Thank you for this response. I dont know what the situation is exactly with SGLTIs However, there does tend to be an issue with losing muacle when losing weight. The challenge is ensuring muscle gain when regaing weight.

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One of the factors with WFPB is the low calorie density. With glp’s you feel fuller at a lower stomach volume of food, and things move through more slowly. In combination GLP + WFPB, for individuals who have 100 lbs to lose – usually no problem!

I’ve got a couple of patients who eat right through 15 mg of Tirzepatide and lose little weight - it’s always high calorie density and little fiber.

Starting these meds is an opportunity to make it easier to change dietary pattern. If the two occur together, the outcomes have been very good.

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In another thread it was said that SGL2i increases the risk of sarcopenia. Of course, it can be due to a calorie deficit (glucose is excreted with the urine)

https://spotify.localizer.co/t/canagliflozin-another-top-anti-aging-drug/91/981

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I would think the issue is that you get muscle loss with fat loss, but because of the difficulties of creating new muscle you then get weakness. The sarcopenia is underlying this and not itself caused by the calorie deficit.

Hence weightloss for older people leads potentially to frailty and maintaining muscle mass is harder. Hence weightloss drugs of any type are not pro longevity/healthspan for older people.

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Some SGLT2I have been linked to lean muscle loss but not all. The meta-analysis addresses this.

As above discussion suggests, the data regarding SGLT2i, and sarcopenia or muscle wasting is conflicting. Apart from discordant findings, there are also various unknowns (Fig. 3). The differences in the results cannot be explained clearly. However, the dose or duration of treatments, concomitant therapies with SGLT2i treatment, characteristics of the study population, the technique used to assess body composition may all play a role for these discordant findings [58].

There are studies that say dapagliflozin decreases fat but not lean muscle.

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Sadly I don’t have access to that commentary. However, I would think this would be quite aging dependent.

(Post moved to SGLT2I topic.)

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Can you please discuss GLP-1RA and SGLT2i in their respective topics? Or start a new weight loss and muscle mass thread? :sweat_smile:

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Main author’s answer:

The survival curves reflect the entire follow-up period. Exposure to SGLT2 inhibitors (like all anti-diabetic drugs in the study) was assessed in chronological order from 1999 to 2018 as a binary variable (yes/no), based on whether patients used the specific drug. This is why the graph shows data for the entire follow-up period, even though these drugs have only been available for the last 10 years.

I don’t understand…

Looks like those who started SGLT2i 10 years into this period already had lower PD risk : Possible this group is more health conscious or has access to better quality health care.

This kind of bias is unavoidable in association studies.

Yes it’s weird but then she told me:

No, the survival curve for SGLT2 inhibitors does not reflect the effects of other drugs prior to the switch. It specifically represents the outcomes for patients from the point they began using SGLT2 inhibitors.
Additionally, the time-dependent model we employed in our analysis accounts for the length of time patients were on different antidiabetic drugs, ensuring the comparisons between medications with varying availability timelines, such as metformin and SGLT2 inhibitors.

If anyone understand please let me know…

Do you have any references that prove this is a common side effect?

The GLP-1 agonists cause weight gain a part of which is muscle loss. After the drug is discontinued, 75% of the weight comes back, but usually not the muscle. That’s what I’ve read and heard about Munjaro and Ozempic.

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Full video of the workshop will be posted here in about two weeks: https://www.nationalacademies.org/event/43073_09-2024_examining-glucagon-like-peptide-1-receptor-glp-1r-agonists-for-central-nervous-system-disorders-a-workshop

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Association between dietary niacin intake and risk of Parkinson’s disease in US adults: cross-sectional analysis of survey data from NHANES 2005-2018

Ling Zhang et al. Front Nutr. 2024.

In the RCS linear test, the occurrence of PD was negatively correlated with dietary niacin intake (nonlinearity: p = 0.232). In stratified analyses, dietary niacin intake was more strongly associated with PD and acted as an important protective factor in patients with fewer years of education (OR: 0.35, 95%CI: 0.13-0.93), married or cohabitating (OR: 0.71, 95%CI: 0.5-0.99), taking dietary supplements (OR: 0.6, 95%CI: 0.37 0.97), non-smokers (OR: 0.57, 95%CI: 0.39-0.85), those with hypertension (OR: 0.63, 95%CI: 0.63-0.95), coronary artery disease (OR: 0.77, 95%CI: 0.6-1), and stroke (OR: 0.75, 95%CI: 0.88-0.98), but the interaction was not statistically significant in all subgroups. Dietary niacin intake was inversely associated with PD risk in US adults, with a 23% reduction in risk for each 10 mg increase in niacin intake.

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This may a good reason to take niacin or one of the NAD boosters like NR or NMN.

Of course it is a Chinese paper, so take it with a grain of salt… or 100.

I wouldn’t jump to conclusions based on an association study about dietary niacin (even less so when it’s a Chinese study in Frontiers). However, there are ongoing RCTs of large dose NR in PD so we’ll soon have an answer to this question…

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More SGTL2i stuff: Canagliflozin - Another Top Anti-aging Drug - #1058 by adssx

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Thank God I was wrong: it seems that low-dose metformin might be great: Metformin decelerates aging clock in male monkeys - #15 by adssx (TBC though…)

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