Unlocking the science: How weight loss medication works and its efficacy
The lowdown on the reliability levels of weight loss drugs.
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Weight loss medications have been all over the news and social media recently, so chances are you’ve heard of them.
Whether you’re all for the use of weight loss medication, or are still a bit sceptical, it’s helpful to understand how these medications actually work, as well as how effective and safe they are for overweight and obese people.
Read as we give you the lowdown on the safety and reliability levels of weight loss medications.
How do these new weight loss medications work?
Originally developed to treat type 2 diabetes, these medications are made up of a molecule that mimics glucagon-like-peptide-1 (GLP-1) activity in the body. GLP-1 is an appetite hormone that your body naturally produces to help regulate hunger.
GLP-1 also stimulates the pancreas to release more insulin when needed, slowing down digestion, and minimising the secretion of glucose into the bloodstream — all of which helps to control blood sugar levels [1].
However, during the testing phase, it became clear that patients being treated with this class of medication weren’t just treating their diabetes. They were also losing a significant amount of weight.
But how? Let’s see what the science says.
On one hand, there’s the physiological effect of slower digestion, which makes you feel fuller for longer, helping to reduce your caloric intake. But the medication also affects people on a neurological level.
They suppress appetite by modifying neural pathways involved in reward, motivation, and addiction — and this is what’s believed to be most responsible for the drug’s unprecedented outcomes [2].
The reason for this is still not entirely clear, but logic suggests that it is related to the pathological pathway behind obesity, which starts with desire.
While we know that humans can use their brains to satisfy desires while navigating physiological changes — for example, by replacing 3 meals with continuous snacking to accommodate a smaller stomach after gastric band surgery — there’s little evidence of us retrieving a desire after it has been neurologically suppressed.
The latter appears to be corroborated by a recent large-scale clinical study that found that these medications had the same appetite-suppressing effect on the brain at the end of the 68-week trial as they did in the early stages [3].
Nevertheless, it is by inducing both a physiological and neurological response that these medications are able to suppress human appetite and, as a result, aid with significant weight loss.
Are they safe?
The short answer is yes, the medication has an excellent safety profile. Although some patients experience adverse events, the vast majority of these are mild to moderate and affect the gastrointestinal system — think nausea, vomiting, and diarrhoea — and such effects subside as your body adjusts to the medication.
Moreover, while no one enjoys experiencing symptoms like these — even if they only occur in the short-term, the discomfort is far outweighed by the reward of tackling obesity and its comorbidities.
Some people might also become alarmed by the figures on serious side effects reported in studies like the 2015 Pi-Sunyer et al. clinical trial we mentioned before. But here’s the thing: these figures always need to be compared to those of the control group.
For example, in the Pi-Sunyer et al study, 6.2% of treatment patients experienced serious adverse events, but so did 5% of patients in the control group. And although 1 treatment patient died from hypertensive heart disease, 2 placebo patients also died — one from pulmonary fibrosis and the other from cardiorespiratory arrest.
Another 2 large-scale trials of the medication have also observed a negligible difference in the incidence of serious adverse events between treatment and control groups, stressing that all events, including deaths, were caused by issues that already existed before the study [4][3].
These facts shouldn’t scare you about the potential side effects of the medications. On the contrary, they should remind you of the dangers of living with obesity.
Yes, receiving guided ongoing treatment might result in some uncomfortable adverse events for a while, but if you stick with it, you have a good chance of losing a substantial amount of weight and lowering serious health risk factors.
This is especially true if you take the medication as a part of a holistic weight loss plan like Juniper’s Weight Reset Program, which includes clinically-proven treatments that target metabolism and overhaul hunger signals, as well as medical advice and health coaching.
When combined with lifestyle changes, they are considered among the most effective methods for long-term weight loss in average patients.
Weight loss medications have been all over the news and social media recently, so chances are you’ve heard of them.
Whether you’re all for the use of weight loss medication, or are still a bit sceptical, it’s helpful to understand how these medications actually work, as well as how effective and safe they are for overweight and obese people.
Read as we give you the lowdown on the safety and reliability levels of weight loss medications.
How do these new weight loss medications work?
Originally developed to treat type 2 diabetes, these medications are made up of a molecule that mimics glucagon-like-peptide-1 (GLP-1) activity in the body. GLP-1 is an appetite hormone that your body naturally produces to help regulate hunger.
GLP-1 also stimulates the pancreas to release more insulin when needed, slowing down digestion, and minimising the secretion of glucose into the bloodstream — all of which helps to control blood sugar levels [1].
However, during the testing phase, it became clear that patients being treated with this class of medication weren’t just treating their diabetes. They were also losing a significant amount of weight.
But how? Let’s see what the science says.
On one hand, there’s the physiological effect of slower digestion, which makes you feel fuller for longer, helping to reduce your caloric intake. But the medication also affects people on a neurological level.
They suppress appetite by modifying neural pathways involved in reward, motivation, and addiction — and this is what’s believed to be most responsible for the drug’s unprecedented outcomes [2].
The reason for this is still not entirely clear, but logic suggests that it is related to the pathological pathway behind obesity, which starts with desire.
While we know that humans can use their brains to satisfy desires while navigating physiological changes — for example, by replacing 3 meals with continuous snacking to accommodate a smaller stomach after gastric band surgery — there’s little evidence of us retrieving a desire after it has been neurologically suppressed.
The latter appears to be corroborated by a recent large-scale clinical study that found that these medications had the same appetite-suppressing effect on the brain at the end of the 68-week trial as they did in the early stages [3].
Nevertheless, it is by inducing both a physiological and neurological response that these medications are able to suppress human appetite and, as a result, aid with significant weight loss.
Are they safe?
The short answer is yes, the medication has an excellent safety profile. Although some patients experience adverse events, the vast majority of these are mild to moderate and affect the gastrointestinal system — think nausea, vomiting, and diarrhoea — and such effects subside as your body adjusts to the medication.
Moreover, while no one enjoys experiencing symptoms like these — even if they only occur in the short-term, the discomfort is far outweighed by the reward of tackling obesity and its comorbidities.
Some people might also become alarmed by the figures on serious side effects reported in studies like the 2015 Pi-Sunyer et al. clinical trial we mentioned before. But here’s the thing: these figures always need to be compared to those of the control group.
For example, in the Pi-Sunyer et al study, 6.2% of treatment patients experienced serious adverse events, but so did 5% of patients in the control group. And although 1 treatment patient died from hypertensive heart disease, 2 placebo patients also died — one from pulmonary fibrosis and the other from cardiorespiratory arrest.
Another 2 large-scale trials of the medication have also observed a negligible difference in the incidence of serious adverse events between treatment and control groups, stressing that all events, including deaths, were caused by issues that already existed before the study [4][3].
These facts shouldn’t scare you about the potential side effects of the medications. On the contrary, they should remind you of the dangers of living with obesity.
Yes, receiving guided ongoing treatment might result in some uncomfortable adverse events for a while, but if you stick with it, you have a good chance of losing a substantial amount of weight and lowering serious health risk factors.
This is especially true if you take the medication as a part of a holistic weight loss plan like Juniper’s Weight Reset Program, which includes clinically-proven treatments that target metabolism and overhaul hunger signals, as well as medical advice and health coaching.
When combined with lifestyle changes, they are considered among the most effective methods for long-term weight loss in average patients.
It’s more than just weight loss
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References
- Tran, K., Park, Y., Pandya, S., et al. (2017) Overview of glucagon-like peptide-1 receptor agonists for the treatment of patients with type 2 diabetes. American Health & Drug Benefits, 10(4), 178-188.
- Müller, T., Finan, B., Bloom, S., et al. (2019) Glucagon-like peptide 1 (GLP-1), Mol Metab, 30:72-130.
- Wilding, J., Batterham, R., Calanna, S., et al. (2021). Once-weekly Semaglutide in adults with overweight or obesity. N Engl J Med, 384: 989-1002
- Rubino, D., Abrahamsson, N., Davies, M., et al. (2021). Effect of continued weekly subcutaneous semaglutide vs placebo on weight loss maintenance in adults with overweight or obesity. JAMA, 325(14): 1414-1425.
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