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Fructose : the truth

anthrax

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Very interesting article on fructose and why it is not evil (yes you can consume fruits !)
A bit long, so if you are tired of reading it all, go to the last paragraph (in bold)

FRUCTOSE
by Lyle McDonald


As with so many other aspects of nutrition, especially bodybuilding and sports nutrition, beliefs about the sugar fructose (more commonly known as fruit sugar) vary widely. On the one hand, because of its low glycemic index (GI) and general lack of insulin response, many people consider fructose an ideal sugar, that should be used to replace other sugars especially for diabetics (1). There is also some indication that fructose may blunt appetite and affect food choice (2,3). Finally, because of the low insulin response, it's been suggested that fructose before or during exercise might allow increased fat utilization during exercise, while still maintaining blood glucose levels (4).

At the other end of the spectrum, because of differences in its metabolism compared to other sugars, and the known effect of fructose on blood triglyceride (fat) levels, many nutritional authorities (most notably John Parillo) consider fructose and fruit a sort of nutritional satan that will only make you fat and that should be eliminated from the diets of bodybuilders

What Is Fructose, How Much Do We Get and
Where Is It Found In the Diet?

Fructose is one of three monosaccharides (single sugar molecules, the other two are glucose and galactose) that occurs naturally in foods. Sucrose (table sugar, a disaccharide) is also 1/2 fructose. However, free fructose only occurs naturally in a few foods, notably some fruits (hence its common name of 'fruit sugar') and honey with the majority of our dietary fructose coming from the ingestion of sucrose. Fructose is also found in small amounts in a few vegetables.

In recent years, the amount of fructose being consumed has increased significantly. One large scale analysis puts average daily amounts in the range of 90-100 grams (8) which is a significant increase over the last 2 decades. This increase has been caused not only by an overall increase in the consumption of sugars, but also because of increased use of high fructose corn syrup (HFS). HFS contains can contain 42% or 55% free fructose, with the remainder being glucose. So, on top of an overall increase in fructose consumption, the use of HFS has caused a significant increase in the consumption of free fructose (8,9).

Additionally, many health-food stores also sell crystalline fructose powder as a sweetener and both crystalline fructose and HFS are used in many commercially produced food products (10).

Fructose Digestion and Metabolism

During digestion in the stomach and small intestines, all dietary carbohydrates are eventually broken down to the monosaccharides glucose, fructose and galactose (found in milk in lactose). These are absorbed via specific transporters in the small intestine, bringing them into the portal vein, next stop the liver.

While the small intestine seems to have an essentially unlimited (estimated around 5000 grams per day) capacity to absorb glucose and galactose, the absorption of fructose is a very different story. The consumption of as little as 35-50 grams of free fructose at once causes gastric upset, gas, bloating and diarrhea in a majority (60% or more) of people (11). However, the addition of glucose to the free fructose prevents the problem. And the ingestion of large amounts of sucrose (again, 1/2 fructose, 1/2 glucose) causes no such problem. It thus appears that our guts have evolved to absorb fructose only in the presence of other sugars and that large amounts of free fructose in the diet are non-physiological for humans. Since HFS also contains a significant amount of glucose, the malabsorption issue may not be a huge one for most processed foods. However, anyone considering using crystalline fructose as a sweetener should consider the potential problems with large amounts of free fructose. I should also mention that some individuals suffer from a hereditary fructose malabsorption syndrome (12), but this is typically identified at a very young age. Fructose free diets can be developed for these individuals.

After digestion, fructose goes to the liver like all sugars, which is where the bulk of its metabolism occurs. This is also where fructose metabolism differs significantly from glucose metabolism, and is the source of much of the debate over the relative 'goodness' of fructose.

Liver Metabolism of Sugars

Although they share many intermediate steps in their metabolism, dietary glucose and fructose follow two distinct pathways in the liver. In fact, it has been known for quite some time that most dietary glucose goes straight through the liver with only minimal metabolism (13) while the majority of fructose is metabolized in the liver (14).

This is part of the reason for the low glycemic index (GI) of fructose. Since it is metabolized almost exclusively in the liver, it has only a very small effect on blood glucose levels. Additionally, and also unlike glucose, the uptake of fructose into liver cells doesn't require insulin. Hence there is no need for the body to secrete insulin in response to dietary fructose ingestion. This is the basis for the claims that fructose is a superior carbohydrate source compared to glucose or sucrose (which recall is half glucose), especially for diabetics (1) who have poor control over blood glucose and insulin levels.

At the same time, because of its extensive metabolism, and the pathways that it follows, in the liver, fructose can have negative effects on the overall metabolism of the body. So first let's compare and contrast the metabolism of glucose and fructose in the liver, and then look at some of the potential negatives of fructose (especially excess fructose) intake.

But Just How Much Are We Talking About?

A cursory examination of the research into fructose feedings in terms of the production of metabolites such as lactate, uric acid and especially VLDL triglycerides has shown distinctly varying results. For example, while some research has clearly shown an increase in VLDL triglyceride levels with fructose feedings (18-23), other research has not (24-28). Why the discrepancy?

As with so many aspects of nutrition, it really comes down to two things: how much fructose they gave, and what population they gave it to. Let's get the population dynamic out of the way first. Studies have examined the effects of fructose in essentially 4 different groups: individuals with normal insulin and triglyceride levels, individuals with normal insulin but high triglyceride levels, individuals with high insulin and normal triglyceride levels, and people with high insulin and triglyceride levels. Different groups show a different susceptibility to the negative effects of fructose (and that still has to take amount into account).

Overall, the last group, those with high insulin and high triglyceride levels tends to be the most sensitive to the negative effects of fructose in terms of increasing VLDL triglyceride levels (3). The other three groups show a distinctly less pronounced effect. This makes some sense as such individuals would normally have skewed physiology to begin with. I should point out that hyperinsulinemic/hypertriglyceridemic folks aren't very indicative of the average lean athlete consuming a healthy bodybuilding/sports oriented diet.

But that brings us back to dose. Even in otherwise healthy individuals, fructose has been found to increase VLDL triglyceride levels so the potential for fat synthesis from fructose is apparently there. Again, looking at the studies as a whole, both negative and positive results are typically found. It's when you start looking at the amounts given, that a pattern starts to develop. First, a select group of studies has used absurd and non-physiological amounts of fructose (200-500 grams per day, more than any human is probably capable of consuming under all but the most forced conditions) and invariably found increased triglyceride levels. Keep in mind that the average American diet only contains about 30-40 grams of fructose per day so we can pretty safely ignore those studies.

Looking at the other studies which gave more reasonable amounts of fructose, as a recent review has done (29), we see a fairly standard pattern: at reasonable amounts of fructose (30-60 grams per day depending on the study), there is no negative effect on VLDL or triglyceride levels. At amounts higher than that (in the range of 80-90+ grams per day), there tend to be an increase in VLDL and triglyceride levels suggesting fat synthesis. This would tend to suggest a distinct cutoff point somewhere between those two values as an approximate maximum of fructose that can be consumed without causing significant triglyceride synthesis.

In contrast, one study comparing 75 grams of fructose to 75 grams of glucose, found that, over 4 hours of study, while there was a small amount of de novo lipogenesis from the fructose, the net effect was that the body burned more fat than it produced (30). The fructose group also showed a higher thermic effect (meaning more calories were wasted as heat), most likely because of the high amount of metabolic processing that went on. However, and perhaps more importantly, despite very little fat synthesis in the fructose group, there was less fat burning in that same group. This occurred with an increased burning of carbohydrate in the fructose group.

So it may be that, while fructose at moderate (<50 g/day or so) amounts doesn't increase fat synthesis per se significantly, it may slow fat loss by decreasing fat burning in the liver. That is, to a degree, the end result may be the same: whether the fructose is causing more fat synthesis, or less fat burning, the net effect on fat loss (which is determined by fat burning - fat intake) may be similar.

As I mentioned above, the metabolic fate of fructose appears to depend on the metabolic state of the liver and the dieter. In the fasted state (as occurs while dieting), fructose will be used for energy and fat synthesis will be negligible, if it occurs at all. Fat burning may be decreased however. In the fed state (as occurs when not dieting), excess fructose can be converted to VLDL TG, increasing heart disease risk and bodyfat.

Fructose Feeding and Exercise Performance

Finishing up, I want to touch on the idea of fructose feeding during exercise. To my knowledge, no studies have examined the consumption of different types of carbohydrates prior to weight training, and all of the research done to date has been in endurance athletes. From a theoretical standpoint (including the low GI/insulin response), there are some good reasons to think that fructose feedings might be superior to glucose during endurance exercise. However, the research to date has not supported the theory. Fructose feeding before or during has been found to be either no better, or in fact worse in terms of performance of endurance exercise (3). As well, there is the issue of gastric upset with high amounts of fructose that limits how much can be given in the first place.

As a final comment, there is the issue of post-workout carbohydrate and recovery. At this point, it should be no surprise to readers that the post-workout consumption of carbs and protein improves recovery, performance and protein synthesis (32,33). Studies examining different types of carbohydrate intake post workout have invariably found that glucose and glucose polymers refill muscle glycogen ideally, while fructose preferentially refills liver glycogen. In that refilling liver glycogen can be important from the standpoint of overall recovery and growth (the details are outside of the scope of this article), consuming a small amount of fructose (10% of the total carbohydrate content or roughly 10-20 grams) in the post-workout shake may be beneficial. But the majority of carbohydrates consumed should come from glucose and glucose polymers.

Summing Up and Practical Recommendations

Ok, an article like this wouldn't be worth much without some actual recommendations and real world application. First and foremost, it should be clear that in large enough amounts, fructose can certainly be detrimental both to health, by raising VLDL cholesterol and triglycerides and possibly to bodyfat levels for the same reason. However, at moderate intakes of fructose, in the range of 50-60 grams per day, fructose appears to pose little problem and certainly is not going to make or break a diet.

For an athlete to avoid all sources of fructose, especially fruit, seems a bit silly and extreme (see below regarding pre-contest bodybuilding prep for a possible exception). However, there is probably a good reason to avoid high fructose corn syrup as much as is reasonably possible. Readers should realize that many sports food companies are using fructose and HFS in their products, so it's possible that athletes are being exposed to larger than normal amounts of fructose in their diets. Athletes and bodybuilders are encouraged to become avid label readers to see if HFS is listed as a primary ingredient.

Individuals who are hyperinsulinemic or have high triglycerides to begin with may question whether using fructose in large amounts is beneficial and should consult with their doctor before making major nutritional changes. The majority of athletes, bodybuilders and otherwise healthy individuals are unlikely to have problems with either hyperinsulinemia or hypertriglyceridemia although it is a possibility.

So, back to the ~50 g/day value. Noting that the average American diet may contain at least double that already, we might assume that athletes shouldn't be adding more fructose or fruit to their diet. But, we really have to ask whether or not that applies to bodybuilders and athletes, who typically avoid the commercial foods which most commonly containing fructose (meaning those containing high fructose corn syrup).

Most bodybuilders and other athletes already avoid the majority of such foods and I would expect that their daily fructose intake is somewhat below the American average. Once again, note that many commercial products aimed at athletes, such as food bars and even some meal replacement powders, are increasing their use of fructose and HFS as a sweetener so it is possible that athletes are getting more fructose or HFS than they're aware of. How much is up to debate and speculation.

So let's address the important question: What about fruit? Can it be part of a healthy bodybuilding/athletic diet, or should it be avoided as Parillo claims? To answer this we really need to look at the amount of fructose found in typical fruits.

On average, fruits such as cherries, pears, bananas, grapes and apples contain anywhere from 5 to 7 grams of fructose in an average sized piece of fruit. Fruits such as strawberries, blueberries, oranges and grapefruit contain 2-3 grams of fructose per 100 gram serving. Honey is an exception, containing 40 grams of fructose per 100 gram serving, but its extreme sweetness would make eating a lot of it difficult. The point being that fruit is actually not a very large source of fructose in the first place. To get 50 grams of fructose per day from fruit alone would require an intake of approximately 10 pieces per day, far more than all but the most extreme intake would provide.


So, summing up, like most aspects of bodybuilding and athletic nutrition, there are few absolutes. While there is no doubt that large amounts of fructose are both non-physiological and potentially harmful, it certainly appears that low to moderate amounts of fructose, and yes fruit, can be included in a bodybuilding or athletic diet. From the standpoint of liver glycogen and maintaining an anabolic state, small amounts of fructose probably should be included in the diet. Considering the other nutrients (fiber, vitamins and minerals) present in fruit, it seems silly to exclude them from the diet based on the rather small amount of fructose present


(References cited following....)
 
References cited:

1. Gerrits, PE and Tsalikian, E. Diabetes and fructose metabolism. Am J Clin Nutr (1993) 58 (suppl): 796s-799s.

2. Moyer, AE and Rodin, J. Fructose and behavior: does fructose influence food intake and macronutrient selection. Am J Clin Nutr (1993) 58 (suppl): 810s-814s.

3. Henry, RR and Crapo, PA. Current issues in fructose metabolism. Ann Rev Nutr (1991) 11: 21-39.

4. Craig, BW. The influence of fructose feeding on physical performance. Am J Clin Nutr (1993) 58 (suppl): 815s-819s.

4a. Web article at: http://www.parrillo.com/sng/tsb_detail.html?cart=3082554946114869&id=45

5. O'Dell, BL. Fructose and mineral metabolism. Am J Clin Nutr (1993) 58: 771s-778s.

6. Dills, Jr. WL. Protein fructosylation: fructose and the Maillard reaction. Am J Clin Nutr (1993) 58 (suppl): 779s-787s.

7. Glinsmann WH and Bowman, BA. The public health significant of dietary fructose. Am J Clin Nutr (1993) 58 (suppl): 820s-823s.

8. http://www.ers.usda.gov:80/publications/SB965/sb965h.pdf Table 2.

9. Vuilleumier, S. Worldwide production of high-fructose syrup and crystalline fructose. Am J Clin Nutr (1993) 58 (suppl): 733s-736s.

10. Hanover, ML and White, JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr (1993) 58 (suppl): 724s-732s.

11. Riby, JE et. al. Fructose absorption. Am J Clin Nutr (1993) 58 (suppl): 748s-753s.

12. Ali, M, et. al. Heriditary Fructose Intolerance. J Med Genet (1998) 35:353-365.

13. McGarry JD et. al. From dietary glucose to liver glycogen: the full circle around. Ann Rev Nutr (1987) 7:51-73.

14. Mayes, PA. Intermediate metabolism of fructose. Am J Clin Nutr (1993) 58 (suppl): 754s-765s.

15. De Jong M et. al. T4 uptake into the perfused rat liver and liver T4 uptake in humans are inhibited by fructose.Am J Physiol (1994) 266(5 Pt 1):E768-E775

16. Hellerstein MK. Synthesis of fat in response to alteration in diet: insights from new stable isotope methodologies. Lipids (1996) 31 (suppl): S117-S125.

17. Acheson KJ et. al. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr (1988) 48: 240-247.

18. Jeppesen, J et. al. Postprandial triglyceride and retinyl ester responses to oral fat: effects of fructose. Am J Clin Nutr (1995) 61: 787-791.

19. Abraha, A et. al. Acute effect of fructose on postprandial lipaemia in diabetic and non-diabetic subjects. Br J Nutr (1998) 80: 169-175.

20. Reiser, S et. al. Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch. Am J Clin Nutr (1989) 49: 832-839.

21. Bantle, JP et. al. Metabolic effects of dietary fructose in diabetic subjects. Diabetes Care (1992) 15: 1468-1476.

22. Bantle, JP et. al. Effect of dietary fructose on plasma lipids in healthy subjects. Am J Clin Nutr (2000) 72: 1128-1134.

23. Swanson, JE et. al. Metabolic effects of dietary fructose in healthy subjects. Am J Clin Nutr (1992) 55: 851-856.

24. McAteer EJ et. al. The effects of one month high fructose intake on plasma glucose and lipid levels in non-insulin-dependent diabetes. Diabetic Medicine (1987) 4: 62-64.

25. Grigorscro, C et. al. Lack of detectable deleterious effects on metabolic control of daily fructose ingestion for 2 Mo in NIDDM patients. Diabetes Care (1988) 11: 546-550.

26. Eunsook, TK et. al. Effects of fructose feeding on blood parameters and blood pressure in impaired glucose-tolerant subjects. J Am Diet Assoc (1988) 88: 932-938.

27. Koivisto VA and Yki-Jarvinen H. Fructose and insulin sensitivity in patients with type 2 diabetics. J Internal Med (1993) 233: 145-153.

28. Malerbi, DA et. al. Metabolic effects of dietary sucrose and fructose in Type II diabetic subjects. Diabetes Care (1996) 19: 1249-1256.

29. Hollenbeck, CB. Dietary fructose effects on lipoprotein metabolism and risk for coronary heart disease. Am J Clin Nutr (1993) 58 (suppl): 800s-809s.

30. Tappy, L, et. al. Comparison of the thermogenic effect of fructose and glucose in normal humans. Am J Physiol (1986) 250: E718-E724.

31. Tittelbach, TJ, et. al. Post-exercise substrate utilization after a high glucose vs. high fructose meal during negative energy balance in the obese. Obes Res (2000) 8: 496-505.

32. Zawadzki et al. Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise. J Appl Physiol (1992) 72: 1854-1859.

33. Rasmussen BB et. al. An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise. J Appl Physiol. (2000) 88:386-92.
 
This is what I've been telling people! BTW, Lyle is IMO the best source available for diet info--and for training info for that matter. Not infallible by any means, but he really tries to be objective and has a great capacity for looking at things from several angles. I'm just waiting for him to write a book about his current theories on training and nutrition so I don't have to keep scouring the net(Though, of course, by the time any book was published he'd probably have changed some opinions.)
 
This is a great post, but it is nothing that cockdezl, MS and myself haven't mentioned numerous times on this board.

The main time to really watch fructose would be on a hypercaloric/high calorie diet, as liver glycogen levels will already be full. However, on a low calorie diet, the liver will be depleted of its glycogen to some degree (will vary) and the consumer will be allowed to eat more fructose. The enzyme that is in small amount will also vary from individual to individual, along with that person's VLDL levels. As Lyle stated, this can vary anywhere between 50-90 mg's.

Fructose would also be best taken before training as it will decrease the amount of triglycerides that would be allow to form. Also, its low GI levels would be ideal as the perfect carb. This too will allow greater workouts to occur towards strength gains. When the liver is fully glycogenated, it is at its best, Lyle has also stated this in the past. Another time on a low calrie diet when fructose would be ideal is before bed with your protein. The low GI would help ensure protein metabolism and synthesis for longer periods throughout the night as compared to other carbs/sugars.

Fructose is a great carb to consume when the consumer knows how to take it correctly.

I would like to touch up on the fruit calorie values that were given in the article. i don't know exactly how accurate they are or in what conditions the fruit were when the values were taken, but this makes a huge difference in the amount of sugar that will have been inverted from starch. Fruit is very unpredictable on its carb calories because of the soils that may have been used to grow in, the time of year, the time it was picked, etc....

The malabsorption syndrome that Lyle mentioned will either be one of two defects:
1. Fructose intolerance or,
2. Essential Fructosuria
however, they are pretty rare, and i'm sure no body reading this board will have them.

Fructose is also the major fuel source for spermatozoa cells. Fructose will be completely oxidized to CO2 & water with these cells through both fructolysis and the citric acid cycle by sperm cells.

Overall, I am in complete agreement with Lyle's article, as I am in most of his work. Therefore, his last paragraph pretty much summed things up....

I'll try to add more on HFCS.

BMJ
 
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