Skip to main content
Missouri Medicine logoLink to Missouri Medicine
. 2022 Nov-Dec;119(6):519–523.

Added Sugars Drive Insulin Resistance, Hyperinsulinemia, Hypertension, Type 2 Diabetes and Coronary Heart Disease

James J DiNicolantonio 1, James H O’Keefe 2
PMCID: PMC9762218  PMID: 36588634

The evidence incriminating insulin and carbohydrate in atherogenesis is strong, and that this scheme would link atherosclerosis with diabetes, obesity, hyperlipemia, lack of physical exercise, and, possibly, hypertension.

– Stout and Vallance–Owen 1969 1

It has been known for over 50 years that abnormal carbohydrate metabolism and elevated insulin levels drive high blood lipids.2 This is because insulin increases the endogenous synthesis of fatty acids (lipogenesis).3 Elevated levels of insulin are found in many diseases states, such as obesity, type 2 diabetes (T2D), hypertension, peripheral vascular disease, and coronary artery disease.4 In individuals who have normal blood pressure, the higher the insulin level the higher the blood pressure.57 Elevated insulin drives salt–sensitive blood pressure and precedes hypertension in many instances.8 For example, insulin resistant individuals have an impaired excretion of sodium in the urine when put on higher sodium intakes.9

Elevated insulin results in sodium and fluid retention.10, 11 Hyperinsulinemia also enhances sympathetic activity and increases plasma noradrenaline levels.1216 This enhanced sympathetic activity also stimulates the renin angiotensin system,13, 17, 18 thereby promoting further sodium retention.

Salt–sensitive hypertensive patients are more insulin resistant.19 Several studies have shown that people with normal blood pressure or high blood pressure who are salt–sensitive are hyperinsulinemic, insulin resistant or both compared to those who are salt–resistant.8, 2028 A large portion of salt–sensitive hypertensives are insulin resistant.25, 29 However, individuals who are insulin resistant still retain their sensitivity to insulin’s ability to promote urinary salt and fluid retention.30 Thus, hyperinsulinemia drives sodium and fluid retention.10, 11, 14, 3034 Improvements in insulin sensitivity via weight loss and exercise decrease salt sensitivity.35 Whatever dietary substance causes hyperinsulinemia leads to sodium and fluid retention and elevated blood pressure. It turns out that the chief dietary culprit driving hypertension may not be salt, but the other white crystal, sugar.16, 3641 Lowering the intake of refined sugars may be an effective strategy for reducing the incidence of hypertension.

Added Sugars Drive T2D and Coronary Heart Disease

The isocaloric replacement of starch, glucose, or a combination of both, with added sugars (sucrose or fructose), increases fasting insulin levels,42, 43 reduces insulin sensitivity,36, 38, 44 increases fasting glucose levels,45 increases glucose and insulin responses to a sucrose load,42, 43 and reduces cellular insulin binding.36 In other words, calorie for calorie, consuming added sugar is more harmful than starch or glucose in regards to worsening hyperinsulinemia, insulin sensitivity and glucose tolerance all of which are risk factors for cardiovascular disease.4649

Individuals who consume 10–24.9% of their calories from added sugars, have a 30% higher risk of mortality from cardiovascular disease compared to those who consume less than 10% of their calories from added sugars.50 A systematic review of 12 studies encompassing over 400,000 people found that the consumption of sugar–sweetened beverages was significantly associated with higher blood pressure and an increased incidence of hypertension.51 Globally, sugar–sweetened beverage consumption is implicated in causing approximately 180,000 deaths per year.52

A diet high in added sugars also increases the prevalence of T2D; in contrast, when sugar intake is restricted the risk of T2D is reduced.5355 In humans, when added sugar is restricted to < 5% of total caloric intake there is an approximate 50% reduction in the prevalence of prediabetes/T2D.53 Overconsuming sugar leads to fat cells that are less sensitive to the effects of insulin, which drives visceral adiposity.56, 57 Consuming a diet high in added sugars for just a few weeks increases triglycerides, uric acid, lowers high–density lipoprotein cholesterol, and alters platelet function,5861 abnormalities that are found in patients with coronary heart disease or with risk factors for coronary heart disease.6265 Conversely, lowering the amount of added sugar in the diet will improve all of these cardiovascular risk factors.42, 61 This suggests that overconsuming added sugars is a major contributor to hypertension, T2D and heart disease. Figure 1 shows the sequence of events for how the overconsumption of added sugars leads to hyperinsulinemia, hypertension, T2D, and heart disease. Figure 1 also depicts how a diet high in added sugars drives hypertension, T2D and heart disease.

Figure 1.

Figure 1

Approximately 13% of the U.S. population consumes at least 25% of their total caloric intake as added sugars.68

Over the past 200 years, the average intake of added sugars went from 4 to 120 pounds per person per year.66 In the United States, around 75% of all packaged food items or beverages contains added sugar.67 Approximately 13% of the U.S. population consumes at least 25% of their total caloric intake as added sugars68 (Figure 1). These current levels of sugar intake are fueling an epidemic of T2D, obesity, and coronary heart disease. Limiting the consumption of foods and beverages that contain added sugar would be a simple and effective strategy for improving the health of the population. One strategy that has already been implemented in the United Kingdom is a tax on sugar–sweetened beverages that contain high levels of added sugar, which has been shown to be effective among people in poorer socioeconomic circumstances.69

When it comes to health, there is nothing sweet about added sugar. Added sugars are used in approximately 75% of packaged foods in the United States.67 The average American consumes a quarter to a half pound of sugar per day.66, 70 What was once a sweet treat in the form of an apple, or a bit of wild honey, now takes a white crystalline form, and it has become a dietary staple that’s hurting the health of the population.

Book Review

The Case Against Sugar

by Gary Taubes

Among Americans, diabetes is more prevalent today than ever; obesity is at epidemic proportions; nearly 10% of children are thought to have nonalcoholic fatty liver disease. And sugar is at the root of these, and other, critical society–wide, health–related problems. The author delves into Americans’ history with sugar: its uses as a preservative, as an additive in cigarettes, the contemporary overuse of high–fructose corn syrup. He explains what research has shown about our addiction to sweets. He clarifies the arguments against sugar, corrects misconceptions about the relationship between sugar and weight loss; and provides the perspective necessary to make informed decisions about sugar as individuals and as a society.

Knopf; Illustrated edition

(December 27, 2016)

Hardcover: 384 pages

ISBN-10: 0307701646

Available on Amazon.com

graphic file with name ms119_p0519f2.jpg

Footnotes

James J. DiNicolantonio, PharmD, (left), and James H. O’Keefe, MD, (right), are at Saint Luke’s Mid America Heart Institute, Kansas City, Missouri.

Disclosure

JHO is an owner of a nutraceutical company.

References

  • 1.Stout RW, Vallance–Owen J. Insulin and atheroma. Lancet. 1969;1:1078–80. doi: 10.1016/s0140-6736(69)91711-5. [DOI] [PubMed] [Google Scholar]
  • 2.Waddell WR, Geyer RP, Hurley N, et al. Abnormal carbohydrate metabolism in patients with hypercholesterolemia and hyperlipemia. Metabolism: clinical and experimental. 1958;7:707–16. [PubMed] [Google Scholar]
  • 3.Kersten S. Mechanisms of nutritional and hormonal regulation of lipogenesis. EMBO reports. 2001;2:282–6. doi: 10.1093/embo-reports/kve071. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Elkeles RS. Insulin and atheroma. Lancet. 1969;1:1211. [PubMed] [Google Scholar]
  • 5.Manolio TA, Savage PJ, Burke GL, et al. Association of fasting insulin with blood pressure and lipids in young adults. The CARDIA study. Arteriosclerosis (Dallas, Tex) 1990;10:430–6. doi: 10.1161/01.atv.10.3.430. [DOI] [PubMed] [Google Scholar]
  • 6.Fournier AM, Gadia MT, Kubrusly DB, et al. Blood pressure, insulin, and glycemia in nondiabetic subjects. The American journal of medicine. 1986;80:861–4. doi: 10.1016/0002-9343(86)90629-7. [DOI] [PubMed] [Google Scholar]
  • 7.Falkner B, Hulman S, Tannenbaum J, et al. Insulin resistance and blood pressure in young black men. Hypertension. 1990;16:706–11. doi: 10.1161/01.hyp.16.6.706. [DOI] [PubMed] [Google Scholar]
  • 8.Sharma AM, Schorr U, Distler A. Insulin resistance in young salt–sensitive normotensive subjects. Hypertension. 1993;21:273–9. doi: 10.1161/01.hyp.21.3.273. [DOI] [PubMed] [Google Scholar]
  • 9.Facchini FS, DoNascimento C, Reaven GM, et al. Blood pressure, sodium intake, insulin resistance, and urinary nitrate excretion. Hypertension. 1999;33:1008–12. doi: 10.1161/01.hyp.33.4.1008. [DOI] [PubMed] [Google Scholar]
  • 10.DeFronzo RA, Goldberg M, Agus ZS. The effects of glucose and insulin on renal electrolyte transport. The Journal of clinical investigation. 1976;58:83–90. doi: 10.1172/JCI108463. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Baum M. Insulin stimulates volume absorption in the rabbit proximal convoluted tubule. The Journal of clinical investigation. 1987;79:1104–9. doi: 10.1172/JCI112925. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Christensen NJ. Acute effects of insulin on cardiovascular function and noradrenaline uptake and release. Diabetologia. 1983;25:377–81. doi: 10.1007/BF00282513. [DOI] [PubMed] [Google Scholar]
  • 13.Rowe JW, Young JB, Minaker KL, et al. Effect of insulin and glucose infusions on sympathetic nervous system activity in normal man. Diabetes. 1981;30:219–25. doi: 10.2337/diab.30.3.219. [DOI] [PubMed] [Google Scholar]
  • 14.O’Hare JA. The enigma of insulin resistance and hypertension. Insulin resistance, blood pressure, and the circulation. The American journal of medicine. 1988;84:505–10. doi: 10.1016/0002-9343(88)90273-2. [DOI] [PubMed] [Google Scholar]
  • 15.Izzo JL, Jr, Swislocki AL. Workshop III––Insulin resistance: is it truly the link? The American journal of medicine. 1991;90:26s–31s. doi: 10.1016/0002-9343(91)90033-t. [DOI] [PubMed] [Google Scholar]
  • 16.DiNicolantonio JJ, Lucan SC. The Wrong White Crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart. 2014;1 doi: 10.1136/openhrt-2014-000167. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Hollenberg NK. The renin–angiotensin system and sodium homeostasis. Journal of cardiovascular pharmacology. 1984;6(Suppl 1):S176–83. doi: 10.1097/00005344-198400061-00028. [DOI] [PubMed] [Google Scholar]
  • 18.DiBona GF. Neurogenic regulation of renal tubular sodium reabsorption. The American journal of physiology. 1977;233:F73–81. doi: 10.1152/ajprenal.1977.233.2.F73. [DOI] [PubMed] [Google Scholar]
  • 19.Lind L, Lithell H, Gustafsson IB, et al. Metabolic cardiovascular risk factors and sodium sensitivity in hypertensive subjects. American journal of hypertension. 1992;5:502–5. doi: 10.1093/ajh/5.8.502. [DOI] [PubMed] [Google Scholar]
  • 20.Zavaroni I, Coruzzi P, Bonini L, et al. Association between salt sensitivity and insulin concentrations in patients with hypertension. American journal of hypertension. 1995;8:855–8. doi: 10.1016/0895-7061(95)00152-F. [DOI] [PubMed] [Google Scholar]
  • 21.Sharma AM, Ruland K, Spies KP, et al. Salt sensitivity in young normotensive subjects is associated with a hyperinsulinemic response to oral glucose. Journal of hypertension. 1991;9:329–35. doi: 10.1097/00004872-199104000-00004. [DOI] [PubMed] [Google Scholar]
  • 22.Fuenmayor N, Moreira E, Cubeddu LX. Salt sensitivity is associated with insulin resistance in essential hypertension. American journal of hypertension. 1998;11:397–402. doi: 10.1016/s0895-7061(97)00490-1. [DOI] [PubMed] [Google Scholar]
  • 23.Galletti F, Strazzullo P, Ferrara I, et al. NaCl sensitivity of essential hypertensive patients is related to insulin resistance. Journal of hypertension. 1997;15:1485–91. doi: 10.1097/00004872-199715120-00017. [DOI] [PubMed] [Google Scholar]
  • 24.ter Maaten JC, Voordouw JJ, Bakker SJ, et al. Salt sensitivity correlates positively with insulin sensitivity in healthy volunteers. European journal of clinical investigation. 1999;29:189–95. doi: 10.1046/j.1365-2362.1999.00445.x. [DOI] [PubMed] [Google Scholar]
  • 25.Ferrannini E, Buzzigoli G, Bonadonna R, et al. Insulin resistance in essential hypertension. The New England journal of medicine. 1987;317:350–7. doi: 10.1056/NEJM198708063170605. [DOI] [PubMed] [Google Scholar]
  • 26.Swislocki AL, Hoffman BB, Reaven GM. Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension. American journal of hypertension. 1989;2:419–23. doi: 10.1093/ajh/2.6.419. [DOI] [PubMed] [Google Scholar]
  • 27.Pollare T, Lithell H, Berne C. Insulin resistance is a characteristic feature of primary hypertension independent of obesity. Metabolism: clinical and experimental. 1990;39:167–74. doi: 10.1016/0026-0495(90)90071-j. [DOI] [PubMed] [Google Scholar]
  • 28.Saad MF, Lillioja S, Nyomba BL, et al. Racial differences in the relation between blood pressure and insulin resistance. The New England journal of medicine. 1991;324:733–9. doi: 10.1056/NEJM199103143241105. [DOI] [PubMed] [Google Scholar]
  • 29.Shen DC, Shieh SM, Fuh MM, et al. Resistance to insulin–stimulated–glucose uptake in patients with hypertension. The Journal of clinical endocrinology and metabolism. 1988;66:580–3. doi: 10.1210/jcem-66-3-580. [DOI] [PubMed] [Google Scholar]
  • 30.Rocchini AP, Katch V, Kveselis D, et al. Insulin and renal sodium retention in obese adolescents. Hypertension. 1989;14:367–74. doi: 10.1161/01.hyp.14.4.367. [DOI] [PubMed] [Google Scholar]
  • 31.Nizet A, Lefebvre P, Crabbé J. Control by insulin of sodium potassium and water excretion by the isolated dog kidney. Pflugers Arch. 1971;323:11–20. doi: 10.1007/BF00586561. [DOI] [PubMed] [Google Scholar]
  • 32.Saudek CD, Boulter PR, Knopp RH, et al. Sodium retention accompanying insulin treatment of diabetes mellitus. Diabetes. 1974;23:240–6. doi: 10.2337/diab.23.3.240. [DOI] [PubMed] [Google Scholar]
  • 33.DeFronzo RA. The effect of insulin on renal sodium metabolism. A review with clinical implications. Diabetologia. 1981;21:165–71. doi: 10.1007/BF00252649. [DOI] [PubMed] [Google Scholar]
  • 34.Reaven GM, Hoffman BB. A role for insulin in the aetiology and course of hypertension? Lancet. 1987;2:435–7. doi: 10.1016/s0140-6736(87)90968-8. [DOI] [PubMed] [Google Scholar]
  • 35.Rocchini AP, Key J, Bondie D, et al. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. The New England journal of medicine. 1989;321:580–5. doi: 10.1056/NEJM198908313210905. [DOI] [PubMed] [Google Scholar]
  • 36.Beck–Nielsen H, Pedersen O, Lindskov HO. Impaired cellular insulin binding and insulin sensitivity induced by high–fructose feeding in normal subjects. The American journal of clinical nutrition. 1980;33:273–8. doi: 10.1093/ajcn/33.2.273. [DOI] [PubMed] [Google Scholar]
  • 37.Gutman RA, Basílico MZ, Bernal CA, et al. Long–term hypertriglyceridemia and glucose intolerance in rats fed chronically an isocaloric sucrose–rich diet. Metabolism: clinical and experimental. 1987;36:1013–20. doi: 10.1016/0026-0495(87)90019-9. [DOI] [PubMed] [Google Scholar]
  • 38.Pagliassotti MJ, Shahrokhi KA, Moscarello M. Involvement of liver and skeletal muscle in sucrose–induced insulin resistance: dose–response studies. The American journal of physiology. 1994;266:R1637–44. doi: 10.1152/ajpregu.1994.266.5.R1637. [DOI] [PubMed] [Google Scholar]
  • 39.Stanhope KL, Schwarz JM, Keim NL, et al. Consuming fructose–sweetened, not glucose–sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of clinical investigation. 2009;119:1322–34. doi: 10.1172/JCI37385. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.DiNicolantonio JJ, O’Keefe JH. Hypertension Due to Toxic White Crystals in the Diet: Should We Blame Salt or Sugar? Progress in cardiovascular diseases. 2016 doi: 10.1016/j.pcad.2016.07.004. [DOI] [PubMed] [Google Scholar]
  • 41.DiNicolantonio JJ, O’Keefe JH, Lucan SC. Added Fructose: A Principal Driver of Type 2 Diabetes Mellitus and Its Consequences. Mayo Clinic proceedings. 2015;90:372–81. doi: 10.1016/j.mayocp.2014.12.019. [DOI] [PubMed] [Google Scholar]
  • 42.Reiser S, Handler HB, Gardner LB, et al. Isocaloric exchange of dietary starch and sucrose in humans. II. Effect on fasting blood insulin, glucose, and glucagon and on insulin and glucose response to a sucrose load. The American journal of clinical nutrition. 1979;32:2206–16. doi: 10.1093/ajcn/32.11.2206. [DOI] [PubMed] [Google Scholar]
  • 43.Reiser S, Michaelis OEt, Cataland S, et al. Effect of isocaloric exchange of dietary starch and sucrose in humans on the gastric inhibitory polypeptide response to a sucrose load. The American journal of clinical nutrition. 1980;33:1907–11. doi: 10.1093/ajcn/33.9.1907. [DOI] [PubMed] [Google Scholar]
  • 44.Gutman RA, Basilico MZ, Bernal CA, et al. Long–term hypertriglyceridemia and glucose intolerance in rats fed chronically an isocaloric sucrose–rich diet. Metabolism: clinical and experimental. 1987;36:1013–20. doi: 10.1016/0026-0495(87)90019-9. [DOI] [PubMed] [Google Scholar]
  • 45.Dunnigan MG, Fyfe T, McKiddie MT, et al. The effects of isocaloric exchange of dietary starch and sucrose on glucose tolerance, plasma insulin and serum lipids in man. Clin Sci. 1970;38:1–9. doi: 10.1042/cs0380001. [DOI] [PubMed] [Google Scholar]
  • 46.Stout RW. The relationship of abnormal circulating insulin levels to atherosclerosis. Atherosclerosis. 1977;27:1–13. doi: 10.1016/0021-9150(77)90018-1. [DOI] [PubMed] [Google Scholar]
  • 47.Zavaroni I, Bonora E, Pagliara M, et al. Risk factors for coronary artery disease in healthy persons with hyperinsulinemia and normal glucose tolerance. The New England journal of medicine. 1989;320:702–6. doi: 10.1056/NEJM198903163201105. [DOI] [PubMed] [Google Scholar]
  • 48.Manolio TA, Savage PJ, Burke GL, et al. Correlates of fasting insulin levels in young adults: the CARDIA study. Journal of clinical epidemiology. 1991;44:571–8. doi: 10.1016/0895-4356(91)90221-t. [DOI] [PubMed] [Google Scholar]
  • 49.DiNicolantonio JJ, JH OK. Added sugars drive coronary heart disease via insulin resistance and hyperinsulinaemia: a new paradigm. Open Heart. 2017;4:e000729. doi: 10.1136/openhrt-2017-000729. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 50.Yang Q, Zhang Z, Gregg EW, et al. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA internal medicine. 2014;174:516–24. doi: 10.1001/jamainternmed.2013.13563. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51.Malik AH, Akram Y, Shetty S, et al. Impact of sugar–sweetened beverages on blood pressure. The American journal of cardiology. 2014;113:1574–80. doi: 10.1016/j.amjcard.2014.01.437. [DOI] [PubMed] [Google Scholar]
  • 52.Singh GMMR, Katibzadeh S, Lim S, Ezzati M, Mozaffarian D. Mortality due to sugar sweetened beverage consumption: A global, regional, and national comparative risk assessment. EPI|NPAM. 2013 [Google Scholar]
  • 53.Reiser S, Bohn E, Hallfrisch J, et al. Serum insulin and glucose in hyperinsulinemic subjects fed three different levels of sucrose. The American journal of clinical nutrition. 1981;34:2348–58. doi: 10.1093/ajcn/34.11.2348. [DOI] [PubMed] [Google Scholar]
  • 54.Basu S, Yoffe P, Hills N, et al. The relationship of sugar to population–level diabetes prevalence: an econometric analysis of repeated cross–sectional data. PloS one. 2013;8:e57873. doi: 10.1371/journal.pone.0057873. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Goran MI, Ulijaszek SJ, Ventura EE. High fructose corn syrup and diabetes prevalence: a global perspective. Global public health. 2013;8:55–64. doi: 10.1080/17441692.2012.736257. [DOI] [PubMed] [Google Scholar]
  • 56.Bruckdorfer KR, Kang SS, Yudkin J. Insulin sensitivity of adipose tissue of rats fed with various carbohydrates. The Proceedings of the Nutrition Society. 1974;33:4a–5a. [PubMed] [Google Scholar]
  • 57.DiNicolantonio JJ, Mehta V, Onkaramurthy N, et al. Fructose–induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity. Progress in cardiovascular diseases. 2018;61:3–9. doi: 10.1016/j.pcad.2017.12.001. [DOI] [PubMed] [Google Scholar]
  • 58.Bruckdorfer KR, Worcester NA, Yudkin J. Influence of diet on rat platelet aggregation. Nutr Metab. 1977;21(Suppl 1):196–8. doi: 10.1159/000176160. [DOI] [PubMed] [Google Scholar]
  • 59.Szanto S, Yudkin J. The effect of dietary sucrose on blood lipids, serum insulin, platelet adhesiveness and body weight in human volunteers. Postgraduate medical journal. 1969;45:602–7. doi: 10.1136/pgmj.45.527.602. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60.Yudkin J, Kakkar VV, Szanto S. Sugar intake, serum insulin and platelet adhesiveness in men with and without peripheral vascular disease. Postgraduate medical journal. 1969;45:608–11. doi: 10.1136/pgmj.45.527.608. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 61.Szanto S, Yudkin J. Plasma lipids, glucose tolerance, insulin levels and body–weight in men after diets rich in sucrose. The Proceedings of the Nutrition Society. 1969;28:11a–2a. [PubMed] [Google Scholar]
  • 62.Knudsen EC, Seljeflot I, Abdelnoor M, et al. Abnormal glucose regulation in patients with acute ST– elevation myocardial infarction–a cohort study on 224 patients. Cardiovascular diabetology. 2009;8:6. doi: 10.1186/1475-2840-8-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 63.Somani BL, Arora MM, Datta SK, et al. Prevalence of unsuspected glucose intolerance in coronary artery disease (CAD) patients: Importance of HbA1c. Medical journal, Armed Forces India. 2013;69:222–7. doi: 10.1016/j.mjafi.2012.11.011. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 64.Szanto S, Yudkin J. Dietary sucrose and platelet behaviour. Nature. 1970;225:467–8. doi: 10.1038/225467a0. [DOI] [PubMed] [Google Scholar]
  • 65.Blake DR, Meigs JB, Muller DC, et al. Impaired glucose tolerance, but not impaired fasting glucose, is associated with increased levels of coronary heart disease risk factors: results from the Baltimore Longitudinal Study on Aging. Diabetes. 2004;53:2095–100. doi: 10.2337/diabetes.53.8.2095. [DOI] [PubMed] [Google Scholar]
  • 66.Bray GA, Popkin BM. 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. 2014;37:950–6. doi: 10.2337/dc13-2085. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 67.Ng SW, Slining MM, Popkin BM. Use of caloric and noncaloric sweeteners in US consumer packaged foods, 2005–2009. Journal of the Academy of Nutrition and Dietetics. 2012;112:1828–34. e1–6. doi: 10.1016/j.jand.2012.07.009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68.Marriott BP, Olsho L, Hadden L, et al. Intake of added sugars and selected nutrients in the United States, National Health and Nutrition Examination Survey (NHANES) 2003–2006. Critical reviews in food science and nutrition. 2010;50:228–58. doi: 10.1080/10408391003626223. [DOI] [PubMed] [Google Scholar]
  • 69.Lean MEJ, Garcia AL, Gill T. Sugar taxation: a good start but not the place to finish. The American journal of clinical nutrition. 2018;108:435–6. doi: 10.1093/ajcn/nqy211. [DOI] [PubMed] [Google Scholar]
  • 70.Cordain L, Eades MR, Eades MD. Hyperinsulinemic diseases of civilization: more than just Syndrome X. Comparative biochemistry and physiology Part A, Molecular & integrative physiology. 2003;136:95–112. doi: 10.1016/s1095-6433(03)00011-4. [DOI] [PubMed] [Google Scholar]

Articles from Missouri Medicine are provided here courtesy of Missouri State Medical Association

RESOURCES