a study at the University of California, San Diego, in which volunteers underwent functional MRI scans as they took small sips of water sweetened with sugar or sucralose. Sugar activated regions of the brain involved in food reward, while sucralose didn’t. In addition to these effects on carbohydrate cravings and weight gain, reports also suggest an association between the consumption of aspartame, a widely used artificial sweetener, and neurological and behavioural reactions. Furthermore, aspartame has also been shown to have the potential to induce serious adverse reactions, including seizures. Thus when trying to be healthy, opting for ‘diet’ options may not be the quick fix it first seems. Not only can artificial sweeteners cause numerous health problems, they can also actively contribute to weight gain, increased BMI and the development of type 2 diabetes. These sweeteners are therefore perhaps not so sweet after all.  Sardesai, VM. & Waldshan, TH. (1991) Natural and synthetic intense sweeteners. J Nutr Biochem. 2(5). 236-44.  Bellisle, F. & Drewnowski, A. (2007) Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 61(6). 691-700.  Rudenga, KJ. & Small. DM. (2012) Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Appetite. 58(2). 504-7.  Yang, Q. (2010) Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings. Yale J Biol Med. 83(2). 101-8.  Fagherazzi, G. et al. (2013). Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidemiologique aupres des femmes de la Mutuelle Generale de l'Education Nationale-European Prospective Investigation into Cancer and Nutrition cohort. Am J Clin Nutr. 97(3). 517-23.  Fowler, SP. et al. (2008) Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 16(8). 1894-900.  Fowler, RP. et al. (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  Frank, GK. et al. (2008) Sucrose activates human taste pathways differently from artificial sweetener. Neuroimage. 39(4). 1559-69.  Lindseth, GN. et al. (2014) Neurobehavioural effects of aspartame consumption. Res Nurs Health. 37(3). 185-93.  Maher, TJ. & Wurtman, RJ. (1987) Possible neurologic effects of aspartame, a widely used food additive. Environ Health Perspect. 75. 53-7.