In this post the Dr. Gloria Sabater , technical director and creator of the master formulas of the Salengei Laboratory, will show us scientific evidence about a myth that is quite widespread in our days: is fruit sugar really bad for our health?

Through a scientific journey, he will provide concise data and evidence that debunks this myth. In this article, we’ll also explore the different types of sugars and examine the benefits of consuming whole fruits instead of products with added sugars.

Investigating the origins of the fructose myth

In recent times and due to the avalanche of information obtained through the internet, and especially on social networks, information without scientific basis has generated concern, which warns about the “dangerous sugar content in fruits”. This has led many people to limit their consumption, fearing adverse effects on their health and, above all, weight gain.

This fear is based on the perception that fructose, the sugar naturally present in fruits, is harmful to our health. However, it is essential to differentiate between fructose added in processed foods, natural fructose present in fruits, and sucrose.

Unfortunately we are becoming more and more accustomed to this type of hoax.

The demonization of fructose

In recent years, a direct causal role between fructose intake and the etiology of the global obesity epidemic has been proposed. However, this proposition is based on controversial interpretations of two distinct lines of research. On the one hand, in mechanistic intervention studies, detrimental metabolic effects have been observed after excessive fructose intake in isolation in animals and humans. On the other hand, the consumption of fructose from added sugars – especially in snacks and drinks – has increased in recent decades and has gone hand in hand with the increase in obesity.

However, both lines of research are currently insufficient to demonstrate a causal role of fructose in metabolic diseases. Most mechanistic intervention studies were conducted on subjects fed large amounts of pure fructose, while fructose is routinely ingested along with glucose and other nutrients.

Based on a comprehensive review of the literature, one study showed that fructose, as commonly consumed in mixed carbohydrate sources, does not exert specific metabolic effects that could explain an increase in body weight. Consequently, public health recommendations and policies that aim solely to reduce fructose consumption, without additional diet and lifestyle goals, would be questionable and impractical (not to say irresponsible). While the available evidence indicates that consumption of sugary drinks is associated with body weight gain, and it is possible that fructose is one of the main components of these drinks, excessive energy consumption is much more important to consider in terms of the obesity epidemic. DOI:10.1017/S0954422414000067

Metabolic Effects of Fructose

Numerous epidemiological studies have presented convincing evidence that there is an association between added sugars (sucrose, fructose, and high-fructose corn syrup) and nonalcoholic fatty liver disease. The liver is where fructose metabolism mainly occurs, with almost 60% oxidation of ingested fructose. Hepatic fructose metabolism stimulates de novo lipogenesis, which increases liver fat.

On the other hand, some studies have shown that a diet that includes whole fruits can result in greater weight loss compared to one that completely restricts fructose. Thus, people who consumed fruits in a controlled way in their diet lost more weight compared to those who only avoided added sugars. This is because the fructose present in fruits is accompanied by fiber, vitamins, minerals, and antioxidants. These have positive effects on health.

Other studies on fructose

A recent meta-analysis of controlled clinical trials concluded that isocaloric carbohydrate exchange for glucose does not induce nonalcoholic fatty liver disease. However, when fructose is the main source of a high-calorie diet, patients have an increase in liver fat and plasma alanine aminotransferases. https://doi.org/10.1111/liv.14360

Indeed, several prospective cohort studies have observed associations between diets containing fruits and vegetables and weight control, weight loss, and obesity risk. A systematic review and meta-analysis of prospective cohort studies from 2015 with 563,277 participants, showed that fruit intake was associated with reductions in body weight and waist circumference and a reduced risk of obesity by 17%. https://doi.org/10.1371/journal.pone.0140846

In the last 50 years, sugar consumption has tripled worldwide. In the United States, there is a great deal of controversy over the widespread use of one added sugar in particular: high-fructose corn syrup (HFCS) which is made from processed corn syrup to obtain an approximately equal mixture of glucose and fructose. https://doi.org/10.1038/482027a

Globally, countries with higher availability of high-fructose corn syrup have a higher prevalence of type 2 diabetes, regardless of obesity. Concomitant with the increased presence of fructose in the diet increases the incidence of obesity, insulin resistance, and systemic arterial hypertension. In addition, increased caloric intake, especially refined sugar and fructose, correlates with increases in dyslipidemia, insulin resistance, and nonalcoholic fatty liver disease https://doi.org/10.2337/dc12-0540

The Effects of Excessive Doses of Fructose

In 1993, some researchers agreed that excessive consumption of fructose (then defined as 7.5% to 70% of total energy intake) induces immediate de novo lipogenesis in both animals and humans. In different experimental settings, it circumvented the substrate inhibition feedback mechanisms that are present for glucose when it enters glycolysis. It was shown that the dietary fructose fraction not converted to lactate in the intestinal epithelium was rapidly absorbed by the liver. It was subsequently converted first to fructose-1-phosphate, and then to triose-phosphate and pyruvate/lactate. Both are potential substrates for liver glycogen synthesis and fatty acid production. This leads to increased release of TAG from the liver into the blood. In addition, fructose was found to stimulate key lipogenic enzymes by activating the sterol regulatory element-binding protein-1c (SREBP-1c) in the livers of mice. https://doi.org/10.1093/ajcn/58.5.754S

High fructose loads (50% of total diet) were also found to lead to an increase in the PPARγ coactivator 1α and 1β (PGC-1α and PGC-1β). This promoted insulin resistance and lipogenesis, as well as decreased insulin receptor activation and phosphorylation of the insulin receptor substrate. Subsequently, lipogenesis induced by this high fructose load was associated with the formation of larger fat deposits in adipose tissue and muscle, in animal models. DOI: 10.1055/s-0029-1211853

Physical activity as a determining factor

Two studies say that no evidence has been found that relatively high levels of sugary drink consumption may be associated with:

• obesity
• diabetes
• Cardiometabolic risk

Professionalathletes who usually consume sugary drinks such as energy drinks. On the other hand, there is evidence that physical inactivity, even for a few days, causes insulin resistance and dyslipidemia in normal healthy individuals. https://doi.org/10.1161/ATVBAHA.107.153288

In this regard, these randomized intra-subject studies in healthy men and women showed that higher plasma concentrations of triacylglycerols, induced by a high-carbohydrate diet, were completely avoided by physical activity. Therefore, the metabolic consequences of a high intake of mixed glucose and fructose can be significantly modulated by exercise. https://doi.org/10.2337/db12-1651 and https://doi.org/10.1161/hq0901.095553

Conclusion on fructose

While fruit consumption in Spain has fallen in recent years due to rising prices (data from the Ministry of Agriculture, Fisheries and Food), less than 10% of most Western populations consume adequate levels of whole fruits and dietary fibre, and typical intake is about half of the recommended levels. Evidence of the beneficial effects of consuming adequate levels of whole fruits has been growing steadily. Especially with regard to its bioactive fiber prebiotic effects and its role in weight management, wellness, and healthy aging.

The assumption that fructose was directly related to the onset of obesity was based on correlation data. Specifically, between the increase in HFCS consumption and the prevalence of obesity in the U.S. This assumption has been considered misleading for a number of reasons.

First, the correlation between HFCS and obesity data only occurred in North America. In Europe, there was also an increase in the prevalence of obesity during the same period, but HFCS was not consumed in significant amounts. That’s why fructose has been disproportionately blamed for the rise in obesity. Scientific evidence suggests that it is no more harmful than other sugars when consumed in similar amounts. Thus, obesity is due more to the excessive consumption of calories and sugars in general, than specifically to fructose.

The reviews often found highlight that many studies on fructose have significant limitations. For example, the lack of adequate controls and the use of excessively high doses, incapable of constituting a humanly sustainable diet.

On the other hand, it is crucial to consider the full context of diet and lifestyle, including physical activity, when assessing the impact of fructose on health.

Because of this, a good public health policy should be based on global scientific evidence and not on myths. It is important to encourage a balanced diet and the reduction of total sugar intake and not just aim for a specific type.