Dear Laura...I take Mounjaro for diabetes, how can I make it suck less?

Welcome to ‘Dear Laura’ - a monthly column where I fashion myself as an agony aunt and answer the questions that readers submit. If you’d like to send in a question for me to answer next month, you can submit it here.

I’m happy to answer Qs about anti-diet nutrition, developing a more peaceful relationship to food and weight-inclusive health, annoying diet trends and news stories, body image challenges, and, of course, challenges with feeding your kiddos. Please give as much detail as you’re comfortable with and let me know if you’d like me to include your name or keep it anon.

Please remember that these answers are for educational purposes only and are not a substitute for medical or nutritional advice; please speak to your GP or a qualified nutrition professional if you need further support.

I wrote the question that follows based on a real person but have edited the details slightly to protect their identity.

Dear Laura,

I have recently started taking Mounjaro to help manage my blood sugar levels. I have a diagnosis of type 2 diabetes and have been trying various medications to bring my HbA1C down, but at my last review, my GP insisted that this was the only option left. After a lot of consideration, I decided to give it a go. I have some other ‘health stuff’ (mental health, chronic illness) that impacts how I move through the world and means that this medication makes a lot of sense for me – I’m not going to be able to ‘gentle nutrition’ my way out of type 2 diabetes. 

But I’m also struggling with the medication on a few different levels. 

Firstly, physically I feel awful; full very quickly after eating, not being able to eat very much at all (especially after being moved up a dose or after my weekly injections), nauseous, bloated, low energy, and constipated. These symptoms are sometimes so bad that they’re debilitating and stop me from seeing friends or being with my family.

Secondly, food has lost a lot of its joy and pleasure, something that was hard won through rebuilding my relationship with food after a years’-long eating disorder and finding fat liberation. I feel really sad about not being able to enjoy things like baking with my kids, or a fancy meal out with friends. I had worked so hard on making peace with food and feeling embodied that this feels like a massive set-back. 

Because I’m fat my doctor isn’t listening to my concerns and doesn’t seem to hear when I say I want the lowest dose that will bring down my HbA1C, rather than the dose that will cause maximum weight loss. He’s also dismissive of the side-effects and I haven’t been offered any nutrition support. 

Right now I’m worried I’m not eating enough to meet my nutritional needs, and nobody can really tell me about the long-term impacts of that. I’m too afraid to start googling how to help my symptoms because everything assumes you want to maximise weight loss. I’d love to hear your take on what the research says about the long-term impacts, how to mitigate them (if that’s even possible) and if there are any non-diet strategies to help make this medication feel less harmful?

Can you also tell me more about how this drug works; is it just because I am eating so little, or is there some other mode of action?

First of all, thank you for this question; I appreciate you speaking to the messiness and complexities of these drugs in a way that isn’t articulated in the almost universally positive media coverage of them. 

Frequently I hear stories about people who quit their gym memberships to take weight-loss injectables. Or they say they can ‘eat whatever they want’ just in smaller quantities. This is a bit like saying if you chew gum you don’t have to brush your teeth. It’s as if we’ve been conflating health with thinness all along…

The framing of advice for these drugs often hinges on how to maximise weight loss, not on how to reduce side-effects or support long-term wellbeing. There is also a ubiquitous idea that these drugs will quieten ‘food noise’. The (anti-fat) assumption here being that you must have a terrible relationship with food to begin with, otherwise you wouldn’t ‘need’ these drugs. But what if you’ve already done a lot of work to heal your relationship with food and your body? Suddenly having to think about food all the time would, I imagine, be very distressing. 

There are a few things I’d like to address in my response:

1. What exactly Mounjaro is and how it works
2. What the long-term impacts of medications like these are
3. How to mitigate the risks and side-effects associated with weight-loss injectables

Before I go on, I want to make it clear that I am not endorsing these medications per se. My personal opinion is that these drugs are prescribed irresponsibly, without a high consent process in place. Meaning that people think they can just chew gum and their teeth won’t fall out. From my experience, doctors – even in specialised weight management settings – aren’t given adequate training on how to manage the side-effects, or how to mitigate the significant risk of malnutrition. And, as I wrote about last week, I think weight-loss injectables will only exacerbate anti-fat bias in medicine and more broadly. 

That said, I understand why people take them; whether to manage type 2 diabetes, as with this reader, or to reduce the burden of anti-fat bias experienced on a daily basis. They are powerful tools for managing blood glucose and there’s emerging evidence that they can help reduce disease risk in other areas. There are also significant potential complications and things we just don’t know about these drugs yet. It’s messy and complicated and I’ve tried my best to distill the things I think are most salient from a nutrition perspective.

For this piece I also checked in with specialist diabetes dietitian and CIHAS reader Rebecca Lawton. You’ll hear from her in a bit. 

What is Mounjaro and how does it work?

Mounjaro is the brand name for a drug called tirzepatide. Tirzepatide contains two different molecules: glucagon-like peptide-1 receptor agonists (GLP-1RAs) and glucose-dependent insulinotropic polypeptide (GIP) agonists. You have probably already heard of GLP-1RAs like semaglutide, found in drugs like Wegovy and Ozempic. Tirzepatide also contains a GIP agonist on top of the GLP-1RA, which may make it more potent for reducing blood sugar levels. 

Both GLP-1 and GIP are hormones that are made by our guts in response to a meal. They help signal to our brains that we’re starting to get full. In response, our bodies slow down digestion; release insulin to help move glucose into our cells; stop our body from producing glucose from the liver and muscle (something that happens when we’re hungry!); and ultimately, to signal that we’ve had enough to eat. 

The way that tirzepatide and similar drugs work is by dialling this normal response to food up to max volume. Typically you’d need to eat a full meal in order to achieve these effects, but with tirzepatide, the effect is achieved with a lot less food. The food stays in the stomach for longer and the whole digestive process is much, much slower; two processes known as delayed gastric emptying and slowed gastric motility respectively. The overall effect is that people eat much, much less food than they ordinarily would.

So to answer the reader’s question, the mechanisms are largely dependent on an overall lower quantity of food being consumed. That said, reductions in HbA1c – which should be the main indicator of ‘success’ in people with type 2 diabetes – can be achieved without changes to weight. Similarly, reduced risk of cardiovascular events appear to precede significant changes in weight.  

What are the long-term impacts of taking medications like these?

In short, we don’t really know. The clinical trials (STEP, SURMOUNT) of GLP1-RA drugs have typically run for 68-72 weeks. Follow-up studies are usually more concerned with outcomes related to weight and HbA1c than nutrition-related outcomes. 

‘I don’t think there is any long-term research as yet,’ Rebecca agrees, ‘but we can look at outcomes from intensive weight loss programs and weight loss surgery to extrapolate what we might expect’. She points to the Look AHEAD trial where participants were required to significantly reduce the energy intake to between 1200-1800kcal depending on their starting weight. ‘There was poorer bone density and increased frailty fractures in the intervention group’. Estimates of energy intake in people taking GLP1-RAs like tirzepatide are as low as 1200 kcal, and could even be lower.

‘We also know that loss of muscle mass is an issue’, Rebecca notes. ‘I do think in the future we are going to see an increase in osteoporosis and fractures due to poorer bone health’.