Tag Archives: sugar

Earlier this month, researchers from the University of Warwick published a study in Nutrition & Diabetes regarding the interaction of methylglyoxal (MG), a reactive glucose metabolite, and HDL cholesterol. HDL is universally known as “good cholesterol” and low HDL is an independent risk factor for cardiovascular disease.¹ The study’s lead author, Dr. Naila Rabbani, claims “MG damage to HDL is a new and likely important cause of low and dysfunctional HDL, and could count for up to a 10% risk of heart disease.”²

Blood MG levels increase with short-term and persistent increases in blood glucose levels.^{3, 4} MG is particularly reactive, up to 40,000 times the reactivity of glucose, but is kept in check by an enzyme called glyoxalase 1 (Glo1).⁵ To address the problems of decreased HDL by way of decreased Glo1 and elevated MG, Rabbani suggests the creation of new food supplements and drugs: “By understanding how MG damages HDL we can now focus on developing drugs that reduce the concentration of MG in the blood.”⁶

While this recent study is an important contribution to scientific literature on “good” and “bad” cholesterol, it begs the question, can’t proper nutrition negate, or at least diminish, the need for proposed new supplements and drugs? According to a 2003 USDA publication, the average American eats an estimated 32 teaspoons of sugar daily.⁷

Sugar sweetened beverages may be uniquely dangerous with respect to decreased HDL levels. A 2012 study found that each additional teaspoon of added sugar per day consumed in beverage form results in a 0.12 mg/dL decrease in HDL.⁸ Since elevated blood glucose levels are associated with elevated MG levels, cutting drastically back on sugar is a logical first step toward establishing healthier MG levels.

The Paleo Diet, of course, eschews sugar, delivering only small amounts of glucose (and fructose) via fruits and vegetables, thereby promoting optimal MG and HDL levels. Other aspects of the Paleo Diet also promote increased HDL. For example, phenolic compounds in olive oil have been shown to increase HDL.⁹ DHA, a particular variety of omega-3 abundant in seafood, increases HDL.¹⁰ Saturated fat, which is embraced by the Paleo Diet, increases HDL.¹¹

An unfortunate trajectory of medical research is the emphasis on developing products designed to address disease symptoms rather than addressing their underlying causes. If we are serious about getting healthy, we must make meaningful lifestyle changes. The diseases of modernity, including cancer, heart disease, and diabetes, are often referred to as lifestyle diseases because they are primarily caused by improper diet, smoking, and sedentary lifestyles.

Supplements and drugs are of little worth absent meaningful lifestyle changes. With respect to cholesterol, this means forgoing added sugar while eating a diet rich in animal foods and vegetables, with modest amounts of fruits, seeds, and nuts. In other words, the Paleo Diet promotes balanced cholesterol levels, making cholesterol-modifying supplements and drugs largely unnecessary.

Christopher James Clark, B.B.A.
@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

References

1. Mahdy, AK, et al. (November 2012). Cardiovascular disease risk reduction by raising HDL cholesterol–current therapies and future opportunities. British Journal of Pharmacology, 167(6). Retrieved September 18, 2014.

2. University of Warwick. (September 1, 2014). Sugar substance ‘kills’ good HDL cholesterol. Retrieved September 18, 2014.

3. Beisswenger, PJ, et al. (April 2001). α-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia. Diabetes Care, 24(4). Retreived September 18, 2014.

4. McLellan, AC, et al. (July 1994). Glyoxalase system in clinical diabetes mellitus and correlation with diabetic .omplications. Clinical Science (London), 87(1). Retrieved September 18, 2014.

5. Thornalley, PJ. (December 2003). Glyoxalase I–structure, function and a critical role in the enzymatic defence against glycation. Biochemical Society Transactions, 31(6). Retrieved September 18, 2014.

6. Ibid, University of Warwick.

7. United States Department of Agriculture, Agriculture Fact Book 2001–2002, March 2003, Office of Communications. Retrieved September 18, 2014.

8. Welsh, JA, et al., (April 2012). The association between sugar intake and HDL levels varies by sugar type and source. The FASEB Journal, 26(Supplement). Retrieved September 18, 2014.

9. Covas, MI, et al., (September 2006). The Effect of Polyphenols in Olive Oil on Heart Disease Risk Factors. Annals of Internal Medicine, 145(5). Retrieved September 18, 2014.

10. Bernstein, AM, et al. (January 2012). A meta-analysis shows that docosahexaenoic acid from algal oil reduces serum triglycerides and increases HDL-cholesterol and LDL-cholesterol in persons without coronary heart disease. Journal of Nutrition, 142(1). Retrieved September 18, 2014.

11. Hayek, T, et al., (April 1993). Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice. Journal of Clinical Investigation, 91(4). Retrieved September 18, 2014.

It’s still mostly fructose.

As I mentioned in my lecture on the realities of food addiction, I am often asked whether honey, a common staple in contemporary Paleo Diets, is beneficial. Typically I recommend a diet low in sugar to most clients, because of the addictive and rewarding properties of the substance.¹ This means honey, which is mostly sugar,² typically gets the “thumbs down” as well. In fact, honey is about 40% fructose, 200% sweeter than glucose, which is found in less sweet carbohydrate sources, and can be used by every cell in your body for energy.³

This is in contrast to fructose, which largely gets handled by the GLUT5 transporter, and is almost entirely cleared in the liver.⁴

Fructose does not raise insulin levels,⁵ reduces leptin (your satiety hormone)⁶ and has many parallels with ethanol (alcohol).⁷ With honey being the food single-handedly highest in fructose, only behind soda and applesauce,⁸ it is generally a good idea to limit intake in today’s modern obesogenic environment.⁹

However, hunter-gatherers have traditionally sought out honey,¹⁰ often enduring great risks to procure the substance.¹¹ While researchers state honey is the most energy dense food in nature,¹², carbohydrate and protein contain 4.1 kcal/gm, Fats (acylglycerols) ~ 8.8 kcal/gm depending upon the acyl group, and ethanol 6.9 kcal/gm. Accordingly, honey contains almost carbohydrate entirely and, therefore, has a caloric density roughly half that of fats. Hence, honey is not the most energy dense food in nature, but rather fat. Hunter gatherers acquired fat (triacylglycerols) from both plant and animal food sources. Concentrated animal triacylglycerol sources include marrow, subcutaneous fat, perinephral fat, mesenteric fat, and retro-orbital fat. Brain, a highly favored food does not contain triacylglycerols but rather is a rich source of fatty acids contained in the phospholipid fraction and, therefore, remains more energetically dense than carbohydrate. Certain plant foods including nuts, some seeds, olives and avocadoes are rich sources of monounsaturated fatty acids. But, honey was a favored food of hunter-gatherers. The Hadza of Tanzania rank honey as their favorite food.¹³

Also of note, is a study barely a week and half old, which describes diet-dependent gene expression in honey bees.¹⁴ This study details the gene expression, which vastly differs between bees fed honey, and those fed either sucrose or high fructose corn syrup (HFCS). This study points out key differences in the gene expression effects of a natural food like honey, compared to man-made creations.

Since it was traditionally thought that bees would respond equally to table sugar and HFCS, as they would to honey, this study is of vast importance, showing the differential responses, genetically, that bees exhibit. This has potential translational implications for humans,¹⁵ which is vital in the obesity pandemic,¹⁶ and the metabolically diseased state,¹⁷ in which we currently live.

Could a simple replacement of natural sweeteners, like honey, with man-made creations, like HFCS, be a potential cause of genetic changes?¹⁸ It seems possible. However, we must proceed with caution, and never base any substantial conclusions on one study, especially when it was not performed on human beings. This study is also supported by another recent finding that HFCS-rich diets may be partially to blame for collapsing bee colonies.¹⁹

Interestingly, some studies have shown honey may instead have potentially “obesity protective” effects.²⁰ This is based on observations in responses to the hormone ghrelin and peptide YY (3-36).²¹ In another study, researchers showed that honey has a gentler effect on blood sugar levels on a per gram basis, at least when compared with sucrose.²²

However, to me, this doesn’t change the biochemistry of fructose, of which honey is largely comprised. It makes more sense to eat whole fruit, starchy sources of carbohydrate and vegetables. It is true that the metabolism and neurochemical responses of pure fructose, such as those used in many studies, may be slightly different than the fructose found in honey. But, in practice, humans consume sweet foods with complete abandon,²³ whether it’s man-made or natural.²⁴ Keep honey as a rare treat, as our hunter-gatherer ancestors (seasonally) did.²⁵ This will limit reward to your brain, which will help to limit more reward-seeking behaviors.²⁶

References

1. Lustig RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013;4(2):226-35.

2. Available at: http://nutritiondata.self.com/facts/sweets/5568/2. Accessed July 23, 2014.

3. Petelinc T, Polak T, Jamnik P. Insight into the molecular mechanisms of propolis activity using a subcellular proteomic approach. J Agric Food Chem. 2013;61(47):11502-10.

4. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010;90(1):23-46.

5. Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 2009;139(6):1257S-1262S.

6. Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008;295(5):R1370-5.

7. Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

8. Available at: http://nutritiondata.self.com/foods-000011000000000000000.html. Accessed April 12, 2014.

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

10. Douard V, Ferraris RP. Regulation of the fructose transporter GLUT5 in health and disease. Am J Physiol Endocrinol Metab. 2008;295(2):E227-37.

11. Marlowe FW, Berbesque JC, Wood B, Crittenden A, Porter C, Mabulla A. Honey, Hadza, hunter-gatherers, and human evolution. J Hum Evol. 2014;71:119-28.

12. Eteraf-oskouei T, Najafi M. Traditional and modern uses of natural honey in human diseases: a review. Iran J Basic Med Sci. 2013;16(6):731-42.

13. Available at: http://www.epjournal.net/articles/sex-differences-in-food-preferences-of-hadza-hunter-gatherers/. Accessed July 23, 2014.

14. Diet-dependent gene expression in honey bees: honey vs. sucrose or high fructose corn syrup. Scientific Reports. 2014;4

15. Purnell JQ, Klopfenstein BA, Stevens AA, et al. Brain functional magnetic resonance imaging response to glucose and fructose infusions in humans. Diabetes Obes Metab. 2011;13(3):229-34.

16. Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

17. Owens S, Galloway R. Childhood obesity and the metabolic syndrome. Curr Atheroscler Rep. 2014;16(9):436.

18. Brown RJ, De banate MA, Rother KI. Artificial sweeteners: a systematic review of metabolic effects in youth. Int J Pediatr Obes. 2010;5(4):305-12.

19. Mao W, Schuler MA, Berenbaum MR. Honey constituents up-regulate detoxification and immunity genes in the western honey bee Apis mellifera. Proc Natl Acad Sci USA. 2013;110(22):8842-6.

20. Erejuwa OO, Sulaiman SA, Wahab MS. Honey–a novel antidiabetic agent. Int J Biol Sci. 2012;8(6):913-34.

21. Larson-meyer DE, Willis KS, Willis LM, et al. Effect of honey versus sucrose on appetite, appetite-regulating hormones, and postmeal thermogenesis. J Am Coll Nutr. 2010;29(5):482-93.

22. Shambaugh P, Worthington V, Herbert JH. Differential effects of honey, sucrose, and fructose on blood sugar levels. J Manipulative Physiol Ther. 1990;13(6):322-5.

23. Bray GA. Fructose: should we worry?. Int J Obes (Lond). 2008;32 Suppl 7:S127-31.

24. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

25. Pontzer H, Raichlen DA, Wood BM, Mabulla AZ, Racette SB, Marlowe FW. Hunter-gatherer energetics and human obesity. PLoS ONE. 2012;7(7):e40503.

26. Volkow ND, Wang GJ, Fowler JS, Tomasi D, Baler R. Food and drug reward: overlapping circuits in human obesity and addiction. Curr Top Behav Neurosci. 2012;11:1-24.

On a scientific level, can food be addictive?¹ The short answer, is yes.² Food addiction is widespread,³ from the increasing obesity pandemic,⁴ to junk food marketing slogans like “I bet you can’t eat just one,”⁵ to the global popularity of coffee chains. But what makes food addictive? There are many factors involved,⁶ as humans are not only highly individualistic (what may be addictive for me, may not be addictive for you),⁷ but our environment has become hyper-stimulatory and obesogenic.⁸

Couple this with the fact processed foods have long-since been manufactured to promote overconsumption,^{9, 10} and you have a recipe for disaster. As if you needed more reasons to adopt a Paleo Diet, I hope to provide a brief insight into the questions behind food addiction, both scientifically and environmentally. However, for those more curious, I am currently lecturing nationwide on this topic, with a video of my lecture and my entire slideshow, embedded below.

Nearly all of us can empathize with the fact that sugar, junk food and fast food are all undeniably addictive.^{11, 12, 13} In a neuroscience study from 2010, researchers showed not only a disruption of sensitivity to brain-stimulation reward (BSR) from eating high fat and/or high carbohydrate food, but also an insensitivity to adverse consequences from consuming the food.¹⁴ This means we become both accustomed to the rewarding neurochemical effects of food and also seek out these foods, even when we know there will be harmful consequences.¹⁵ These are two behavioral aspects, which are also exhibited in drug addiction,¹⁶ reinforce studies showing the neurophysiology of food addiction overlaps with drug addiction,¹⁷ specifically via the nucleus accumbens, and the downregulation of D2 (dopamine) receptors.¹⁸

Taken together, the data supports the notion that obesity and drug addiction may arise from similar neuroadaptive responses in brain reward circuitries.¹⁹ In another study, researchers posit that intense sweetness from food surpasses cocaine reward.

Our findings clearly demonstrate that intense sweetness can surpass cocaine reward, even in drug-sensitized and -addicted individuals. We speculate that the addictive potential of intense sweetness results from an inborn hypersensitivity to sweet tastants. In most mammals, including rats and humans, sweet receptors evolved in ancestral environments poor in sugars and are thus not adapted to high concentrations of sweet tastants. The supranormal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction. ²⁰

In another interesting study, Oreo cookies were found to be as addictive as cocaine.²¹ In a different study, obese subjects showed greater activation in the bilateral hippocampus/parahippocampal gyrus, but lean subjects showed more activation in the posterior insula portion of the brain.²² Some scientists have speculated that exorphins from food may have lead humans to initially adopt agriculture,²³ which was a more laborious and challenging way of life.

Cereals and dairy foods are not natural human foods, but rather are preferred because they contain exorphins. This chemical reward was the incentive for the adoption of cereal agriculture in the Neolithic. Regular self-administration of these substances facilitated the behavioural changes that led to the subsequent appearance of civilisation.

Other studies have delved into the rewarding properties of both high caloric, and neurologically rewarding foods, such as chocolate.²⁴ Take note of the following image, illustrating how chocolate ‘cravers’ elicit completely different responses, neurologically, than ‘non-cravers.’

In addition to ‘craving,’ there is a host of activity seen within the human brain, in response to rewarding foods or food-based cues.²⁵ Activity is seen in the orbitofrontal cortex, amygdala, insula, nucleus accumbens, dorsal striatum, and many other regions.

It’s fascinating that genetic vulnerabilities can increase predisposition to both obesity and drug addiction. This should come as no surprise to those who are well-versed in science. Oftentimes genetics and environment converge to cause dysfunction, both neurologically and physically.²⁶ As stated by researchers:²⁷

Neuroimaging studies in obese subjects provide evidence of altered reward and tolerance. Once obese, many individuals meet criteria for psychological dependence. Stress and dieting may sensitize an individual to reward. Finally, fast food advertisements, restaurants and menus all provide environmental cues that may trigger addictive overeating.

So how does one avoid addiction to food? The simplest method is to adopt a Paleo Diet. Then you will be avoiding processed foods, which are (by nature) addictive,²⁸ since food chemists utilize a technique termed ‘the bliss point’ to keep consumers coming back for more. You will also be avoiding the opioid peptides found in dairy,²⁹ as well as the opioid peptides found in grains.³⁰ Enjoy real foods, and watch your health soar, as your addictions to sugar and other rewarding chemicals,³¹ vanish.

Is Food Addictive from PaleoHacks

References

1. Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept?. Obes Rev. 2013;14(1):19-28.

2. Liu Y, Von deneen KM, Kobeissy FH, Gold MS. Food addiction and obesity: evidence from bench to bedside. J Psychoactive Drugs. 2010;42(2):133-45.

3. Fortuna JL. The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs. 2012;44(1):56-63.

4. Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC. The obesity pandemic: where have we been and where are we going?. Obes Res. 2004;12 Suppl 2:88S-101S.

5. Bernhardt AM, Wilking C, Adachi-mejia AM, Bergamini E, Marijnissen J, Sargent JD. How television fast food marketing aimed at children compares with adult advertisements. PLoS ONE. 2013;8(8):e72479.

6. Pedram P, Wadden D, Amini P, et al. Food addiction: its prevalence and significant association with obesity in the general population. PLoS ONE. 2013;8(9):e74832.

7. Heber D, Carpenter CL. Addictive genes and the relationship to obesity and inflammation. Mol Neurobiol. 2011;44(2):160-5.

8. Berthoud HR. The neurobiology of food intake in an obesogenic environment. Proc Nutr Soc. 2012;71(4):478-87.

9.Gearhardt AN, White MA, Potenza MN. Binge eating disorder and food addiction. Curr Drug Abuse Rev. 2011;4(3):201-7.

10. Available at: http://courses.bio.indiana.edu/L104-Bonner/F12/imagesF12/L8/BlissPoint.html. Accessed July 17, 2014.

11. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

12. Gearhardt AN, Grilo CM, Dileone RJ, Brownell KD, Potenza MN. Can food be addictive? Public health and policy implications. Addiction. 2011;106(7):1208-12.

13. Blumenthal DM, Gold MS. Neurobiology of food addiction. Curr Opin Clin Nutr Metab Care. 2010;13(4):359-65.

14. Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

15. Parylak SL, Koob GF, Zorrilla EP. The dark side of food addiction. Physiol Behav. 2011;104(1):149-56.

16. Avena NM, Bocarsly ME, Hoebel BG, Gold MS. Overlaps in the nosology of substance abuse and overeating: the translational implications of “food addiction”. Curr Drug Abuse Rev. 2011;4(3):133-9.

17. Meule A. Are certain foods addictive?. Front Psychiatry. 2014;5:38.

18. Halpern CH, Tekriwal A, Santollo J, et al. Amelioration of binge eating by nucleus accumbens shell deep brain stimulation in mice involves D2 receptor modulation. J Neurosci. 2013;33(17):7122-9.

19. Kenny PJ. Reward mechanisms in obesity: new insights and future directions. Neuron. 2011;69(4):664-79.

20. Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS ONE. 2007;2(8):e698.

21. Levy A, Salamon A, Tucci M, Limebeer CL, Parker LA, Leri F. Co-sensitivity to the incentive properties of palatable food and cocaine in rats; implications for co-morbid addictions. Addict Biol. 2013;18(5):763-73.

22. Bragulat V, Dzemidzic M, Bruno C, et al. Food-related odor probes of brain reward circuits during hunger: a pilot FMRI study. Obesity (Silver Spring). 2010;18(8):1566-71.

23. Available at: http://www.ranprieur.com/readings/origins.html. Accessed April 11, 2014.

24. Asmaro D, Liotti M. High-caloric and chocolate stimuli processing in healthy humans: an integration of functional imaging and electrophysiological findings. Nutrients. 2014;6(1):319-41.

25. Kenny PJ. Reward mechanisms in obesity: new insights and future directions. Neuron. 2011;69(4):664-79.

26. Tsuang MT, Stone WS, Faraone SV. Genes, environment and schizophrenia. Br J Psychiatry Suppl. 2001;40:s18-24.

27. Garber AK, Lustig RH. Is fast food addictive?. Curr Drug Abuse Rev. 2011;4(3):146-62.

28. Ifland JR, Preuss HG, Marcus MT, et al. Refined food addiction: a classic substance use disorder. Med Hypotheses. 2009;72(5):518-26.

29. Kurek M, Przybilla B, Hermann K, Ring J. A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy Immunol. 1992;97(2):115-20.

30. Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides. 1984;5(6):1139-47.

31. Blum K, Liu Y, Shriner R, Gold MS. Reward circuitry dopaminergic activation regulates food and drug craving behavior. Curr Pharm Des. 2011;17(12):1158-67.

Your book was recommended to me by a certified nutritionist/pharmacist, who has known me since 1990. May 2001, I was diagnosed with breast cancer-infiltrating, T1, node negative. I had a lumpectomy, chemotherapy and radiation. I was cancer free until March 2004 when it returned to my spine, the L-1 disk. After weekly rounds of chemotherapy for six months at Duke University, followed up with five weeks of radiation, I was finally in remission. Tumor markers on April 8 were 89.6. By December 15 they had dropped to 22.

Every three weeks I receive Herceptin and Zometa every three months. Since December 15 until May 21, we noticed a trend of my tumor markers rising: 22 to 28.4.

After talking with my certified nutritionist/pharmacist, who knows of all the drugs I am on, he recommended your diet. I started it immediately on May 26. My latest tumor marker of July 21 was 26. I am looking forward to the next tumor marker test in early September to see if this downward trend continues. I am convinced that sugar negatively affects my body and probably feeds the cancer. In addition, I have lost 12 pounds of the 25 pounds that I put on due to chemotherapy and radiation. I am 5’11” and weighed 163 prior to my first cancer treatment in 2001. I am now 10 pounds from my goal.

Thank you for a succinctly written book.

Debbie

LOREN CORDAIN, PH.D.

Tag Archives: sugar

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