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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 (for example, see web article reference 4a).
Along similar lines, Dan Duchaine, in his book "Bodyopus" stated that removing fruit at the end of a diet increased fat loss. Because of some of the known metabolic effects of excess fructose consumption (discussed below) including increased blood triglyceride levels, increased uric acid and even impaired copper absorption (3,5). There is also some in vitro indication that fructose may increase protein cross linking, which is associated with a number of different potential negative health issues (6).
Because of the varying data on fructose,there is a considerable amount of debate regarding the effects of fructose on public health even outside of the bodybuilding nutrition arena (7). So what is the truth about fructose? Is it an ideal sugar that should be used freely, or a nutritional evil that should be avoided? As is usually the case, the answer is somewhere in the middle of the two extremes and the goal of this article will be to set the record straight regarding fructose. We'll start by looking briefly at fructose absorption and metabolism before addressing the metabolic effects on the body. back to top
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). back to top
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. back to top
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.
Figure 1 gives a partial overview comparing glucose and fructose metabolism. I want to note a few things. First, I left out the majority of enzymes that are involved in the various metabolic pathways (see ref 2 or any good biochemistry book for the full pathways and enzymes). Most of that was to make the graphic a little less busy, part of it was because it just wasn't that important in the overall scheme of things. The enzymes I did include are the ones in boxes, since they are the key enzymes we need to focus on. back to top
As you can see from the graphic, the number of different paths that fructose can take in the liver are much more complex than glucose. Let's look at glucose first. In short, glucose can either be stored as glycogen, by being phosphorylated to glucose-6-P first, or go straight to blood glucose. Under most conditions, the majority of dietary glucose leaves the bloodstream immediately to enter the bloodstream.
Fructose on the other hand, follows an entirely different set of pathways and I want to look at some of the steps now. First and foremost, note that the phosphorylation of fructose occurs via a different enzyme (fructokinase) than that of glucose (glucokinase). I should also mention that fructokinase is essentially found only in the liver which simply means that muscle is unable to utilize fructose for the most part. You might as well think of fructose as 'liver food' for lack of a better way of looking at it.
In fact, all fructose entering the liver must be phosphorylated first which leads to one of the potential problems with excess fructose ingestion. In large amounts, and usually with infusion, fructose does two things. First, it depletes the liver of ATP (which is broken down to ADP to provide the P for that step), which can limit the liver's ability to perform other metabolic functions such as the uptake and conversion of T4 to T3 (15).
At the same time (biochemical steps not shown), the breakdown of ATP and subsequent depletion of cellular phosphate can lead to the production of a waste product called uric acid, which must then be excreted. Excess uric acid can cause gout in sensitive individuals and large infusions of fructose have been shown to deplete liver ATP, increase uric acid production, and cause symptoms of gout in some people (3).
Once phosphorylated, fructose-1-P is then broken down to the two breakdown products shown. I should mention that the fructose malabsorption syndrome mentioned above is caused by a lack of the Aldolase B enzyme (12). These are called triose sugars, which can go into a number of different pathways. The topmost pathway shows DHAP and glyceraldehade 3-P reconverting to fructose 1-6-bis-P, then up to liver glycogen via the same pathway that glucose would have followed.
Alternately, glyceraldehyde 3-P can be converted to pyruvate which can be converted to lactate (a waste product), or be further broken down to Acetyl-CoA. Acetyl Co-A is sort of a metabolic middleman produced from the breakdown of carbohydrates, fats and protein. You may note how non-esterified fatty acids, just a fancy name for fatty acids, can be broken down to Acetyl-CoA as well.
What pathways Acetyl-CoA follows will depend on the overall metabolic state of the liver. If the liver is in the 'fed' state (meaning that liver glycogen is fairly full), acetyl-CoA can go through de novo lipogenesis (DNL, the pathway to the left) to acyl glycerols and combined with cholesterol to produce very low density lipoprotein triglycerides. This is the pathway that anti-fructose individuals such as John Parillo have focused on. If the liver is in the 'fasted' state (meaning that liver glycogen is depleted), acetyl-CoA can be used for energy, producing Co2, or be used to produce ketone bodies.
Now, the key aspect that individuals such as Parillo have focused on is the fact that fructose enters the various metabolic pathways without being regulated by phosphofructokinase (PFK). The issue is that PFK is highly regulated and normally acts to control how much glucose can go into the other pathways that fructose can enter more readily. Thus, he is correct in stating that fructose has a much higher *tendency* to be converted to fat than glucose.
That is, while DNL from glucose is thought to be of minimal importance under all but the most extreme (700-900 grams per day for 5 days) carbohydrate overfeeding (16,17), overfeeding fructose has a much higher tendency to promote VLDL triglyceride formation. This is not only important from the aspect of bodyfat and appearance but increased VLDL levels in the bloodstream are a known independent risk factor for cardiac disease. Thus, increases in VLDL from fructose feedings could have potential health risks outside of increasing bodyfat storage. back to top
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.
In contrast, in a study of obese individuals given either high fructose or high glucose feedings prior to exercise, researchers found no difference in fat burning after the workout when the groups were dieting. The same study found that there was significantly less fat burned after exercise when the groups were not restricting calories (31). Of course, there are metabolic differences between obese individuals and very lean bodybuilders so you have to be careful extrapolating from these studies.
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. back to top
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 we come back to Parillo's frequent story about the bodybuilder at 4% bodyfat who gains fat by replacing rice with bananas, his supposed real-world 'proof' that fruit makes you fat. Well, first we have to ask how relevant an example (male at 4% bodyfat) is to the majority of athletes and bodybuilders. That is, while it may be worthwhile to exclude sources of fructose at the end of a pre-contest diet(as Dan Duchaine suggested in "Bodyopus"
because of decreases in fat burning, that hardly applies to the majority of athletes under most circumstances.
Secondly, there is the example of bananas, a fruit which is very high on the Glycemic Index and contains far more glucose than anything else. 300 calories of bananas is approximately 3 medium bananas which would contain 15-21 grams of fructose far below the level needed to promote fat synthesis. While Parillo conveniently blames the lipogenic effect of the rice/banana switch on fructose, it's more likely that the other sugars present, and the insulin spike from such a high GI food were to blame.
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. back to top
References available upon request
