Fructose

We evolved with little sugar

Fructose is a toxin in excess

References

We evolved with little sugar

Sugar was never a regular, daily part of our diet as we humans evolved. The most sugar that paleolithic people and hunter-gatherers ever had was from a wild, low-sugar fruit tree that happened to be in season, or some occasional painfully-obtained honey. Sugar in the quantity that most people consume it today is toxic and causes all sorts of serious problems. (14)

Today's modern diet is high in sugars. In the USA high fructose corn syrup (HFCS) is added to almost all processed foods and drinks. In addition, the use of pesticides dramatically increases the level of sugar in the crop. A 2018 study showed that the level of fructose is increased by 40-68%. (16)

Most people (yes, the majority of people) are sugar addicted. Fructose has properties which make it a primary cause of overweight and obesity.

When you eat a starchy food or dairy food, mostly glucose and galactose are digested. They find their way into your bloodstream where a little is stored as glycogen in your muscles and liver. The remainder is stored as fat.

Extended periods of high blood glucose are responsible for today's plague of degenerative diseases (such as Alzheimer's, atherosclerosis, bacterial infections, cancers, diabetes, heart disease, kidney disease (15), mental disorders, metabolic syndrome and strokes. (9, 10, 11, 13, 14)

Fructose is a toxin in excess

The fructose component of our diets is particularly damaging. Fructose does not directly raise your blood glucose level - that is why it has a low GI (glycemic index). Low GI foods are generally a good thing, but not when the low GI is caused by fructose. You cannot metabolise fructose like most other sugars, and your cells cannot use fructose as a fuel. Instead, your liver has to dispose of all the fructose that you consume. Fructose has to be processed in a similar way to another carbohydrate, alcohol. Your liver slowly converts fructose to triglycerides and several toxic by-products. In the same way as alcohol, fructose puts a heavy load on your liver. Did you know that excessive fructose can cause liver cirrhosis? (1, 2, 3, 13)

Fructose reacts with proteins to form highly toxic and aging advanced glycation end products (AGEs). They hasten your aging, damage your skin, stiffen blood vessels and cause kidney disease. (4, 5, 6, 13, 15) Fructose also reacts with polyunsaturated oils to form toxic products. Gout, obesity, metabolic syndrome, (8, 12, 13, 14) diabetes, (8, 13, 14) Alzheimer's, (17) heart disease (12, 13, 14) and infections (7, 14) are also outcomes of a high-fructose diet.

Fructose inhibits the production of nitric oxide. Nitric oxide is an antioxidant produced by sunshine on the skin, and from a good diet. It is critical for good health. (18)

All the above assumes that you were able to digest the fructose in the first place. Most people (yes, most people) cannot properly digest all the fructose they get every day from an apparently normal and healthy diet. If you are eating large quantities of fruit thinking it's healthy, well think again. A normal healthy adult can properly digest 25-50 grams of fructose per day. Many people have difficulty digesting less than that, and a few have difficulty digesting any fructose at all. In the year 2000, the average fructose consumption per person in the USA was 79 grams per day. (14)

If you have flatulence, diarrhoea, bloating or indigestion after eating fruit or sweet foods, it is a sign of fructose malabsorption. Other symptoms that can occur within a day or two are fatigue, lack of energy / tiredness, brain fog and negative emotions.

In one study, diabetes and kidney disease were healed after two months on a ketogenic diet. (15) Basically this is a no sugar, no carbohydrate diet - but it is especially important to avoid fructose at this time.

References

1. Robert H. Lustig. Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nature clinical practice. Endocrinology & metabolism 2 (8): 447-58.

2. Isganaitis E; Lustig RH. Fast food, central nervous system insulin resistance, and obesity. 2005. Arterioscler. Thromb. Vasc. Biol. 25 (12): 2451-62.

3. Lim, Jung; Michele Mietus-Snyder, Annie Valente, Jean-Marc Schwarz and Robert H. Lustig. The role of fructose in the pathogenesis of naFlD and the metabolic syndrome. May 2010. Nature reviews. Gastroenterology & hepatology. 7 (5): 251-264.

4. Schalkwijk CG. et al. Fructose-mediated non-enzymatic glycation: sweet coupling or bad modification. Diabetes Metab Res Rev. 2004 Sept-Oct; 20(5):369-82.

5. Hipkiss AR. Dietary restriction, glycolysis, hormesis and ageing. Biogerontology. April 2007; 8(2):221-4.

6. Gaby AR. Adverse effects of dietary fructose. Alt Med Rev. Dec 2005: 10(4):294-306.

7. Bergheim I. et al. Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin. J Hepatol. June 2008; 48(6):983-92.

8. Heather Basciano, Lisa Federico, Khosrow Adeli. Fructose, insulin resistance, and metabolic dyslipidemia Nutrition & Metabolism 2005, 2:5

9. Perez-Pozo SE, Schold J, Nakagawa T, Sanchez-Lozada LG, Johnson RJ, Lillo JL. Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response. Int J Obes (Lond). 2010 Mar;34(3):454-61. Epub 2009 Dec 22.

10. Johnson RJ, Perez-Pozo SE, Sautin YY, Manitius J, Sanchez-Lozada LG, Feig DI, Shafiu M, Segal M, Glassock RJ, Shimada M, Roncal C, Nakagawa T. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. 2009 Feb;30(1):96-116. Epub 2009 Jan 16.

11. Bray GA. How bad is fructose? Am J Clin Nutr. 2007 Oct;86(4):895-6.

12. Peter Mirtschink, Jaya Krishnan, Fiona Grimm, Alexandre Sarre, Manuel Horl, Melis Kayikci, Niklaus Fankhauser, Yann Christinat, Cedric Cortijo, Owen Feehan, Ana Vukolic, Samuel Sossalla, Sebastian N. Stehr, Jernej Ule, Nicola Zamboni, Thierry Pedrazzini, Wilhelm Krek. HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease. Nature 522, 444-449 (25 June 2015) doi:10.1038/nature14508.

13. Gitanjali M. Singh, Renata Micha, Shahab Khatibzadeh, Stephen Lim, Majid Ezzati, Dariush Mozaffarian, on behalf of the Global Burden of Diseases Nutrition and Chronic Diseases Expert Group (NutriCoDE). Estimated Global, Regional, and National Disease Burdens Related to Sugar-Sweetened Beverage Consumption in 2010. CIRCULATION AHA. (AHA - American Heart Association) 114.010636. Published online before print 29 June 2015. doi: 10.1161/CIRCULATIONAHA.114.010636.

14. Loren Cordain, S Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A Watkins, James H O'Keefe, Janette Brand-Miller. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.

15. Michal M. Poplawski, Jason W. Mastaitis, Fumiko Isoda, Fabrizio Grosjean, Feng Zheng, Charles V. Mobbs. Reversal of Diabetic Nephropathy by a Ketogenic Diet. Published: 20 April 2011. doi.org/10.1371/journal.pone.0018604.

16. Matthew A. Cutulle, Gregory R. Armel, Dean A. Kopsell, Henry P. Wilson, James T. Brosnan, Jose J. Vargas, Thomas E. Hines, Rebecca M. Koepke-Hill. Several Pesticides Influence the Nutritional Content of Sweet Corn. J. Agric. Food Chem., DOI: 10.1021/acs.jafc.7b05885. Published online 12 February 2018.

17. Richard J. Johnson, Dean R. Tolan, Dale Bredesen, Maria Nagel, Laura G. Sanchez-Lozada, Mehdi Fini, Scott Burtis, Miguel A. Lanaspa, David Perlmutter. Could Alzheimer's disease be a maladaptation of an evolutionary survival pathway mediated by intracerebral fructose and uric acid metabolism? 11 January 2023, American Journal of Clinical Nutrition. DOI: 10.1016/j.ajcnut.2023.01.002.

18. Kobayashi J, Ohtake K, Uchida H. NO-Rich Diet for Lifestyle-Related Diseases. Nutrients. 2015 Jun 17;7(6):4911-37. doi: 10.3390/nu7064911. PMID: 26091235; PMCID: PMC4488823.