Imeglimin. A new and novel drug thats better than Metformin

#64

For anti aging I added dapaflozen (??) an SGLT2, 10mg AM, and may not be getting the most out of taking this by takiing in AM vs in front of food.

Talk here of taking imeglimin WITH metformin any thoughts of imeglimin with a SGLT-2?

tnx to all, curt

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#65

Deborah, we are similar. My A1c is 5.6, my FBS is 92, and my fasting insulin is 2 -4 (I’m an omnivore). My c-peptide is 1.5. I am also taking 1g of Metformin. By all accounts, it seems I have some beta-cell insufficiency and a slow phase 1 insulin response. Have you done any genetic analysis? I did. Using my 23andMe data and running it through Rhonda Patrick’s genetic service I learned that I have several variants that predispose me to diabetes: SLC30A8, IRS1, ACE, CRY2. The first is a zinc waster, which means I don’t absorb zinc well and zinc is necessary to produce insulin. Sure enough, I tested on the low end of normal. I have upped my zinc and we will see it’s impact in upcoming tests. My IRS1 variant impairs insulin signaling and could be ameliorated by reducing saturated fat (at least according to Rhonda’s site). If you haven’t already, a genetic analysis could provide some interesting data for you. I will be ordering Imeglimin from Maulik soon, too. And thanks to Charles for alerting me to the possibility of Met/Imeg combo therapy. BTW, have you tried this glucose metabolism calculator? It provides some interesting metrics that were new to me. Glucose Metabolism Interpreter.

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#66

Thanks for your post, Kebossit. A while back I did do the Rhonda Patrick report on my 23&Me data. Just revisited it, and it showed a low adiponectin level, and a risk of obesity. The obesity risk was also highlighted in my Promethease report. This confirms what I have long felt was true – I gain weight so easily and have to watch calories very carefully – while also needing to work extra hard, and find low-calorie high protein nutrition to grow some muscle. The Rhonda Patrick report also highlighted a tendency to develop diabetes. So this, combined with the recent insights that genetics control about half – much higher than previously thought – of your health/longevity: a giant “Oy vay,” as they say.

This is all so discouraging, but knowing is better than not knowing. When I have told people that my mother is 99 (but very severely demented) and my grandmother lived to 103, they respond “You’ve got great genetics.” NOT! Could be worse, but I do not want to be a skinny, frail, demented centenarian.

If it were not for this forum, I would likely still be blithely believing I was quite OK doing what I was doing, which wasn’t nothing but: now I know I need to work much harder. So, even though rapamycin in particular does not seem to be an intervention that is matched with my body or my genes, (or my age) I have learned so much, and confirmed so much that I already sensed but could not verify until now. Thank you all!

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#67

Ya, I also have low adiponectin and an obesity gene (FTO) per Rhonda. I am curious why you don’t think rapa would work for you…especially since we seem to have some similar genes and maybe age (I am 59 on Saturday). Low muscle mass? It is on my to-do list.

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#68

I had similar problems with lower digestive tract problems and occasional bouts of unexpected diarrhea. This was after I stopped taking metformin, which acts as a strong laxative for me. May be an effect of polypharmacy or too many supplements. Old age is certainly a factor. When I was young, I had a cast-iron stomach that would tolerate most anything.

My first line of defense was to take 2 mg of loperamide daily. This is a safe dose for long-term use. This worked quite well, but didn’t address the underlying problem.

I eventually concluded that my gut bacteria might be a problem due to occasional antibiotic use, including the DAV protocol “Three-drug combination therapy for anti-aging.”

So, how to address the problem of gut bacteria? Some forum members suggest eating a lot of yogurt, as well as kimchi and sauerkraut. I think that is a good suggestion, but I don’t like any of them.

My solution, which is working quite well, is to take probiotics daily. I have tried them occasionally in the past and was not impressed. But I think I was using the wrong protocol.

The key, from my experience, is to take the probiotic if it is not already in an enteric-coated capsule and put it in a slightly larger enteric-coated capsule. Gut bacteria need sufficient fiber to thrive. I don’t get enough fiber in my protein-weighted diet. I cannot tolerate most fiber supplements, such as inulin, because they cause a lot of gas. I use “Advanced Acacia Fiber Powder, Organic Soluble Fiber Leaky Gut Repair Powder.” Natural Supplement Prebiotic for Gut Repair" from Amazon. I really like this fiber because it dissolves in my coffee without adversely affecting the taste.

My protocol is not medical advice. Just the result of an N=1 experiment.:

So, I have solved the problem for me. Take any good probiotic bacteria supplement; I really don’t think it matters. I would start with a known good bacteria that is often prescribed for children, Lactobacillus Breve. I started with this and had very good results. You must take it in an enteric-coated capsule to see results within a reasonable amount of time. It takes about 30 days to see results from a probiotic supplement, along with a daily dose of fiber. You can take loperamide daily while you are doing this. It has no adverse effects on the gut bacteria.

Claude:

General Safety of Low-Dose Daily Use

For mild, chronic loose stool issues, low-dose daily loperamide is actually commonly used and considered reasonable in several clinical contexts:

  • Crohn’s disease: It’s frequently used as an adjunct for mild functional diarrhea, but with an important caveat — it should generally not be used during active flares or if there’s any risk of toxic megacolon (a serious complication). During remission or for residual loose stools, it’s often appropriate.
  • Polypharmacy/supplement-induced loose stools: This is a very common and generally safe application for loperamide, as the cause is functional rather than inflammatory.

Key Considerations

Dose: 2 mg/day is a low, conservative dose (the typical acute dose is 4 mg initially, then 2 mg after each loose stool, up to 16 mg/day). So 2 mg daily is well within a safe range for most people.

Drug interactions matter: Since polypharmacy is already a factor, it’s worth flagging that some medications (like certain antifungals, antibiotics like clarithromycin, or HIV medications) can raise loperamide blood levels and increase cardiac risk — though this is mainly a concern at higher doses.

Supplement interactions: Some supplements (like grapefruit-related compounds or St. John’s Wort) can affect how loperamide is metabolized.

When NOT to use it:

  • During a Crohn’s flare with significant abdominal pain or fever
  • If the diarrhea may be from an active infection (C. diff, for example)
  • If there’s blood in the stool

Long-term use: Regular use can sometimes mask underlying problems that need attention, so it’s worth periodically reassessing why the loose stools are happening rather than just controlling symptoms indefinitely.

Bottom Line

For the scenario you describe — mild, non-inflammatory loose stools in the context of Crohn’s (not actively flaring) or polypharmacy effects — 2 mg of loperamide daily is generally considered a safe and reasonable approach by most gastroenterologists. It’s not habit-forming and doesn’t carry significant systemic risk at that dose.

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#69

There was a time when I had gut issues and nothing seemed to work. What cleared it up were oregano pills. I read about it somewhere online and didn’t really expect it to work but in about a week’s time I had significant improvement.

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#70

Good question. I am curious about this also.

So, here is the prompt I gave to Google Gemini 3 Pro:

Role: pharmacist and longevity researcher. Task: identify and summarize research papers from the past 5 years that cover simultaneous dosing imeglimin with a SGLT-2 inhibitor, isolating the claims made in these papers.
Part 3: Claims & Verification

  1. Extract Claims: Identify every specific biological, medical, or protocol claim made in the study.
  2. Verify Externally: Search for “[Claim] meta-analysis”, “[Claim] Cochrane review”, “[Claim] RCT”.
  3. Assess Hierarchy of Evidence: Evaluate support using this strict hierarchy:
    • Level A: Human Meta-analyses / Systematic Reviews.
    • Level B: Human RCTs.
    • Level C: Human Observational / Cohort Studies.
    • Level D: Pre-clinical (Animal/In vitro). Flag heavily if claim relies on this level.
    • Level E: Expert Opinion / Anecdote.
  4. Detect Translational Uncertainty: If a claim is based on mouse/worm/yeast data but presented as human advice, label this as a “Translational Gap.”

STRICT CITATION PROTOCOL (MANDATORY):

  • Hyperlink Syntax: Use inline Markdown hyperlinks: Title (Year).
  • Verification: Do not generate a URL unless you have accessed the live webpage. Fallback to Title (Year) if the direct link is unstable.
  • Search Query: For every claim, execute: “[Topic] study [Journal Name] [Year]”.
  • Link Validation: Prioritize nlm.nih.gov, doi.org, nature.com, science.org. If no link is found, state “Source unverified in live search.”

Output Constraints:

  • Use Markdown formatting.
  • Do not use LaTeX, python code, or special characters that break simple text parsers or reveal formatting codes, etc…
  • Tone: Objective, critical, “Tell it like it is.” No hype.

Output: Provide a bulleted list of claims with their associated Evidence Level (A-E) and supporting external citations.

Gemini 3 Pro Response:

Claims & Verification: Imeglimin and SGLT-2 Inhibitor Co-Administration

The following claims regarding the simultaneous dosing of imeglimin and SGLT-2 inhibitors are extracted from literature published between 2021 and 2026.

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#71

Just started today, 2x 1000mg

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#72

Is anyone pairing this with retatrutide? Curious to hear about experiences.

Claude seems to think these would be synergestic, and in my opinion, Reta + SGLT-2 + imeglimin is probably a much more beneficial stack than whatever crazy & expensive things other biohackers are carrying out (e.g. reta + tesamorelin — which is probably the safest among the other crazy stuff going on in that space).

Excerpt of chat with Claude:

" Here’s the reasoning for why imeglimin (the “glimin” class oral antidiabetic, approved in Japan) could complement retatrutide (Lilly’s GIP/GLP-1/glucagon triple agonist):

Complementary mechanisms

Retatrutide acts at the receptor level — it agonizes GLP-1R, GIPR, and GcgR to drive weight loss, improve incretin signaling, and increase energy expenditure. Imeglimin works at the cellular/mitochondrial level, amplifying glucose-stimulated insulin secretion and preserving β-cell mass, while also enhancing insulin action in the liver and skeletal muscle PubMed Central. These are largely non-overlapping targets.

Countering retatrutide’s glucagon-driven hepatic glucose output

This is arguably the most compelling rationale. Retatrutide’s glucagon receptor agonism is intended to increase energy expenditure and lipolysis, but glucagon also stimulates hepatic gluconeogenesis — a potential glycemic liability. Imeglimin directly targets excess hepatic gluconeogenesis as one of its three core mechanisms PubMed Central, which could offset this side effect of glucagon agonism.

β-cell protection

Retatrutide drives sustained metabolic stress (weight loss, altered fuel partitioning). Imeglimin’s mitochondrial mechanism — rebalancing respiratory chain activity and reducing reactive oxygen species — preserves β-cell mass and function PubMed Central, which could support long-term durability of glycemic benefit.

Additive glucose-dependent insulin secretion with low hypoglycemia risk

Like GLP-1 receptor agonists, imeglimin enhances insulin secretion in an exclusively glucose-dependent manner, but their mechanism of action at the cellular level diverges PubMed — imeglimin works through NAD⁺/ATP amplification rather than receptor signaling. So combining them adds two independent glucose-dependent insulin-secretion pathways without substantially increasing hypoglycemia risk.

Residual insulin resistance

Retatrutide’s primary benefit is weight-mediated metabolic improvement. But imeglimin targets multiple mechanisms — increasing insulin sensitivity, decreasing gluconeogenesis, increasing β-cell function, and improving mitochondrial function PubMed Central — potentially addressing insulin resistance that persists beyond what weight loss alone corrects."

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#73

@shc I agree re reta + imeg + sglt2 and I’ve been doing GH secretagogs early AM and before bed: Ipamorelan 300mcg + CJC 300 mcg + tesamorlan 300mcg. I agree prob too much pressure from secretagogs. Its said that your body can only respond with so much GH release from the secretagog input and anything more then your body can put to use is wasted. Per my costs so low I con’t care about wasting a peptide. IE nexaph.com and chinese places another 20% cheaper.

I’m 72yo male, fit and no GH secretagogs my IGF-1 is just 159, 2 hr after this dose my IGF-1 is 250 and has seen higher. So the rule that GH secretagogs loose effectiveness above age XX is maybe true in general but the healthiier you are the more you work on rebuilding your organs, pineal gland, thymus via the various bioregulators; epitalon, pinealon, chronuluten, vesugen, vilon, livagen, cartalax cortagen, et al (they have some cross talk) the more you get your organs to still produce as I’ve have tested to show.

I just need to share from the body builder / health groups that there are some 20% of non responders to Reta and they have to move back to Tirzepatide. Side effects reported can be: hyper to hypo glucose even early AM during sleep. Papitation, tacacardia at night, even an increase in appitite which is more often then reduction. So some folks combine semaglutide or tirzepatide with reta. Some lower percent up to 50/50 to reta.

Just reporting that 100% reta can be tolerated by alot of folks, some do have to swap to tirz or combine with sema or tirz.

I’ve heard that if you are on 3mg/week in multiple doses tirzepatide that reta might need 4mg. IMHO though I’d still swap mg for mg onto reta and titrate up as you search for results.

I do 1mg / week 50:50 tirz and reta not for weight loss but for HRT a forever protocol.

Another issue: GLP-1’s interact with mitchondria function along with MANY other compounds: SLU-PP-332, 5amino-1q, even Urolithin-a, SS31, MOTSC and prob many other compounds. Meaning you may without knowledge amplify the effect of reta by adding some seemingly unrelated compound and now you have side effects, nausia, total constipation by adding an unrelated compound but under the hood there IS a connection.

The single common thread to me is lower doses of everything and very very careful titration up ideally just one thing at at time and give a month for the connectedness to settle out. I wish this was all simpler but its not.

Good luck, curt

PS hate to not mention, its common wisdom in the health coach circles that all this is useless completely and practically useless if ALL of your hormones are not up to 40yo levels: E, P, testosterone and free-T3 above 3.2 etc etc etc. I will add that fasting glucose and insulin needs to be well under insulin resistant. GLP-1 is NOT a cure for insulin resistance as is marginally wrongly touted. Get your diet fixed THEN GLP-1. I can share cheap blood testing and mail order T, E, P hormone sourcing with just an emailed blood test. Thyroid, ideally is NP thyroid a desicated till needs a local prescriber.

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#74

Alone for replace metformin? Or with met, acarbose, sglt2, etc.

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#75

Just noticed this message from a while back… here is the response from Gemini 3 Pro:

Contraindication Analysis: Imeglimin and Rapamycin (Sirolimus)

There is currently no scientific or clinical evidence indicating that imeglimin is contraindicated for individuals taking rapamycin. On the contrary, existing pharmacokinetic and pharmacodynamic data suggest the two compounds are structurally independent and potentially synergistic in mitigating the metabolic side effects of mTOR inhibition.

Pharmacokinetic (PK) Independence

The primary safety concern when stacking compounds with rapamycin is the modulation of cytochrome P450 3A4 (CYP3A4), as rapamycin is heavily dependent on this enzyme for hepatic metabolism.

  • Renal Excretion vs. Hepatic Metabolism: Imeglimin is excreted largely unchanged in the urine via active renal secretion (utilizing OCT1/OCT2 and MATE transporters). It undergoes minimal hepatic metabolism.
  • Absence of CYP Interference: In vitro and in vivo human studies confirm that imeglimin has no significant induction or inhibition potential toward CYP450 enzymes, including CYP3A4. Therefore, co-administering imeglimin will not artificially elevate or depress systemic rapamycin trough levels, avoiding acute toxicity or sub-therapeutic dosing.

Pharmacodynamic (PD) Synergy

Rapamycin is utilized in longevity protocols to inhibit the mTORC1 pathway, a mechanism that reliably delays cellular senescence but frequently induces metabolic toxicity. Long-term sirolimus use dampens peripheral insulin signaling and increases hepatic gluconeogenesis, often resulting in insulin resistance, hyperglycemia, and hypertriglyceridemia (clinically documented as New-Onset Diabetes After Transplantation, or NODAT).

Imeglimin presents a compelling mechanistic countermeasure to this specific side-effect profile:

  • Mitochondrial Rescue: Rapamycin-induced insulin resistance is driven by peripheral tissue metabolic stress. Imeglimin targets mitochondrial bioenergetics (mildly inhibiting Complex I while stimulating Complex II), reduces reactive oxygen species (ROS), and upregulates glucose-stimulated insulin secretion without exhausting $\beta$-cells.
  • Clinical Application for mTOR Toxicity: Recent clinical reviews explicitly identify medications targeting compromised mitochondrial function, specifically citing imeglimin, as therapeutic interventions to rescue blood sugar control and metabolic homeostasis in patients suffering from immunosuppressant-induced diabetes (including those on sirolimus).

Knowledge Gaps & Required Data

While informed speculation strongly supports the safety and metabolic utility of this combination, significant evidentiary gaps remain in the literature.

  • Translational Void: There are zero Randomized Controlled Trials (RCTs) directly evaluating the co-administration of imeglimin and rapamycin in healthy human populations for healthspan extension or sarcopenia prevention.
  • Data Requirements: To definitively validate this protocol, crossover clinical trials are required. These studies must quantify whether imeglimin’s activation of upstream metabolic sensors (such as Akt or AMPK) unintentionally blunts rapamycin’s geroprotective mTORC1 suppression at the skeletal muscle or organ level. Furthermore, continuous glucose monitoring (CGM) and cross-sectional lipid tracking in a co-administered cohort are required to quantify the exact magnitude of imeglimin’s rescue effect on rapamycin-induced dyslipidemia.
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#76

Imeglimin Shows Sustained Real-World Efficacy in Aging Diabetics, But High-Dose Metformin Combo Triggers Gut Distress

Mitochondrial modulators are gaining traction in the longevity and metabolic health space, and imeglimin—a novel oral tetrahydrotriazine—is showing promise outside of strictly controlled clinical trials. A new retrospective cohort study analyzed the 12-month real-world efficacy of imeglimin in individuals with type 2 diabetes. The drug, which targets mitochondrial complex I to enhance insulin secretion and suppress hepatic gluconeogenesis, effectively reduced HbA1c by an average of 0.8% across all age groups over the study period.

Crucially for longevity protocols targeting older demographics, imeglimin maintained its efficacy and favorable tolerability profile in the very elderly, including those aged 75 and older. However, the data revealed a significant translational caveat for combination therapies: co-administering imeglimin with high-dose metformin (1,000 mg/day or more) significantly increased the frequency of gastrointestinal disturbances. Because both drugs inhibit mitochondrial complex I and share structural similarities, their stacked use likely amplifies gut toxicity. Patients whose biguanide doses were reduced or discontinued when starting imeglimin experienced fewer GI events, but they also saw less robust HbA1c reductions compared to those who maintained their biguanide dose, highlighting a stark efficacy-versus-tolerability trade-off.

Beyond glycemic control, the study noted favorable off-target metabolic effects. Over 12 months, subjects exhibited significant reductions in body weight, triglycerides, and liver enzymes, specifically ALT, AST, and gamma-GTP. These secondary outcomes suggest imeglimin may possess hepatoprotective properties, potentially offering a therapeutic vector against metabolic dysfunction-associated steatotic liver disease (MASLD), a major driver of systemic aging.

  • Paper: Real-world effectiveness and safety of imeglimin: a single-center retrospective cohort study in Japan
  • Context: This research was conducted by scientists at the Central Japan International Medical Center, Gifu University, and Kyoto University in Japan.
  • Journal: It was published in Frontiers in Clinical Diabetes and Healthcare.
  • Impact Evaluation: The impact score of this journal is 2.2, evaluated against a typical high-end range of 0–60+ for top general science, therefore this is a Low impact journal.
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#77

Looking at imeglimin literature, I was currently focusing on the effect on mitochondria, and a few papers were interesting enough to share here in a batch (with brief commentary from me).

There has been talk here about imeglimin vs metformin in regard to exercise, and a question about the possibility that imeglimin might be similarly suboptimal in the context of exercise. It seems not. In fact, there might be synergies between imeglimin and exercise - at least resistance exercise (free article).

Combination of imeglimin and resistance exercise improves mitochondrial function and glucose metabolism in skeletal muscles

“These findings suggest that the combination of imeglimin and RT [Resistance Training] is a promising therapeutic approach to enhance mitochondrial function and glucose metabolic capacity.”

There have been suggestions that some drugs that were used in T2DM were actually beneficial for CV health, such as SGLT2i. Well, it looks like perhaps imeglimin might join the club, insofar as it might mitigate atherosclerosis - who knew!

Molecular mechanism for pancreatic β-cell dysfunction and atherosclerosis

“Recently we have reported that imeglimin exerts beneficial effects on mitochondria morphology in β-cells and/or number and quality of insulin granules. In addition, we have reported that imeglimin shows favorable effects against the development of atherosclerosis independently of glycemic and lipid control.”

That part about the effect on atherosclerosis was independent of glycemic and lipid control is very important, because it tells us that this effect is not solely due to imeglimin being an anti-diabetic agent, and also because it can be used as an addition to LLT (statins, ezetimibe etc.), and the effects on atherosclerosis should therefore stack.

How does imeglimin work in beta cells? Overview.

Current understanding of imeglimin action on pancreatic β‐cells: Involvement of mitochondria and endoplasmic reticulum homeostasis

A big part of fighting aging is centered around the inflammatory process that is downstream from LPS propagation. It looks like imeglimin might be helpful here (free article).

Imeglimin attenuates NLRP3 inflammasome activation by restoring mitochondrial functions in macrophages

“We demonstrated for the first time that imeglimin reduces LPS-induced NLRP3 inflammasome activation by inhibiting mPTP opening in THP-1 macrophages. These results suggest that imeglimin could be a promising new anti-inflammatory agent for treating diabetic complications.”

The next paper speaks for itself - mitochondrial ROS is a fundamental driver of aging, so it’s nice to see imeglimin might be helpful here (free article).

Suppressing Mitochondrial ROS Production is Beneficial in Multiple Preclinical Models of Human Disease

Finally, the last paper is just a case report, but I liked it because it used three classes of drugs, which many of us have an interest in: SGLT2i, ARB and glimin. As a small additional factor, the ARB in question is olmesartan which I have increasing interest in.

Mitochondrial Nephropathy With m.5538G>A Mutation Within the tRNA-Trp Region Assessed by Mitochondrial Function Analysis: A Case Report

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#78

I use acarbose 100mg each meal, dapa 10mg and tirz 3mg + the imeglimin

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#79

Do you track your blood glucose at all with a CGM? I would love to see your charts… how is your waking blood glucose? Any issues with low blood sugar… low energy, etc.?

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#80

A few week report on imeglimin + dapaflogzen (??) an SGLT2. I put on a CGM, continuous glucose monitor, stelo, not that good but works and cheap.

500mg am imeglimin was ok, + 10mg dapa was ok slightly better. taken upon rising, before brushing teeth re timing. I have a pronounced dawn effect of a 30pt rise from pre wakening in bed. 75-80 rising to 110-120.

Upping to the suggested 1000mg imeg at rising + 10mg dapa knocked that back down under 100.

Flat through AM, early afternoon. Then prior to dinner, 4pm for us, I take another 500mg imeg + 10mg dapa (though std dose is 10mg alll day) and I’m flat through our meat dinner, wine, cheese desert, often some dark chocolate that has std sucrose…

I’m VERY happy getting this imeg tip here from THIS thread. THANK YOU guys!!!

Next experiment is to add a blood pressure drug; telimsartan, a low toxisity, gp for general health drug similar to imeg in that it has wider benefits then just small nudges on blood pressure that I don’;t have any problem with. This prospect came to me as a low toxic low risk alternative to carderine a thermogenic with a cancer rumor (probably out of context). Reading that telimisartan also nudges better glucose control.

IMHO lower glucose (70-90 flat all day is the goal) thus lower to flat insulin leads to lower all forms of inflammation, leads to lower inflam-aging and lower disease.

Both of us have taken this groups guessing and moved to 6mg rapa every 2 weeks. I do more due to my past testing experience of low absorption re my blood testing.

Good luck and health to all, curt

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#81

Maybe a bit impatient (on my part) but I think we are due another update from you @cl-user on imeglimin. Share what you can, FG, Exercise, any effect on markers (if you had labs lately) etc…Thanks,

#82

@Kelman Wearing a CGM, Lingo, seemed to work the best. I wore 2 Stelo’s both died in the 2nd week.

1000mg imeglimin upon waking, and 500mg prior to dinner. And 10mg dapaflogzen (??) at AM and either 5mg or 10mg of dapa upon dinner;

Diet: low carb high protein and 2 meals aday. AM might be protein powder + left over meat/fish/cottage cheese, or all of the above. And at 4pm some meat or fish. A french style desert or 2nd course of cheese. Usually some dark chocolate. I aim for 120grams of protein. Honestly probably under 50g of carbs. Fat is just in the cheese and flat iron steak. I do add ghee, butter, to coffee/bone broth each AM. I also add a teaspone of sheep tallow to a vitamin mix; adding steric acid and also a teaspone or 2 of high oliec olive oil. Decently high fish oil incluiding decently high dosing of PRMs from prodrom.com .

YET without this glucose control my glocose will have a dawn effect running from 90’s while sleeping up into 120/130 by 8am without a food based reason. Through the day normal glucose will vary between 120 and down to 90’s. An allopathic endo would say my glucose is perfect. An anti-aging researcher would say I’m too high.

You’d think this low carb (IE <<100g/day some might say is lowish carb, yet I think I’m under 50) I’d be bouncing at 70 with ease. My wife can, not so much me. But she has a slow pancreas/eyelets and she can spike. She’s slow at uptake new things so so far is not on these drugs.

Post imeg/dapa; sleeping glucose bounces off 70 and always under 80, dawn effect very slight up to 90, and day time can drop into the 80s, and stay flat under 90 through dinner. Even small carbs, berries, chocolate can have little effect. Crap deserts with synthetic ultra-glycemic can spike to 120 even 130 but that is low compared to naked of 140-150.

No side effects; stomach, intestinal, any… Pills chew easily and swallow with water quickly. Are cheap from alldaychemist.com. Or other Indian sources.

IMHO these 2 drugs are life time and can’t see any reason to not take.

Its 5pm, less then 45 min post dinner just tested for ketones with a keto-mojo. 0.2. Which is amazing given I should have some insulin… Which I must not have much else I’d not be producing ketones this close to food!! Meaning these drugs allow my insulin to stay so low I still produce ketones. Which IMHO is the total goal, super low insulin.

With peptide boosts of HGH, the secretagogs, minor excersize grows good muscle. Even on rapa, low carb, low insulin. I have very good muscle. Can curl 45# hand weights x 10 reps. Most body builders believe one needs to feed carbs and run insulin high to grow muscle…

Pre drugs my fasting insulin was under 3.5, very very low. I’m taking these drugs to go from good glucose control to excellent. This all is on top of the usual; Alpha lipoic acid and friends.

My total cholesterol is too low at 165, 72 HDL. At 72yo male I’d prefer LDL above 125 maybe more. Some I believe because we eat only regeneratively grown grass finished beef; an example is flat iron steaks from piedmontese.com, miller bio farm in PA, Frankies grass finished beef… Piedmontese is easiest to order from. Also very very good frozen trout from smokeinchimneys.com . Grill fast on charcole stuffed with onion, dill and lemon. 3.5min a side.

Good luck, curt

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#83

Thanks @curt504 (Curt), great info and explanation as usual. Have couple questions below:

Are you saying that you chew Imeglimin and Canagliflozin? I thought you are not supposed to chew them??? Plus I take Empagliflozin first thing in the morning (25mg) do you think i should split and take 1/2 in AM and the other half with/pre dinner? I thought SGLT2i’s are supposed to be empty stomach?

Care to explain why you think an LDL-C of 125 is better than 72 or said in a different way are you trying to commit suicide LOL. If you are afraid, you might start third world war :joy::joy:by saying that LDL-C at high levels is not dangerous, you can DM me, I’m very interested in your reasoning. I’ve been in a quest to severely crush my LDL-c as of late but I’m afraid i might be turning myself into one of those supercentenarian Japanese woman with a heartbeat of 25 per minute (that have forgotten to die, yet they’re not alive either :joy:) as opposed to my usual raging (with hormones) bull LOL.

Thanks for the sources of grass fed beef, and trout. might try in future.