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Comment by CJefferson | Hacker News Reader

I've recently started taking 'liraglutide', which is an appetite suppressant.

I haven't been taking it that long, but so far it's amazing -- I eat a balanced meal with an approriate amount of calories in it, and then I am full, and don't want to eat any more. Sometimes I snack and eat a biscuit, but then I don't feel any need to eat a second biscuit.

I'm not saying this is a long-term solution for me, or people in general, but what it has shown me is some people (me included) have managed to mess up their digestive systems badly enough it is incredibly hard to eat healthily -- I previously lost 8 stone (50 kg), but I was hungry every minute of every day, no matter what I tried. Once I had a bad patch I ended up putting all the weight back on.

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'an appetite suppressant' is really underselling liraglutide. It also corrects insulin resistance, which accounts for some degree of it's effectiveness as a weight loss aid beyond it's effects on slowing the GI tract.

GLP-1 agonists are truly an amazing class of drugs. It's absolutely absurd that they're generally not covered by insurance for non-diabetics, even when they yield such obvious benefits for obese people.

>It also corrects insulin resistance

Is liraglutide doing that directly, or is it mediated by people eating less sugar?

Directly. It stimulates insulin release from the pacreas.

Eesh… that doesn’t seem great. How does this not cause further habituation?

Human and animal studies demonstrate that it doesn't seem to worsen insulin resistance if treatment is ceased, but probably doesn't significantly improve it either.

Weird. That's quite intriguing.

Within the UK they remain restricted too.

However, more and more at target populations i.e. obesity + diabetes/obesity related secondary condition or even at risk for diabetes i.e. ethnicity based.

Are being offered these treatments.

It really will be a new age for obese patients.

The first and exercise tactic is a lost battle, ideally we'd be bringing up a generation that can manage their weight but we've failed at that. This is a really good option.

Metformin is similarly excellent drug even in absence of diabetes.

As a non-diabetic (though demonstrably insulin resistant and leptin resistant), I've found metformin's gastro side effects and impact on blood glucose levels to be annoyingly unpredictable. Metformin also causes a noticeable drop in testosterone that can be especially counterproductive for men if weight loss/maintenance is a goal and one already has relatively low baseline testosterone levels.

Definitely heard that the gastro side effects are unacceptable to many and can even impact social life.

I'd heard a bit about the testosterone, i.e. that you don't get the testosterone rise associated with successful management for diabetes. And perhaps Metformin short circuits that. Also that it might correlate with the life expectancy improvement and it does make sense since Metformin is also used for PCOS with wide ranging benefits not limited to insulin resistance but actually reducing androgenic effects of the condition.

Do you think you'll continue with Metformin? I've genuinely was close to starting on it some years back (despite having no (pre) diabetes.).

Metformin never really yielded noticeable benefits for me (neither in terms of fat loss nor any bloodwork metrics) above and beyond other lifestyle changes I had already made, so I discontinued it after a trial period of about 4 months.

The MD I was working with argued that I could have seen a impact on weight loss if taking a more extreme approach to dieting (basically an extremely high protein, moderate fat, moderate carb diet with 300-400 calories of intake every ~4 hours from sunrise to sunset) in conjunction with the metformin, but that approach didn't really fit my lifestyle at the time. If done correctly, this ostensibly maximizes the gluconeogenesis inhibition effect of metformin in conjunction with minimizing fatty acid synthesis by keeping blood levels at a consistent glucose deficit (thus encouraging lipolysis). I was also unconvinced that this isn't a just-so story, and thus I preferred to take a traditional 'keto' diet route (which has a lot more evidence backing it).

The MUFAs in olive oil and a-linolenic acid (like from flax seed) are natural GLP-1 agonists:

https://nutritionandmetabolism.biomedcentral.com/articles/10...

Edited to add: https://pubs.rsc.org/en/content/articlelanding/2020/fo/d0fo0...

I’m not overweight and I tried liraglutide for other reasons and it had the same effect on me.

Obviously it’s the whole “is your blue my blue?” conundrum, but at least some of us that aren’t overweight could also eat all day too. Dieting for anyone is hard. It seems like once you go below what your body is used to you’re going for be super hungry.

Interesting. Does that help with all forms of caloric intake? Alcoholic / sugar beverages included?

In general, yes, but beverage intake results can vary a lot based on behavioral factors. If one frequently drinks sugary beverages or even alcohol to attempt to sate a hunger drive (e. g., due to leptin resistance), it could dramatically reduce intake of those things. But if intake of those beverages are driven by other factors such as poor judgement in beverage selection for hydration or alcoholism, it's not likely going to result in much of a change.

As far as medical solutions go, something like naltrexone is probably a better fit for discouraging unhealthy food/beverage selection, especially (but not necessarily) when paired with bupropion. The combo dramatically blunts the positive neurochemical effects of eating artificially sweet/salty/fat foods + drinking alcohol (and nearly eliminates the perceptible benefits of alcohol as well - it's a very surreal experience).

Was it hard to get it? Is it expensive?

https://m.goodrx.com/victoza

$1000 for 3 pens.

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