Thanks a lot for your Pita data - I am just in the midst of considering swapping to it and this has helped my decision.
as for SGLT2's, I too have been researching whether to add them. Let me provide my GPT summary to support yours - as it adds some extra info ontop of yours,
particularly regarding HCT:
My prompt was:
'
Are SLG2 medications like Jardiance valuable for AAS users? i know they have kidney protective properties, however I have also heard they restructure muscle morphology and deplete it of glycogen.'
GPT (Model GPT 5-Thinking):
Short answer: probably “sometimes,” not “routinely.”
TL;DR
SGLT2 inhibitors (e.g., empagliflozin/Jardiance) are genuinely kidney- and heart-protective—even in many people
without diabetes. That’s the upside. The trade-offs for lifters are: a small daily energy leak via glycosuria (often ~60–90 g glucose/day), a fuel-shift toward fat/ketone use (less glycolysis), a modest
rise in hematocrit (bad if AAS already pushes Hct high), mild diuresis, and higher rates of genital yeast infections. Evidence for “muscle remodeling” is real but subtle: more intramyocellular lipid droplets and a tilt toward fat oxidation rather than frank muscle loss; meta-analyses do show a small average
lean-mass drop unless diet/training offset it. Net: if you have albuminuria/CKD or HF risk, they can be very valuable; if you’re a healthy, high-Hct, high-intensity athlete chasing a pumped look, they’re usually not worth it
prophylactically.
New England Journal of Medicine+1Lippincott Journals
The upside (why lifters consider them)
1) Real kidney protection, even without diabetes.
Large RCTs (DAPA-CKD, EMPA-KIDNEY) show slower eGFR decline and fewer renal/CV deaths in CKD across etiologies. Mechanistically they restore tubuloglomerular feedback, reduce intraglomerular pressure, and improve tubular energetics. Benefits extend to non-diabetics.
New England Journal of Medicine+1PMCLippincott Journals
2) Heart-failure protection and BP/weight effects.
They reduce HF hospitalization across EF ranges, lower systolic BP a few mmHg, and trim weight mostly via fat+water. Uric acid also falls (less gout risk).
PMC+1PubMed
Heuristic: If you’ve developed
albuminuria or early CKD (which AAS, high BP, and high Hct can aggravate), an SGLT2 inhibitor is one of the few interventions with hard outcome data.
The trade-offs that matter to AAS users
A) Fuel shift, not “muscle wipe-out.”
In humans, short-term SGLT2 use
reduced glycolytic flux markers and
increased intramyocellular lipid droplet size/number, with higher acyl-carnitines and gene expression favoring fat oxidation. That’s a “fasting-like” metabolic tilt, not muscle damage. In training terms: a nudge toward fat/ketone use and away from high-rate glycolysis.
PubMedJCI Insight
B) Lean-mass signal is small but real on average.
Meta-analyses show modest reductions in fat-free mass (~0.9–1.5 kg over months), typically ~25–35% of total weight loss. In resistance-trained lifters eating enough, this is likely attenuated, but it’s a signal you’d plan around.
PMC
C) Glycogen & “flatness.”
Typical glycosuria runs
~60–90 g/day, i.e., ~240–360 kcal/day. If you don’t replace those carbs/calories and fluids, you may look flatter (less glycogen + water). That’s fixable by eating/drinking more; there’s no strong human evidence of chronic muscle glycogen depletion at rest, just a
substrate shift.
PMCDiabetes Journals
D) Hematocrit goes up.
SGLT2 inhibitors commonly raise Hct ~2–4% via increased erythropoiesis. Great for HF/CKD outcomes;
not great if you’re already polycythemic from AAS. If your Hct rides ≥52–54%, this can push you into the red zone.
Annals of Palliative MedicineAmerican Heart Association JournalsNew England Journal of Medicine
E) Volume & electrolytes.
Mild osmotic diuresis means more peeing and a small plasma-volume dip. Combine that with contest-prep restrictions or sauna sessions and you’re courting lightheadedness and performance hits if you don’t compensate.
Lippincott Journals
F) Infections & rare events.
Genital mycotic infections are
2–3× more common; absolute rates in men are typically a few percent per year (higher with prior history). UTIs aren’t clearly increased. Rarely,
euglycemic ketoacidosis can occur—even without diabetes—especially with low-carb diets, fasting, illness, or peri-op states.
Naturedrc.bmj.comPMC+1
Do they “restructure muscle morphology” and “deplete glycogen”?
- Morphology: Human biopsy/MRS work shows more/larger lipid droplets inside muscle fibers and a shift toward fatty-acid use after ~5 weeks of dapagliflozin; mitochondrial function didn’t worsen. That’s metabolic re-programming, not sarcomere loss. Animal data sometimes show fiber-type shifts toward oxidative phenotypes. PubMed
- Glycogen: The drug increases urinary glucose loss; if you don’t replace it, you’ll run slightly “carb-poorer.” Studies emphasize reduced glycolysis rather than measured muscle glycogen depletion in healthy athletes. Practically: the look/performance downsides are preventable with extra carbs, sodium, and fluids. PubMedDiabetes Journals
Where they make sense for AAS users (big-picture framework)
Green light (strong rationale):
- You have CKD signals: ACR ≥30 mg/g or a clear downward eGFR trend despite controlling BP. Run ARB/ACEi at target dose plus consider SGLT2 (empagliflozin 10 mg) and monitor Hct closely. This mirrors trial populations and guideline logic; benefits likely outweigh physique downsides. New England Journal of Medicine+1KDIGO
Yellow light (case-by-case):
- Borderline albuminuria or long AAS history + hypertension, but normal Hct and no dehydration-heavy prep → plausible kidney insurance, but manage the carbohydrate/water gap and watch Hct trends. Lippincott Journals
Red light (generally avoid prophylactically):
- Hct already high (≥52–54%), frequent dehydration/cutting, low-carb/fasting phases, or recurrent genital candidiasis. Here the SGLT2 liabilities (Hct, diuresis, euDKA risk) can outweigh a speculative renal gain in an otherwise normal kidney. AHA Journalsdrc.bmj.com
Practical heuristics if you do use one
- Dose used in trials: empagliflozin 10 mg daily (may titrate to 25 mg in diabetes; kidney/HF trials often used 10 mg). You’ll see a small eGFR dip in the first weeks (hemodynamic), then a flatter slope. New England Journal of Medicine+1
- Pumps & performance: Add ~60–90 g carbs/day (and water + sodium) to offset glycosuria and diuresis; expect a slightly “drier” look otherwise. PMC
- Hematocrit: Recheck CBC after 4–8 weeks; if you already flirt with 52–54%, this might tip you over—plan accordingly. Annals of Palliative Medicine
- Sick-day/low-carb rule: Hold the drug during illness, surgery preps, prolonged fasting, or very low-carb phases to reduce euDKA risk. Resume when eating normally. PMC
- Hygiene & risk reduction: Rinse/dry after training; treat early symptoms of candidal balanitis; prior infections predict recurrence—if that’s you, consider avoiding. drc.bmj.com
Bottom line for your use-case
- Kidney protection: Real and clinically meaningful—if you have documented CKD/hyperfiltration, this is one of the rare pills with outcome wins. New England Journal of Medicine+1
- Physique/performance: Expect a fuel shift (less glycolysis, more fat/ketone use) and a small, preventable tendency toward “flatness.” No good human data show pathologic glycogen depletion in healthy athletes. PubMed
- AAS-specific caution: The hematocrit rise is the main clash with AAS. If your Hct already runs high, SGLT2s are usually a bad add unless the kidney/HF indication is compelling and you’re managing Hct proactively. Annals of Palliative Medicine
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I find it useful knowing the ratio for physiques that look good, because it helps me steer my own goals. Sort of sets body weight aside, to a degree. I prioritise my own training based on keeping ratios a certain rate, e.g chest > midsection.
