Weight-Loss Injectable Medications
There has been a storm of weight loss medications hitting the market over the last few years. Examples of these medications include Semaglutide (Saxenda), Liraglutide (Wegovy and Ozempic) and Tirzepatide (Mounjaro). These medications mimic the “incretin” hormones which we secrete in response to the consumption of dietary fat. The incretin hormones include Glucagon-like peptide -1 (GLP1) and Gastric inhibitory peptide (GIP) and they trigger appetite suppression (see “weight regulation” tab). Dietary fat consumption triggers the release of other appetite suppressive hormones such as cholecystokinin, leptin, peptide YY and amylin. Weight loss injectable medications do not mimic any of these other hormones. In other words, dietary fat has a powerful effect on appetite suppression comparable to and possibly better than weight loss injectable medications.
Our bodies have an innate ability to regulate weight via homeostatic mechanisms (refer to “weight regulation” and “glucose homeostasis” tabs). Carbohydrate consumption results in an insulin spike, which reduces the activity of hormone-sensitive lipase, which is needed to access stored fat as an energy source. When calories are restricted without carbohydrate restriction, this triggers homeostatic mechanisms that minimise weight loss, such as a reduction in metabolic rate and the stimulation of hunger. In contrast, when carbohydrate intake is reduced (but intake of fats and proteins are maintained), insulin levels are low and hormone-sensitive lipase is active. This enables us to mobilise stored fat for energy, which prevents activation of homeostatic mechanisms that would otherwise help to minimise weight loss. This combined with the appetite suppressive effects of dietary fat consumption allows us to introduce intermittent fasting without hunger. Logic tells me this is safe. As a species, we have evolved over 300, 000 years thriving on a mostly ketogenic diet (meat, eggs, veg, nuts, seeds) with limited periods of higher carbohydrate intake (berries in summertime). What happens if we interfere with nature? What happens if we inject medications that over-ride hunger when we don’t have access to our stored fats? The following questions come to mind.
How is this any different to the Minnesota Starvation study or the Biggest Loser study discussed earlier?
If we are calorie restricting without access to stored fats, what is the impact on our BMR? Where is this weight loss coming from? Lean muscle mass? Bone density?
When we administer synthetic (exogenous) hormones, such as testosterone or prednisone, we suppress our own ability to make these hormones. Are we going to suppress our ability to make GLP1 and GIP?
Chronically elevated levels of insulin results in the development of insulin resistance. The instructions for all injectable medications include the recommendation to increase the dose as the effect wears off. Are we going to build resistance to exogenous (factory made )and endogenous (made by our bodies) GLP1 and GIP?
What happens when we cease these medications?
How can we safely use injectable weight loss medications?
Injectable weight loss medications need to be used as a TOOL to help complement the metabolic and hormonal processes that are activated with LCWF. They should never be prescribed as a primary means of treatment to support calorie restriction without carbohydrate restriction. In the early stages of implementing LCWF changes, these medications are helpful to quieten food noise and combat sugar addiction. They may serve as effective confidence boosters. They may be reintroduced for a few weeks if patients are straying from LCWF changes. These medications should be used intermittently at a minimally effective dose. This prevents reliance on the medications for sustainable weight loss.
