Does Fruit Make You Fat?

ALPHARAJNutrition, SkepticismLeave a Comment

There is a unique category of experts in the fitness industry who I like to call ‘wannabe myth-busters’. These are the types who claim to be unbiased and scientific, when all they really do is add more nonsense to the already overflowing pool of misinformation.

One of their many questionable claims revolves around the idea that “fruit is fattening”.

As such, we’ve received many questions from people infected with their pseudoscience who are now afraid to eat fruit because they think the fructose will magically “turn to fat” or that they’ll end up with diabetes, obesity, or some other health problem.

One of those questions comes from our friend, Yash. You can read it by clicking on the link below:

So what’s all the fuss about?

The argument against fruit takes the following form:

“Fructose (unlike glucose) is only metabolized in the liver and can either be converted into liver glycogen or fat. Since liver glycogen stores are full after a meal, any fructose consumed (in the form of fruit or table sugar) will be converted into fat.”

Sounds convincing?

If only human metabolism was that simple.

There are two assumptions being made here:

1) Fructose is ONLY metabolized in the liver

2) Fructose has ONLY two fates: to be stored as liver glycogen or fat

Both these assumptions represent an over simplistic (and incomplete) understanding of human metabolism, a lack of critical thinking skills and a total disregard for scientific research.

Let’s break them down.

Premise 1: Fructose is ONLY metabolized in the liver.

This is false.

Fructose is not only metabolized in the liver, but it is also metabolized in the intestine, testis, kidney, skeletal muscle, fat tissue and brain [1, 2].

Premise 2: Fructose has ONLY two fates – to be stored as liver glycogen or fat.

This is also false.

The following images illustrate the metabolic fates of dietary fructose:

Approximately 50% of ingested fructose is converted in the liver to glucose, 25% to lactate, 15% to 18% to glycogen, and a few percent is metabolized to carbon dioxide. Only a very small percentage (on the order of 1%–5%) is converted to free fatty acids [3, 4].

It is this conversion to fatty acids, a process called de novo lipogenesis (DNL), which the anti-fructose zealots tend to fuss about.

But did it ever occur to them that dietary fat is stored as body fat much more easily than fructose (or any carbohydrate for that matter) because there’s no conversion needed at all – duh!

Stephan Guyenet destroys their argument with one simple quote:

“If fructose is fattening due to its ability to become fat, then dietary fat should be even more fattening because it doesn’t have to undergo an inefficient conversion process – it’s already fat.”

So even at the most basic level of reasoning the idea that fructose after a meal will make you fat because it can be “converted into fat” just doesn’t make sense.

Also it’s worth mentioning that DNL is a highly inefficient pathway in the human body. Almost every study ever conducted on this subject has shown that under normal dietary conditions, DNL is so minute and insignificant that it contributes virtually nothing measurable to body fat [5, 6].

I can end the post on this note. But there’s still room to add more nails to the coffin.

One thing the anti-fructose brigade fails to realize is that humans have been ingesting fructose for thousands of years.

In fact, hunter gatherer tribes all over the world have consumed large amounts of fructose in the form of fruit and honey (which is 38-64% fructose).

For example, the Hadza from Tanzania, get 15% of their calories from honey. Their average body fat percentage is 11% for males and 20% for females – both incredibly lean by any standard [7].

Let’s examine some more research.

• In 1971, Meyer and colleagues found that over the course of six months, an ad-libitum diet which consisted of 82% of calories from fruit helped overweight subjects lose a large amount of body fat [8].

• In 1997, Surwit et al. compared the six-week effects of two diets that consisted of identical total calories, one had 43% of the total calories as sucrose (which is 50% fructose), and one had only 4% of the total calories as sucrose. The result: no significant differences were seen in the loss of body weight or body fat between the high- and low-sucrose groups [9].

• Similarly in 2005, Rodriguez et al. had 15 obese subjects randomly assigned to either a high fruit diet or a low fruit diet [10]. Both the groups lost weight “but the cholesterol fall was higher in obese subjects receiving the diet containing more fruit.”

• In 2009, Alinia et al. published a meta-analysis that examined the relationship between fruit intake and body weight [11]. The following is a direct quote from the study: “We identified three intervention, eight prospective observational, and five cross-sectional studies that explored this relationship. Two of the intervention studies showed that fruit intake reduced body weight, five of the prospective observational studies showed that fruit consumption reduced the risk of developing overweight and obesity, and four of the cross-sectional studies found an inverse association between fruit intake and body weight. The majority of the evidence points towards a possible inverse association between fruit intake and overweight.”

• And finally in 2011, a study by Madero et al. had obese subjects randomly assigned to calorie-matched diets that were either low-fructose (less than 20 g/day) or moderate-fructose (50-70 g/day) mostly from whole fruit [12]. The moderate-fructose group lost significantly more weight than the low-fructose group (4.19 kg versus 2.83 kg, respectively). The authors concluded, “For weight loss achievement, an energy-restricted moderate natural fructose diet was superior to a low-fructose diet.”

Ouch! That last one is definitely going to ruffle some feathers in the anti-fructose lobby.

Now before I get accused of cherry picking “fructose friendly” research, I’d like to point out a few limitations of the studies which are used to demonize fructose.

Admittedly, there are studies which shows negative effects of fructose consumption.

The main problem with these studies – almost all of them are done on rats who feasted on an excessively high amount of fructose far beyond anything which the average human being consumes. The same can be said for some of the research done on humans – a large amount of isolated fructose is fed to the subjects, whereas under normal dietary conditions fructose is consumed with glucose in moderate amounts (usually in the form of fruit or table sugar).

So far, we’ve seen that fruit consumption isn’t going to jeopardize your fat loss efforts. But it only gets better from here.

Can fruit help you get leaner?

We know that fructose helps maintain liver glycogen. Why is this important? Because glycogen-mediated liver cell swelling is one of the body’s most potent anabolic/anti-catabolic signals.

In other words, fruits can help you preserve muscle mass when you’re in a caloric deficit.

To top it off, fruits are rich in micronutrients, they have a low calorie:satiety ratio (due to their high fiber/water content) and they are bloody delicious – making them an ideal food to consume when you’re attempting to lose fat.

The Bottom Line:

Don’t fall for anti-fructose mythologies. They’re promoted by pseudo-experts who’re on a mission to develop irrational fears and obsessive tendencies about food.

At the end of the day, body fat accumulation will only occur when the rate of fat formation exceeds the rate of fat burning over a significant period of time. And that is primarily dictated by energy balance.


1. Hundal, Harinder S., et al. “GLUT5 expression and fructose transport in human skeletal muscle.” Skeletal Muscle Metabolism in Exercise and Diabetes. Springer US, 1998. 35-45.

2. Douard, Veronique, and Ronaldo P. Ferraris. “Regulation of the fructose transporter GLUT5 in health and disease.” American Journal of Physiology-Endocrinology and Metabolism 295.2 (2008): E227-E237.

3. Sun, Sam Z., and Mark W. Empie. “Fructose metabolism in humans-what isotopic tracer studies tell us.” Nutr Metab (Lond) 9.1 (2012): 89.

4. Rippe, James M., and Theodore J. Angelopoulos. “Sucrose, high-fructose corn syrup, and fructose, their metabolism and potential health effects: what do we really know?.” Advances in Nutrition: An International Review Journal 4.2 (2013): 236-245.

5. Hellerstein, M. K., et al. “Measurement of de novo hepatic lipogenesis in humans using stable isotopes.” Journal of Clinical Investigation 87.5 (1991): 1841.

6. Hellerstein, M. K. “De novo lipogenesis in humans: metabolic and regulatory aspects.” European journal of clinical nutrition 53 (1999): S53-S65.

7. Marlowe, Frank W., and Julia C. Berbesque. “Tubers as fallback foods and their impact on Hadza hunter‐gatherers.” American Journal of Physical Anthropology 140.4 (2009): 751-758.

8. Meyer, B. J., et al. “Some physiological effects of a mainly fruit diet in man.” South African Medical Journal 45 (1971): 191-195.

9. Surwit, Richard S., et al. “Metabolic and behavioral effects of a high-sucrose diet during weight loss.” The American journal of clinical nutrition 65.4 (1997): 908-915.

10. Rodríguez, M. Cristina, et al. “Effects of two energy-restricted diets containing different fruit amounts on body weight loss and macronutrient oxidation.” Plant foods for human nutrition 60.4 (2005): 219-224.

11. Alinia, Sevil, O. Hels, and I. Tetens. “The potential association between fruit intake and body weight–a review.” Obesity Reviews 10.6 (2009): 639-647.

12. Madero, Magdalena, et al. “The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial.” Metabolism 60.11 (2011): 1551-1559.

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