Tag Archives: fructose

Obesity | The Paleo Diet

Unfortunately, 70% of the United States is now overweight.1 And nearly half of that 70% is obese – a truly scary prospect for the future of our nation’s health.2 But despite this alarming obesity epidemic (technically it is a pandemic, because the entire world is suffering from this problem) there has never been more debate about what exactly is causing the issue.3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 While this article will cover specific transcription factors and antioxidant pathways, the big bullet points for preventing obesity are simple.26 27 28 29 30 31 32 33 34 35

For starters, we are eating too many calories.36 37 38 39 Secondly, we are eating too much sugar and not enough nutrients.40 41 42 43 44 45 46 47 48 49 50 Third, we are not getting enough exercise.51 52 53 And lastly, we are stressed like never before, and sleeping less than ever.54 55 56 57 58 59 In a way, the rest of the debate is just minutia, because until we fix these four problems, we are not going to be able to stop this boat from capsizing.

Booth FW, Laye MJ. Lack of adequate appreciation of physical exercise’s complexities can pre-empt appropriate design and interpretation in scientific discovery. J Physiol. 2009;587:5527–5539.

But if we are to delve into the details of obesity, there are two dichotomous factors, which are at play. As I mentioned, too much sugar is a cornerstone of our nation’s various health problems. The fructose transporter GLUT5 plays a specific role in this problem, since we are taking in far too much fructose in our collective diet.60 61 62 63 64 By contrast, if we were to eat more vegetables and other healthful foods, we would see better results via the Nrf2 pathway.65 66 67 68 69 70 Most of us are aware that free radicals are categorized as ‘bad’ and antioxidants as ‘good’.71 But the details behind these scientific terms remain elusive, for most of the population.

Evolution of the consumption of high-fructose corn syrup (HFCS) and sucrose in the United States between 1970 and present. HFCS has increased rapidly to replace 50% of the sucrose consumption. Over this period, not only total sugar consumption but also total calorie intake and total fat intake have increased significantly. (USDA)

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Fructose metabolism in liver cells. Fructose metabolism (grey arrows) differs from glucose (black arrows) due to 1) a nearly complete hepatic extraction and 2) different enzyme and reactions for its initial metabolic steps. Fructose taken up by the liver can be oxidized to CO2 and then converted into lactate and glucose; glucose and lactate are subsequently either released into the circulation for extrahepatic metabolism or converted into hepatic glycogen or fat. The massive uptake and phosphorylation of fructose in the liver can lead to a large degradation of ATP to AMP and uric acid.60

Summary of the potential mechanisms for fructose-induced insulin resistance.60

The research on fructose has been steamrolling the scientific community since the viral popularity of pediatric endocrinologist Robert Lustig’s lecture, a few years ago.72 73 74 75 Not surprisingly, the food and beverage industry is trying like mad to stop any bad publicity from arising from the scientific community, around their sugary cash cow.76 But the actual, unbiased data has been very damning.77 78 79 80 Take the following chart, which shows that fructose in beverages, which do not list it on the label, often contain quantities of fructose that surpass the amount of the substance in beverages which do list it on the label.

Fructose concentration and fructose-to-glucose (F:G) ratio: juices. Concentration of fructose (g/L) in juices is displayed on the left y axis (open bars) and the F:GAdjusted is shown on the right y axis (solid bars). * Products with high-fructose corn syrup listed as an ingredient on the label. F:GAdjusted, the F:G ratio adjusted for other detected disaccharides.

Walker, R.W.; Dumke, K.A.; Goran, M.I. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition 2014, 30, 928–935.

In an evolutionary sense, this level of fructose consumption is out of control and unprecedented.81 82 83 We’ve known for thousands of years, humans consumed about 20g of fructose each day.84 85 Their intake came from fruit and honey,86  vastly different than more concentrated sources of fructose, like soda. For one thing – there is no fiber in soda, which might slow down hepatic absorption of fructose. Oh, and for those curious, we are now consuming about 80g of fructose per day, on average.87 88

Proposed pathways and mechanisms underlying the differential effects of fructose compared with glucose consumption on adipose deposition, postprandial lipid metabolism glucose tolerance/insulin sensitivity.

Stanhope, K. L., & Havel, P. J. (2010). Fructose consumption: Recent results and their potential implications. Annals of the New York Academy of Sciences, 1190, 15–24. doi:10.1111/j.1749-6632.2009.05266.x

But why is fructose so harmful, and how does the GLUT5 transporter factor into this issue? GLUT5 was successfully cloned around 20 years ago and was initially described as a glucose transporter, until it became clear that it was specifically related to fructose.89 The brain and kidneys have both shown levels of GLUT5 mRNA and/or protein.90 This (indirectly) means that by eating too much fructose, your brain processes might be impaired.91 92 93 Since we now know that high levels of HA1c correlate with dementia, this shouldn’t be shocking news.94

Your small intestine has the greatest amount of GLUT5, and it also controls the availability of fructose to other areas.95 Interestingly, intestinal GLUT5 mRNA levels and fructose transport rates are very low until fructose is introduced, or after a few weeks of development (this appears to be genomic).96 97 98 99 The problems start to arise when too much fructose is introduced (via processed foods, usually) too early, creating a baseline of consumption, which seems to need to be satisfied.100 101 102 103 Though the science is still out, this ‘created need’ may force children to overeat, and as a result, become overweight and/or obese.

The GLUT5 transporter has been linked to hypertension, and also to diabetes.104 105 Since the United States spends over $240 billion on diabetes annually, scientific research into the area of GLUT5 should be pushed to the forefront, with the hope being that by better understanding the transport and processing of fructose, we can help improve the rates of disease – if not prevent them entirely.106

For example, diabetes profoundly affects GLUT5 expression in the small intestine.107 By down-regulating GLUT5 protein levels in those with high blood sugar, we may have a mechanism to help diabetics. Of course, there are many potential areas of research, which could be interesting for the GLUT5 transporter. But for the brevity of this article, I will stop here.  I invite those further interested to research the GLUT5 transporter, via easily using a search engine to locate articles on PubMed relating to the topic.

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

One of the many issues with fructose is that it helps to cause non-enzymatic glycation – in layman’s terms; fructose helps to age your liver.108 This shouldn’t be surprising. Remember – increased dietary intake of sugar was linked to dementia – premature aging/degradation of brain tissue usually due to excessive buildup of the beta amyloid protein.109

By contrast, activation of the Nrf2 pathway may help to stop aging – not just in your liver, but also throughout the body.110 The Nrf2 pathway helps in regulating over 500 cytoprotective genes, which give your cells multiple layers of protection.111 112 Interestingly, research has found that dietary flavonoids help to activate this pathway, and thus, your diet can truly determine whether you age quickly or slowly.113 It really is this simple. Sort of.

NRF2, p53 and FOXOs support complementary antioxidant pathways.

Gorrini, C., Harris, I. S. & Mak, T. W. Modulation of oxidative stress as an anticancer strategy. Nature Rev. Drug Discov. 12, 931–947 (2013).

You see, in science, one must resist the urge to oversimplify, and in this case we must remember to not forget all the other stressors to our cells. This means sleep quantity and quality, exercise, stress from work, genetics, epigenetics, pollution – it is truly a never ending list. However, we very much have control over what we put in our mouths.

Differential responses to rising oxidative stress.

Stefanson, A. L., & Bakovic, M. (2014). Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals. Nutrients, 6(9), 3777–3801. doi:10.3390/nu6093777

The Nrf2 pathway has been recently found to react to apigenin and luteolin (dietary phytochemical flavones) in a favorable way.114 The antioxidant pathway is activated upon ingestion of apigenin and luteolin, and the flavones may be responsible for vital anti-inflammatory effects.

Schematic representation depicting some of the various cytoprotective proteins that are upregulated by Nrf2. Flavonoid-mediated protection from ischemic/hemorrhagic stroke, traumatic brain injury, and/or other neuropathies may result in large part from Nrf2 regulation of these pathways.113

In fact, activation of the Nrf2 pathway is being studied fairly extensively, in regards to cancer prevention and treatment.115 Since dietary activation is very cheap (especially when compared to pharmaceutical drugs) this research could pave the way for widespread effective change in our world’s health. Mandatory spinach and kale consumption might be a potential guideline – if one was to hypothesize about potential ways this research could be implemented on a widespread basis.

Schematic representation depicting the potential mechanisms by which flavanol-mediated Nrf2 induction leads to activation of cytoprotective pathways after stroke, traumatic brain injury, and/or other neurodegenerative diseases. Flavanols may induce Nrf2 through binding to receptors seated on the plasma membrane and subsequent initiation of intracellular signaling cascades. Alternatively, passive diffusion or active transport through the plasma membrane may permit direct cytosolic dissociation of the Keap1/Nrf2 complex or activation of second messengers that regulate Nrf2 translocation into the nucleus. Upon nuclear translocation, Nrf2 binds to AREs on the promoter regions of cytoprotective genes to regulate heme/biliverdin, glutathione, NAD(P)H, and/or other protective pathways.113

So, if your diet is making you fat, old and sick, you now have some great motivation to affect change. What can be more powerful than that? By loading up on neuro-protective vegetables and healthy fats, as well as quality proteins (which contain essential amino acids) you will be helping to fight back against cellular aging, obesity and illness.

And good news – a Paleo Diet – by its very nature – eliminates all the bad choices for you, and emphasizes all the best foods. The work has already been done. It couldn’t get any easier. You have a path towards obesity, dementia and medication. You also have a path towards health, wellness and vitality. The choice is yours – so choose wisely.

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114 Paredes-gonzalez X, Fuentes F, Jeffery S, et al. Induction of NRF2-mediated gene expression by dietary phytochemical flavones apigenin and luteolin. Biopharm Drug Dispos. 2015;

115 Jaramillo MC, Zhang DD. The emerging role of the Nrf2-Keap1 signaling pathway in cancer. Genes Dev. 2013;27(20):2179-91.

Soy, Sugar's Cohort in Causing Obesity | The Paleo Diet

Since the 1930s, the US government has been heavily subsidizing corn, soy, wheat, and other so-called staple crops. Subsequently, these foods have remained artificially cheap for decades, leading to enormously increased consumption.

For a new study, just published in PLOS One, scientists at UC Riverside compared the effects of diets high in soybean oil with those high in fructose and/or coconut oil. They concluded that soybean oil, when consumed at typical American consumption levels, causes significant liver damage and promotes obesity and diabetes even more so than fructose.1

“This was a major surprise for us—that soybean oil is causing more obesity and diabetes than fructose—especially when you see headlines everyday about the potential role of sugar consumption in the current obesity epidemic,” said Poonamjot Deol, the study’s lead scientist.2

This study is believed to be the first comparing the effects of unsaturated fat, saturated fat, and fructose on obesity, diabetes, insulin resistance and nonalcoholic fatty liver disease. While excessive sugar consumption has rightfully been criticized during the past several years, this study shows that industrial seed oils, particularly soybean oil, can be just as dangerous.

Soybean oil features prominently in many processed foods, especially margarine, salad dressings, and snack foods. It’s also the preferred cooking oil throughout the restaurant industry. In 2007, around 80 million tons of edible vegetable oils were produced globally, about half of which was soybean oil.3

Just how much money goes into keeping soy cheap and plentiful? Between 1995 and 2012, US soy subsidies totaled an astounding $27.8 billion, second only to corn, which amounted to $84.4 billion for the same period. In 2014, the US government replaced direct payments to farmers with Price Loss Coverage (PLC) and Agricultural Risk Coverage (ARC), but these new programs still cost taxpayers two-thirds as much as the direct payments did.4

Annual consumption of soybean oil increased from a miniscule 0.01 kg per person in 1909 to 11.2 kg in 1999.5 So what has been the impact on health? The UC Riverside scientists fed mice diets with 40% of calories coming from fat and supplemented those diets with fructose. Diet 1 consisted of 36 kcal% from coconut oil and 4 kcal% from soybean oil. Diet 2 consisted of 21 kcal% from coconut oil and 19 kcal% from soybean oil. These diets were formulated to mimic American consumption patterns with respect to saturated fat, soybean oil, and fructose.

Mice on Diet 2, the high soybean oil diet, exhibited increased weight gain, adiposity, fatty liver, insulin resistance, and diabetes, compared to mice on Diet 1. The scientists believe the mechanisms behind these outcomes involve changes in gene expression. Diet 2, for example, caused significant global dysregulation of several genes, particularly cytochrome P450, related to diabetes, obesity, lipid metabolism, and cancer.

Fructose had less severe metabolic effects than did soybean oil, which was a surprise to the scientists. More importantly, they determined that fructose combined with soybean oil works synergistically to undermine health.

Fructose induced neither diabetes nor insulin resistance in this study, although it did induce obesity. The scientists point out that fructose and its metabolic impact are very hotly debated within the nutrition science community. Further research will yield a more evolved perspective on fructose, but this study stresses the importance of dietary context. In other words, fructose seems to be much more damaging when paired with unhealthy oils compared to healthy sources of fat.

Many people within the Paleo community are concerned about fructose, even going so far as to completely eliminate fruit from their diets. While this might be appropriate for some people, it’s probably unnecessary for others. The fat in the Paleo diet comes mostly from high-quality sources of saturated and monounsaturated fat, with minimal amounts of high-quality polyunsaturated fat. The current study shows how foods interact and why a holistic approach to diet is essential. If America is serious about reversing degenerative diseases, soybean oil must share the spotlight with sugar during the many ongoing national discussions about nutrition.

 

REFERENCES

[1] Deol, P., et al. (July 2015). Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver. PLOS One, 10(7).

[2] University of California – Riverside. (2015, July 22). Soybean oil causes more obesity than coconut oil, fructose: Scientists found mice on high soybean oil diet showed increased levels of weight gain, diabetes compared to mice on a high fructose diet or high coconut oil diet. ScienceDaily.

[3] Rosillo-Calle, F. (2009). A global overview of vegetable oils, with reference to biodiesel. CEP/Imperial College, Luc Pelkmans, VITO and Arnaldo Walter, UNICAMP for IEA Bioenergy Task 40.

[4] Haspel, T. (February 18, 2014). Farm bill: Why don’t taxpayers subsidize the foods that are better for us? The Washington Post.

[5] Blasbalg, TL, et al. (March 2011). Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. The American Journal of Clinical Nutrition, 93(5).

Does Fructose Promote Overeating? | The Paleo Diet

In the early 1980s, public health authorities began warning that saturated fat was driving obesity and various degenerative diseases. During this same period, high-fructose corn syrup (HFCS) rose to prominence, sneaking itself into processed foods, especially sodas, cookies, and cakes.

Saturated fat consumption fell. Sugar consumption and overall caloric intake rose. Obesity, metabolic syndrome, type-2 diabetes, and other diet-related diseases got worse. These disturbing facts have prompted nutrition scientists to begin investigate fructose (a primary type of sugar) as a possible driver of the obesity crisis.

Does fructose uniquely promote overeating? Does fructose affect satiety differently than other sugars, particularly glucose?

Before looking into these questions, we should note that fructose is almost always accompanied by glucose in natural foods. The following chart, for example, shows the sugar content of common foods.

Does Fructose Promote Overeating? | The Paleo Diet

Almost all foods containing sugars, including vegetables, include both glucose and fructose (as well as sucrose, which is 50% fructose and 50% glucose). The ratio of fructose to glucose for most foods hovers around 50:50 and generally never exceeds 70:30.

It’s been suggested that high-fructose corn syrup is more dangerous than table sugar because it contains proportionally more fructose, a modest 55% compared to 50% for ordinary table sugar. According to the numbers in the chart, if fructose were inherently more dangerous than glucose, we would have to conclude that apples and pears are worse than bananas and blueberries.

So is there any evidence that fructose promotes overeating? Is snacking on apples rather than bananas a bad idea? In 2013, a study published in the Journal of the American Medical Association sparked headlines like, “Fructose changes brain to cause overeating, scientists say,” and “Revealed: fructose ‘may spur overeating.’”1, 2

From the actual study, we read, “Glucose but not fructose ingestion reduced the activation of the hypothalamus, insula, and striatum—brain regions that regulate appetite, motivation, and reward processing; glucose ingestion also increased functional connections between the hypothalamic-striatal network and increased satiety.”3

It seems convincing. But was this study representative of real-world scenarios? Let’s see how the study was organized. The scientists worked with 20 normal-weight subjects (10 men, 10 women) without diabetes and a mean age of 31. The study was a blinded, random-order crossover design (so far so good).

Following an overnight fast, subjects drank 300ml of cherry-flavored water with either 75g of fructose or 75g of glucose. 60 minutes later, blood samples were drawn and the subjects completed a series of surveys rating “feelings of hunger, satiety, and fullness on a scale of 1 to 10.”

First of all, 75g of sugar, whether fructose or glucose, is an inordinately large amount to consume at one time. Roughly equivalent to 2.5 cans of soda, this might not be reflective of real-world consumption patterns. More importantly, however, we never consume foods or beverages sweetened entirely by fructose or by glucose. Invariably, both sugars are present, typically in 50:50 ratios.

This study made headlines because it contradicted previous studies. A 2007 study, for example, tested energy balance and satiety of high-fructose corn syrup (55% fructose, 45% glucose) compared to sucrose (50% fructose, 50% glucose). The scientists found that glucose and fructose contribute to satiety through different biochemical mechanisms, but overall there are no significant differences between sucrose- and HFCS-sweetened drinks with respect to satiety and energy balance.4

Ultimately, the fructose/overeating issue comes down to quantity and form (whole foods versus liquids). Fructose appears to have bidirectional effects. In other words, effects on certain biomarkers (fasting triglycerides, insulin sensitivity, etc.) at moderate doses may be absent or even opposite those observed at very high/excessive doses.5

Very high/excessive doses are almost certainly detrimental, but moderate doses, especially when consumed as whole foods, can be very beneficial. Researchers from the Harvard School of Public Health, for example, determined that consumption of whole fruits, particularly blueberries, grapes, and apples, is associated with decreased type-2 diabetes risk, whereas consumption of fruit juice is associated with increased risk.6

THE BOTTOM LINE

Foods containing fructose, especially fruits and vegetables, are healthy when consumed as part of a balanced Paleo diet. Eating a couple pieces of fruit each day doesn’t promote overeating, but drinking 4 cans of soda or fruit juice might. More research must be done to better understand fructose, but when you read that fructose is dangerous, ask about the quantity, source, and form (liquid/whole food) of fructose. Also keep in mind that glucose almost always accompanies fructose in real foods, so studies on pure fructose consumption may not be relevant to real-world eating.

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

Christopher James Clark | The Paleo Diet TeamChristopher 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] CBS/Associated Press. (January 2, 2013). Fructose changes brain to cause overeating, scientists say. CBS News. Retrieved from //www.cbsnews.com/news/fructose-changes-brain-to-cause-overeating-scientists-say/

[2] Associated Press. (January 2, 2013). Revealed: fructose ‘may spur overeating.’ The Independent. Retrieved from //www.independent.co.uk/life-style/health-and-families/health-news/revealed-fructose-may-spur-overeating-8434959.html

[3] Page, KA., et al. (January 2, 2013). Effects of Fructose vs Glucose on Regional Cerebral Blood Flow in Brain Regions Involved With Appetite and Reward Pathways. Journal of the American Medical Association, 309(1). Retrieved from //jama.jamanetwork.com/article.aspx?articleid=1555133

[4] Soenen, S., et al. (December 2007). No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads. American Journal of Clinical Nutrition, 86(6). Retrieved from //ajcn.nutrition.org/content/86/6/1586.full

[5] Livesey, G. (April 22, 2009). Fructose Ingestion: Dose-Dependent Responses in Health Research. The Journal of Nutrition, 139(6). Retrieved from //jn.nutrition.org/content/139/6/1246S

[6] Muraki, I., et al. (August 29, 2013). Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies. British Medical Journal, 347. Retrieved from //www.bmj.com/content/347/bmj.f5001

Honey: The Sticky Truth

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
Metabolism and Honey

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

Metabolic Effects of Fructose: Honey

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.
Differences in Honey Gene Expressions

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

Honey: Chart 4

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: //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: //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: //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.

Fructose Content In Fruit | The Paleo Diet

Good day!  I am about 6 months into the paleo lifestyle, have been crossfitting for a couple years, loving it, and seeing great results.  I have been following a lot of your literature and what I love most about paleo is that it is undeniably the ultimate way to lead a healthy life. I love that it proves its findings on a cellular level, you just can’t debate that!!   I am torn now though because as an athlete I am getting mixed reviews on fructose. I’m reading its toxic and mostly useless and harmful to the liver.  But in your paleo for athletes book a lot of stage 1-3 suggests fruits with high glycemic load. Can u shine some light on this for me? of everything I read an hear I always standby you and Robb Wolfe most.

Thanks, curious and confused fan #1,350,785 : )

 

Dr. Cordain’s Response:

Hi Eric,

Thanks for your kind words about the Paleo Diet. Unless someone is overweight, obese or has any symptoms (high blood pressure, abnormal blood lipids, type 2 diabetes) of the metabolic syndrome there really is no need to restrict fresh fruits.  At my website, I list the fructose content of all common fruits (here).  You can see that most dried fruits are quite high in fructose and should be eaten sparingly by most people.  Some fruits like tomatoes, lemons, limes, avocadoes, apricots and grapefruit are quite low in fructose and typically even overweight or people with the metabolic sydrome need not restrict these fruits.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

Affiliates and Credentials