The TRUTH is here!

Sugar and other chemically-designed sweeteners:
​A systematic review of (>55) medical journals and peer-review studies.
Will arrive the day when bottles and cans of Soda, Diet Soda or Caffeine-and-sugar-laden Energy Drinks will have the same front as a packet of cigarette?

Warning
* if your tastebuds and brain are in constant need of sugar, if you experience dips in energy all throughout the day every day; then it is time to address your sugar needs (if not addiction). Remember sugar is a drug and coming off it is as difficult and 'painful' as Cocaine (for example). If you need help reducing your sugar intake or need more information, or a boost in motivation, please contact me today for a free telephonic assessment today!

   We can also discuss any of the articles in my newsletters to help you fully understand Stress and many of the Stress-related conditions and how far it can go...
   If you have recently been diagnosed with Type-II Diabetes or immune condition, and stressing about your new way of life, I would recommend to see me immediately, as Type-II Diabetes may be reversible if you are willing to make changes. An immune condition took years, if not decades to settle in, and might require more work but as Amy Meyer, specialist in autoimmune conditions and Thyroid Dysregulation, explains in her books, nothing is impossible 
   Type-II Diabetes is a Diet-and-Lifestyle induced condition! 

   If you have seen a health practitioner and he/she is asking for you to take pills for the rest of your life, and you are experiencing several if not all of the side-effects – while, not changing your diet or lifestyle –, then the approach is not for you, and you need to understand that you are the only one responsible for your state of health, and that you need to make change happen, with the right support. Then, and only then, will you be able to be the hero of your own journey.
   And, it all start with your own inner-conversations. Be positive and be open for change, and give yourself a chance! ​

picture source:
http://therenegadepharmacist.com/diet-coke-exposed-happens-one-hour-drinking-diet-coke-coke-zero-similar-diet-soda/?utm_content=buffer4d012&utm_medium=social&utm_source=facebook.com&utm_campaign=buffer#post/null

​And you thought you knew all about Artificial Sweeteners and that they are the best alternative to sugar? ​

If you think that using chemically-made sweeteners is the answer, you may have to think this again. Research shows that Artificial Sweeteners have the same impact on blood sugar levels and on Insulin spikes; however, like chemically-designed drugs they have side-effects too. Studies have demonstrated that sweeteners can, like sugar, be the cause of Type-II diabetes and inflammation.


 And here is the proof:

Artificial sweeteners regular use is, research shows, a leading cause of disturbed symbiotic Microbiome (the good gut bacteria), AKA Dysbiosis, a leading cause of inflammation, Obesity (including, in children), Type-II Diabetes, and subsequently autoimmune conditions

This is what we already know about sugar and High-Fructose Corn Syrup
​
"Temporal patterns over the past three to four decades have shown a close parallel between the rise in added sugar intake and the global obesity and type 2 diabetes (T2D) epidemics. Sugar-sweetened beverages (SSBs), which include the full spectrum of soft drinks, fruit drinks, energy and vitamin water drinks, are composed of naturally derived caloric sweeteners such as sucrose, high fructose corn syrup, or fruit juice concentrates. Collectively they are the largest contributor to added sugar intake in the US diet. Over the past 10 years a number of large observational studies have found positive associations between SSB consumption and long-term weight gain and development of T2D and related metabolic conditions. Experimental studies provide insight into potential biological mechanisms and illustrate that intake of SSBs increases T2D and cardiovascular risk factors. SSBs promote weight gain by incomplete compensation of liquid calories and contribute to increased risk of T2D not only through weight gain, but also independently through glycemic effects of consuming large amounts of rapidly absorbable sugars and metabolic effects of fructose."
Vasanti, SM. Frank, BH. (2012). Sweeteners and Risk of Obesity and Type 2 Diabetes: The Role of Sugar-Sweetened Beverages. Current Diabetes Reports. 12 (2), pp 195–203.

This is what research shows about Artificial Sweeteners 

"Highlights:

• Similar to sugar-sweetened beverages, artificially sweetened (diet) beverages (ASB) are linked to obesity.
• ASB may increase the risk for diabetes, metabolic syndrome, and cardiovascular disease. 
• ASB may increase the risk for negative outcomes by interfering with learning.
• Reductions in sweetener use, including low-calorie sweeteners, may be warranted

The negative impact of consuming sugar-sweetened beverages on weight and other health outcomes has been increasingly recognised; therefore, many people have turned to high-intensity sweeteners like aspartame, sucralose, saccharin as a way to reduce the risk of these consequences. However, accumulating evidence suggests that frequent consumers of these sugar substitutes may also be at increased risk of excessive weight gain, metabolic syndrome, type 2 diabetes, and cardiovascular disease. This paper discusses these findings and considers the hypothesis that consuming sweet-tasting but non-calorie or reduced-calorie food and beverages interferes with learned responses that normally contribute to glucose and energy homeostasis. Because of the interference, frequent consumption of high-intensity sweeteners may have the counterintuitive effect of inducing metabolic derangements."
Withers, SE. (2013). Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends in Endocrinology & Metabolism. 24 (9), pp. 431–441.

   "Epidemiological data have demonstrated an association between artificial sweetener use and weight gain. [...] Eighteen studies were identified. Data from large, epidemiologic studies support the existence of an association between artificially-sweetened beverage consumption and weight gain in children."
Brown, RJ. de Banate, MA. Rother, KI. (2010). Artificial Sweeteners: A systematic review of metabolic effects in youth. International Journal of Pediatric Obesity. 5 (4), pp. 305–312.

"At least daily consumption of diet soda was associated with a 36% greater relative risk of incident metabolic syndrome and a 67% greater relative risk of incident type 2 diabetes compared with nonconsumption. [...] Association between diet soda consumption and type 2 diabetes were independent of baseline measures of adiposity [fatty tissue] or changes in these measures, whereas association between diet soda and metabolic syndrome were not independent of these factors" and concluded: "Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident metabolic syndrome components and type 2 diabetes."  
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), pp. 688–694.

"Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment." writes Suez, et al (2014. p. 181), adding: "We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage."
Suez, J. et al. (2014). Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 514, pp. 181–186.

   "Since their discovery, the safety of artificial sweeteners has been controversial. Artificial sweeteners provide the sweetness of sugar without the calories. As public health attention has turned to reversing the obesity epidemic in the United States, more individuals of all ages are choosing to use these products. These choices may be beneficial for those who cannot tolerate sugar in their diets (e.g., diabetics). However, scientists disagree about the relationships between sweeteners and lymphomas, leukemias, cancers of the bladder and brain, chronic fatigue syndrome, Parkinson's disease, Alzheimer's disease, multiple sclerosis, autism, and systemic lupus."
Whitehouse, CR. Boullata, J. McCauley, LA. (2008). The Potential Toxicity of Artificial Sweeteners. Workplace Health & Safety . 56(6), pp. 251–261.

   A case-control Canadian study using 480 men and 152 women observed that using artificial sweeteners has a significant dose-response relationship for both duration and frequency of use, putting diabetics at a higher risk (33%) of bladder cancer than the normal population.
Howe, GR. et al. (1977). ARTIFICIAL SWEETENERS AND HUMAN BLADDER CANCER. The Lancet. 310(8038), pp. 578–581.

---

More References:
American Dietetic Association. (2004). Position of the American Dietetic Association: Use of nutritive and nonnutritive sweeteners. Journal of the American Dietetic Association. 104(2), pp. 255–275. Google Scholar
Arnold, DL. (1983, April). Two-generation saccharin bioassays. Environmental Health Perspectives. 50, pp. 27–36. Google Scholar
Arnold, DL. (1984). Toxicology of saccharin. Fundamental and Applied Toxicology. 4(5), pp. 674–685. Google Scholar
Aspartame Information Center. (2006). Aspartame Information Center homepage. Retrieved April 28th, 2017, from: www.aspartame.org. Google Scholar
Bellisle, F. Drewnowski, A. (2007). Intense sweeteners, energy intake and the control of body weight. European Journal of Clinical Nutrition. 61(6), pp. 691–700. Google Scholar
Beverage Institute for Health & Wellness. (2006). Beverage science Q&A: Aspartame. Retrieved April 28th, 2017, from:               www.beverageinstitute.org/ingredients/pdf/Aspartame.pdf. Google Scholar
Bigal, ME., Krymchantowski, AV. (2006). Migraine triggered by sucralose: A case report. Headache. 46(3), pp. 515–517. Google Scholar
Blumenthal, HJ. (1997). Chewing gum headaches. Headache. 37(10), pp. 665–666. Google Scholar
Butchko, HH. Stargel, WW. (2001). Aspartame: Scientific evaluation in the postmarketing period. Regulatory Toxicology and Pharmacology. 34(3), pp. 221–233. Google Scholar
Calorie Control Council. (2007, Fall). Saccharin: How sweet it is. Retrieved April 28th, 2017, from:                                                       www.saccharin.org/facts_policy.html. Google Scholar
Centers for Disease Control and Prevention. (2007). US obesity trends 1985–2006. Retrieved April 28th, 2017, from:                     www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm. Google Scholar
Dills, WL. (1989). Sugar alcohols as bulk sweeteners. Annual Review of Nutrition. 9, pp. 161–186. Google Scholar
EDInformatics. (1999). Science of cooking: Sucralose. Retrieved April 28th, 2017, from:                                                                         www.edinformatics.com/math_science/science_of_cooking/sucralose.htm. Google Scholar
European Food Safety Authority. (2007). Neotame as a sweetener and flavor enhancer: Scientific opinion of the Panel on Food Additives, Flavourings, Processing Aids and Materials in Contact with Food. Retrieved April 28th, 2017, from:
www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1178659409273.htm. Google Scholar
Ferland, A. Brassard, P. Poirier, P. (2007). Is aspartame really safer in reducing the risk of hypoglycemia during exercise in patients with type 2 diabetes? Diabetes Care. 30(7), p. 59. Google Scholar
Filer, LJ. Stegink, LD. (1988). Effect of aspartame on plasma phenylalanine concentrations in humans. In Wurtman RJ. Ritter-Walker, E. (Eds.). Dietary phenylalanine and brain function. Boston: Birkhauser. pp. 18–40.  Google Scholar
Food and Drug Administration. (2006). Artificial sweeteners: No calories…sweet! Retrieved Retrieved April 28, 2017, from:         www.fda.gov/fdac/features/2006/406_sweeteners.html. Google Scholar
Frey, GH. (1976). Use of aspartame by apparently healthy children and adolescents. Journal of Toxicology & Environmental Health. 2(2), pp. 401–415. Google Scholar
Fukushima, S. et al. (1983). Differences in susceptibility to sodium saccharin among various strains of rats and other animal species. Gann, 74(1), pp. 8–20. Google Scholar
Gallus S. et al. (2007). Artificial sweeteners and cancer risk in a network of case-control studies. Annals of Oncology. 18(1), pp. 40–44. Google Scholar
Garland, EM. et al. (1993). Effects of dietary iron and folate supplementation on the physiological changes produced in weaning rats by sodium saccharin exposure. Food & Chemical Toxicology. 31(10), pp. 689–699. Google Scholar
Grice, HC. Goldsmith, LA. (2000). Sucralose: An overview of the toxicity data. Food and Chemical Toxicology. 38(Suppl. 2), S1–S6. Google Scholar
Health Canada. (2007). Questions and answers: Saccharin. Retrieved April 28, 2017, from:
www.hc-sc.gc.ca/fn-an/securit/addit/sweeten-edulcor/saccharin_qa-qr_e.html. Google Scholar
Institute of Medicine. (2005). Dietary reference intakes for energy, carbohydrates, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Washington, DC: National Academy Press. Google Scholar
International Sweeteners Association. (2008). Saccharin fact sheet. Retrieved April 28, 2017, from:
www.sweeteners.org/pdf/fs-Saccharin_English.pdf. Google Scholar
Knopp, RH. Brandt, K. Arky, RA. (1976). Effects of aspartame in young persons during weight reduction. Journal of Toxicology and Environmental Health. 2(2), pp. 417–428. Google Scholar
Lenoir, M. Serre, F. Cantin, L. Ahmed, SH. (2007). Intense sweetness surpasses cocaine reward. Retrieved April 28, 2017, from: 
​www.pubmedcentral.nih.gov/picrender.fcgi?artid=1931610&blobtype=pdf. Google Scholar
Lieberman, HR. Caballero, B. Emde, GG. Bernstein, JG. (1988). The effects of aspartame on human mood, performance, and plasma amino acid levels. In Wurtman R. J., Ritter-Walker E. (Eds.), Dietary phenylalanine and brain function.  Boston: Birkhauser. pp. 198–200. Google Scholar
Mayhew, DA. Comer, CP. Stargel, WW. (2003). Food consumption and body weight changes with neotame, a new sweetener with intense taste: Differentiating effects of palatability from toxicity in dietary safety studies. Regulatory Toxicology and Pharmacology. 38(2), pp. 124–143. Google Scholar
Mazur, RH. (1984). Discovery of aspartame. In Stegink LD. Filer LJ. (Eds.), Aspartame: Physiology and biochemistry. New York: Marcel Dekker. pp. 3–9. Google Scholar
McLean Baird I. Shephard, NW. Merritt, RJ. Hildick-Smith, G. (2000). Repeated dose study of sucralose tolerance in human subjects. Food and Chemical Toxicology. 38(Suppl. 2), S123–S129. Google Scholar
Mukherjee, A. Chakrabarti, J. (1997). In vivo cytogenetic studies on mice exposed to acesulfame-K a non-nutritive sweetener. Food and Chemical Toxicology. 35(12), pp. 1177–1179. Google Scholar
Negro, F. Mondardini, A. Palmas, F. (1994). Hepatotoxicity of saccharin. The New England Journal of Medicine. 331(2), pp. 134–135. Google Scholar
Nofre, CC. Tinti, JM. (2000). Neotame: Discovery, properties, utility. Food Chemistry. 69, pp. 245–257. Google Scholar
O'Donnell, K. (2005). Carbohydrates and intense sweeteners. In Ashurst P. R. (Ed.), Chemistry and technology of soft drinks and fruit juices (2nd ed.), pp. 68–89. Hereford, UK: Blackwell Publishing Ltd. Google Scholar
Palese, M. Tephly, TR. (1975). Metabolism of formate in the rat. Journal of Toxicology and Environmental Health. 1(1), pp. 13–24. Google Scholar
Renwick, AG. (2006). The intake of intense sweeteners: An updated review. Food Additives and Contaminants. 23(4),  pp. 327–338. Google Scholar
Roberts, A. Renwick, AG. Sims, J. Snodin, DJ. (2000). Sucralose metabolism and pharmacokinetics in man. Food & Chemical Toxicology. 38(Suppl. 2), S31–S41. Google Scholar
Roberts, HJ. (2007). Aspartame-induced thrombocytopenia. Southern Medical Journal. 100(5), p. 543. Google Scholar
Sedova, L. et al. (2007). Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome. American Journal of Physiology-Endocrinology & Metabolism. 292(5), E1318–E1324. Google Scholar
Soffritti, M. et al. (2007). Lifespan exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats. Environmental Health Perspectives. 115(9), pp. 1293–1297. Google Scholar
Stegink, LD. (1976). Absorption, utilization, and safety of aspartic acid. Journal of Toxicology and Environmental Health. 2(1), pp. 215–242. Google Scholar
Stegink, LD. Filer, LJ. Baker, GL. (1977). Effect of aspartame and aspartate loading upon plasma and erythrocyte free amino acid levels in normal adult volunteers. Journal of Nutrition. 107(10), pp. 1837–1845. Google Scholar
Stegink, LD. Shepherd, JA. Brummel, MC. Murray, LM. (1974). Toxicity of protein hydrolysate solutions: Correlation of glutamate dose and neuronal necrosis to plasma amino acid levels in young mice. Toxicology. 2(3), pp. 285–299. Google Scholar
Stokes, AF. Belger, A. Banich, MT. Taylor, H. (1991). Effects of acute aspartame and acute alcohol ingestion upon the cognitive performance of pilots. Aviation Space & Environmental Medicine. 62(7), pp. 648–653. Google Scholar
Sweeteners Holdings, Inc. (2002). Neotame. Retrieved April 28th, 2017, from: www.neotame.com. Google Scholar
Swithers, SE. Davidson, TL. (2008). A role for sweet taste: Calorie predictive relations in energy regulation by rats. Behavioral Neuroscience. 122(1), pp. 161–173. Google Scholar
Tennant D. (2002). Estimation of food chemical intake. In Kotsonis F. N., Mackey M. A. (Eds.), Nutritional toxicology (2nd ed.), pp. 263–286. New York: Taylor & Francis. Google Scholar
Waisman, HA. Harlow, HF. (1965, February 12). Experimental phenylketonuria in infant monkeys: A high phenylalanine diet produces abnormalities simulating those of the hereditary disease. Science. 147, pp. 685–695.Google Scholar
Weihrauch, MR. Diehl, V. (2004). Artificial sweeteners: Do they bear a carcinogenic risk? Annals of Oncology. 15, pp. 1460–1465. Google Scholar
World Health Organisation. (2004). Harmonization project document no. 1 IPCS risk assessment terminology: Definition of key terms (pp. 10–15). Geneva: Author. Google Scholar

​Just in case you wandered... This simplified illustration shows the impact of regular soda consumption within one hour.
(this information has not been verified. It is just distributed for information purposes)