Treatment of obesity is a challenging activity in our modern society, including scientific approach and some the current weight-loss programs. One of the surprising scientific discovery it’s the suggestion that Viagra could be useful to treat obesity in humans.
A study published in Federation of American Societies for Experimental Biology, revealed both mice and mice cells that a signaling messenger called Cyclic guanosine monophosphate (cGMP) would have on fat tissue. Normally, cGMP is a common regulator most physiological function including blood vessels, relaxation of vascular smooth muscles lead to vasodilation and increased blood flow. Viagra also enhance the vasodilatory by blocking an enzyme that breaks down cGMP, term phosphodiesterases (PDE 5) that increase levels of cGMP could be considered to contribute to potential changes in the fat cells.
Viagra experiment was done within seven days. During this period the mice were split into two groups, with one group being given 12mg/kg Viagra and the other group being given a placebo containing 0.9% salt. These treatments were administered on a daily basis. Once the treatments were finished, the researchers compared changes in weight and body composition before and after the treatment between the groups. In addition to that the researchers also looked at tissue samples taken from the mice’s abdominal region. The key findings indicated that the weight and body composition was not affected in either group. However, the observation of the samples of abdominal cells suggested that, for the mice in the Viagra group, the white fat cells had changed to have some features of brown adipose tissue (known for their ability to generate heat from fat). Based on this, the researchers argued that Viagra could contribute to “browning” of white fat cells, which could be useful for considering obesity treatments.
Although this study outlined an intriguing hypothesis for the underlying mechanism of browning, it is clear that the many limitations of the study demonstrated that the findings are too small and too recent to warrant the conclusions. The fact that the findings cannot be extrapolated to humans at this stage is obvious given that this was an animal study that had a very short duration. Similarly, several factors such as whether all the mice were obese, ages of the mice and levels of stress tolerance that could have contributed to different reactions between the groups were not specified, thus making it challenging to rule out alternative explanations.
What stood out the most for us when reading the article was the absence of two distinctions in particular. The first one was the researchers’ failure to make a distinction between browning cells and brown cells when discussing their results, thus making it difficult to know whether their ability to create heat from fat comes from an identical process and is comparable to other studies of brown cells. Consequently, this omission led to the study’s main strength of explaining an underlying relationship between Viagra and fat cells becoming subject to more questions than answers. The second distinction was the fact that the researchers gave the mice very high doses of Viagra, which were much higher than the current doses prescribed for erectile dysfunction treatment in humans. This, of course, made us wonder for whom they were designing this treatment and where the value of the finding lies.
If high doses are likely to be considered unsuitable for humans, then they are even more unlikely to be a prescribed by most clinicians. While the findings in this study can raise hope, it is important to know that they are far from being established facts in the scientific community and even further from being considered safe and reliable treatments in the clinical community. You can read more about the study
Treatment of obesity is a challenging activity in our modern society, including scientific approach and some the current weight-loss programs. One of the surprising scientific discovery it’s the suggestion that Viagra could be useful to treat obesity in humans.
A study published in Federation of American Societies for Experimental Biology, revealed both mice and mice cells that a signaling messenger called Cyclic guanosine monophosphate (cGMP) would have on fat tissue. Normally, cGMP is a common regulator most physiological function including blood vessels, relaxation of vascular smooth muscles lead to vasodilation and increased blood flow. Viagra also enhance the vasodilatory by blocking an enzyme that breaks down cGMP, term phosphodiesterases (PDE 5) that increase levels of cGMP could be considered to contribute to potential changes in the fat cells.
Viagra experiment was done within seven days. During this period the mice were split into two groups, with one group being given 12mg/kg Viagra and the other group being given a placebo containing 0.9% salt. These treatments were administered on a daily basis. Once the treatments were finished, the researchers compared changes in weight and body composition before and after the treatment between the groups. In addition to that the researchers also looked at tissue samples taken from the mice’s abdominal region. The key findings indicated that the weight and body composition was not affected in either group. However, the observation of the samples of abdominal cells suggested that, for the mice in the Viagra group, the white fat cells had changed to have some features of brown adipose tissue (known for their ability to generate heat from fat). Based on this, the researchers argued that Viagra could contribute to “browning” of white fat cells, which could be useful for considering obesity treatments.
Although this study outlined an intriguing hypothesis for the underlying mechanism of browning, it is clear that the many limitations of the study demonstrated that the findings are too small and too recent to warrant the conclusions. The fact that the findings cannot be extrapolated to humans at this stage is obvious given that this was an animal study that had a very short duration. Similarly, several factors such as whether all the mice were obese, ages of the mice and levels of stress tolerance that could have contributed to different reactions between the groups were not specified, thus making it challenging to rule out alternative explanations.
What stood out the most for us when reading the article was the absence of two distinctions in particular. The first one was the researchers’ failure to make a distinction between browning cells and brown cells when discussing their results, thus making it difficult to know whether their ability to create heat from fat comes from an identical process and is comparable to other studies of brown cells. Consequently, this omission led to the study’s main strength of explaining an underlying relationship between Viagra and fat cells becoming subject to more questions than answers. The second distinction was the fact that the researchers gave the mice very high doses of Viagra, which were much higher than the current doses prescribed for erectile dysfunction treatment in humans. This, of course, made us wonder for whom they were designing this treatment and where the value of the finding lies.
If high doses are likely to be considered unsuitable for humans, then they are even more unlikely to be a prescribed by most clinicians. While the findings in this study can raise hope, it is important to know that they are far from being established facts in the scientific community and even further from being considered safe and reliable treatments in the clinical community. You can read more about the study