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Educational Blog - GLP-1 Receptor Agonists
Introduction
In recent years, GLP-1 receptor agonists like semaglutide (brand names: Ozempic
and Wegovy) have gained popularity for weight loss and diabetes management. These medications are even being explored for potential use in dementia treatment. However, as a vitalistic naturopathic physician, I believe it’s essential to take a step back and look at the long-term effects of these medications, especially for off-label use. In this article, we’ll dive into the facts and the risks surrounding GLP-1 medications.
What is GLP-1?
GLP-1, or glucagon-like peptide-1, is a naturally occurring hormone that plays a vital role in regulating blood sugar levels. It promotes insulin secretion, reduces glucagon release, slows gastric emptying, and helps promote satiety. Initially, synthetic GLP-1 receptor agonists were developed as a treatment for type 2 diabetes. Pharmaceutical companies then began to focus on their weight loss benefits, with Ozempic and Wegovy becoming popular options for people looking to lose weight.
Off-Label Use of GLP-1 Medications for Weight Loss
Soon after the introduction of Ozempic and Wegovy, providers observed that patients using these drugs were experiencing significant weight loss—a benefit that wasn't initially expected. This "side effect" soon became the primary reason for prescribing these drugs. Today, GLP-1 receptor agonists are commonly prescribed for weight loss in individuals who do not have diabetes. While this has been celebrated as a breakthrough in obesity management, it raises concerns from a vitalistic perspective. Overriding the body’s natural regulatory mechanisms for weight management may have long-term implications that we don’t fully understand.
GLP-1 and Dementia: The Next Frontier?
Recent headlines suggest that GLP-1 medications may have the potential to prevent or treat dementia. While preliminary studies are promising, we need more research before jumping to conclusions. Neurological protection is a complex, multifactorial
issue, and using metabolic drugs to address brain diseases should be carefully scrutinized.
As a naturopathic physician, I understand that blood sugar dysregulation plays a significant role in cognitive decline. In fact, Alzheimer’s disease is often referred to as “Type 3 Diabetes”, a term reflecting how poor glucose control can impair brain function. So, the question is: Should we focus on synthetic hormones, or is it more effective to address the root cause through dietary changes, therapeutic movement, and natural supplements?
For most people, supporting blood sugar regulation naturally through lifestyle changes can be a far safer and more sustainable solution for brain health. But, of course, every individual’s situation is unique, and medications may be necessary in some cases. The key is to understand that these should be one tool in the toolbox, not the first-line solution.
The Thymus Cancer Connection: Why You Should Be Concerned
One of the most troubling aspects of GLP-1 receptor agonists is the potential link to cancer. Preclinical studies have shown that these medications caused medullary thyroid carcinoma and thymus tumors in rodents. While we cannot directly translate these findings to humans, the black box warning on these drugs indicates a serious potential risk.
The thymus plays an essential role in immune system development, especially during early life. As a practitioner who values the body’s inherent intelligence, I am deeply concerned about the potential impact of these medications on such a crucial organ. This is particularly troubling when these drugs are used for non-life-threatening conditions such as cosmetic weight loss.
Vitalistic Reflections: A Holistic Approach to Health
From a vitalistic perspective, our goal is not to suppress symptoms but to understand why the body is expressing an imbalance and to support its natural healing potential. Chronic weight gain, cognitive decline, and metabolic dysfunction often stem from lifestyle choices, nutrition, trauma, and environmental toxins.
While pharmaceutical interventions like GLP-1 agonists may offer short-term relief, they can sometimes mask symptoms without addressing the root causes of the problem. It’s critical that we continue to demand long-term safety data, engage in honest discussions about risks, and commit to root-cause healing through natural, holistic methods.
Conclusion: The Big Question
Before embracing any new drug as a panacea, we must ask ourselves: What are the long-term effects? Are we supporting or suppressing the body’s wisdom? Are we treating the whole person, or just chasing numbers on a scale?
At Rising Phoenix Naturopathy, I am committed to exploring safe, sustainable solutions that support your body’s natural healing ability. GLP-1 medications may be useful in certain situations, but it is important to remain cautious and prioritize personalized care that addresses the root causes of disease.
If you have any questions or want to discuss more, please feel free to email me at info@RisingPhoenixNaturopathy.com
Citations
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Bjerre Knudsen L, Madsen LW, Andersen S, et al. Glucagon-like Peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology. 2010;151(4):1473-1486. doi:10.1210/en.2009-1272
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Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183
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Nørgaard CH, Friedrich S, Hansen CT, et al. Treatment with glucagon-like peptide-1 receptor agonists and incidence of dementia: Data from pooled double-blind randomized controlled trials and nationwide disease and prescription registers. Alzheimers Dement (N Y). 2022;8(1):e12268.
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Espinosa De Ycaza AE, Brito JP, McCoy RG, Shao H, Singh Ospina N. Glucagon-Like Peptide-1 Receptor Agonists and Thyroid Cancer: A Narrative
Review. Thyroid. 2024;34(4):403-418. doi:10.1089/thy.2023.0530
5. Madsen LW, Knauf JA, Gotfredsen C, et al. GLP-1 receptor agonists and the thyroid: C-cell effects in mice are mediated via the GLP-1 receptor and not associated with RET activation. Endocrinology. 2012;153(3):1538-1547. doi:10.1210/en.2011-1864