Geneva forces you to go through a doctor
But can you get that much data on so many metabolites just via blood drops?
What are the key benefits of doing the test, do you think? Have you read good reviews or research on the panel of tests?
$620 here:
ION-Sales-Sheet.pdf (6.2 MB)
They test 8-oxo-G and some oxidation byproducts (which gives you option to test/retest after interventions like metformin or anti-glycation drugs)
Also theyâre a good way to test for rare nutritional deficiencies
I wonder if the test result ranges are simply the US normal range, the generally accepted as âhealthyâ range, or the optimal for longevity range⌠Do you have any idea?
you might need to centrifuge it, which is harder with mobile phlebotomy⌠(getlabs). am asking rn
Wow this is way more complicated than I first thoughtâŚ
- Contact Getlabs: If you have concerns about the complexity of your blood draw or need to discuss equipment requirements (like a centrifuge), reach out to Getlabs directly at hello@getlabs.com or through their Contact Page. They may offer accommodations or clarify any misunderstandings.ââ
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there are CENTRIFUGES at biomakerspaces!! [but they often have limited hoursâŚ]
LOOKS LIKE ARCPOINT LABS CAN DO THE CENTRIFUGE
wow, mobile phblebotomist from getlabs.com came over and made it all super-easy (theyâll take care of the centrifuge and shipping), I really got lucky b/c I wasnât compared for the complexity but theyâve done it before!
Got my report⌠Some parts are really scary. Trying to run thru o3.
CHAL-Genova-Diagnostic 2025.pdf (533.6 KB)
Idgaf but there are some strong concerns
Ugh I really need to semaglutide more
I was so healthy a few years ago and something happened recently. I really donât think it was the life altering accident, but it could have contributedâŚinasmuch as it increased appetite
Oxidative vs Reductive stress â a side-by-side read of your ION ÂŽ panel
(all values already corrected for the very low urine creatinine, i.e. á 4)
âStress dialâ | Key lab pointers from your report | Net push |
---|---|---|
Oxidising-side drivers | ⢠Pyroglutamate = 9.5 mmol / mol Cr (high-normal) â glutathione is being spent faster than average⢠8-OH-dG â 3â4 Âľg / g Cr after dilution correction â some DNA oxidation, albeit mild⢠Orotate â 0.27 mmol / mol Cr â nucleotide ârepair debrisâ⢠Low Îł-tocopherol and low Ď-3 index â fewer lipid-phase antioxidants | Moderately â |
Reducing-side drivers | ⢠Whole-blood GSH = 786 Âľmol LâťÂš â 60-ish percentile; plenty of reducing buffer⢠β-Hydroxybutyrate = 0.8 mmol / mol Cr (after correction) â fasting/ketosis raises the NADH:NADâş ratio (âreductive pushâ)⢠Serine â, Taurine â â both sulphur-rich, antioxidant amino acids ⢠Riboflavin-FAD demand (borderline glutarate) suggests parts of the ETC want more oxidising power | Mild â |
Neutral / missing | ⢠Lipid peroxides not reportable (Cr too low) â would have sharpened the oxidation picture⢠No oxidised : reduced glutathione ratio (GSSG/GSH) in this panel | â |
Quick index:
Think of oxidative-stress âpressureâ as how hard your antioxidant bank account is being tapped; reductive-stress âpressureâ as how over-stuffed that bank is with reducing equivalents.
- Withdrawal rate (oxidative): mild-to-moderate â enough to lift pyroglutamate and flirt with the 8-OH-dG cut-off, but not deplete glutathione.
- Deposit rate (reductive): low-to-mild â ketosis and ample GSH give a reductive nudge, yet no markers show the overshoot seen in true reductive stress (e.g., high lactate : pyruvate, high reduced/oxidised GSH ratio, suppressed ROS-dependent signalling metabolites).
Verdict
Your chemistry tilts slightly oxidative overall: glutathione is plentiful, but youâre using it; DNA-oxidation debris is detectable; lipid-phase defences are under-supplied. Reductive stress does not appear dominantâthereâs a gentle reductive push from fasting/ketones, but nowhere near the âstuck in over-reductionâ profile seen in heart-failure or chronic hyper-NADH states.
Tightening the redox balance
Goal | Practical lever | Expected shift |
---|---|---|
Lower oxidative withdrawals | ⢠2â4 g EPA + DHA/d⢠100 IU mixed tocopherols⢠NAC 600 mg Ă 2 + glycine 3 g at night⢠Polyphenol-rich plants (berries, cocoa, green tea)⢠Normal-volume morning urine on next lab â lipid-peroxide data | â 8-OH-dG, normalise pyroglutamate |
Avoid over-reduction | ⢠Keep β-hydroxybutyrate in nutritional-ketosis range only when intended (⤠1.0 mmol / mol Cr)⢠Riboflavin-5â˛-phosphate 20 mg for FAD enzymes | Keeps NADH:NADâş and FAD-linked dehydrogenases balanced |
Monitor | ⢠Add oxidised & reduced GSH or GSSG/GSH ratio next panel⢠Include plasma lactate : pyruvate or β-HB : AcAc if you stay low-carb | Gives a direct reductive-stress gauge |
If those tweaks pull pyroglutamate and 8-OH-dG further into the green while GSH stays robust, youâll know the redox seesaw is centred. Should new data ever show an excessive drop in ROS-dependent markers (e.g., chronically very low 8-OH-dG, suppressed NRF2 activity, rising lactate : pyruvate), then weâd revisit reductive stressâbut at present your profile is âmild oxidative > mild reductive.â
What a lab panel
can
âand canâtâtell you about energy surplus
A Genova IONÂŽ profile is superb for vitamin, redox, and mitochondrial clues, but it is not a calorie counter. None of its biomarkers quantifies how much food goes down the hatch. What we can do is look for the typical biochemical fingerprints of chronic over-feeding vs. neutral or hypocaloric states and see which side your data lean toward.
âCalorie-surplus flagsâ most labs show | Your result | Interpretation |
---|---|---|
Persistent glycolytic spill-over (high lactate, high pyruvate and no ketosis) | Lactate 7.5 mmol /mol Cr (low-normal) and β-hydroxyÂbutyrate 0.8 mmol /mol Cr after dilution-correction CHAL-Genova-Diagnostic 2025.pdf](file-service://file-G3N327fubLTMQt2dUnHoLW) | Pattern fits light ketosis / low-carb utilisation, not chronic over-glucose. |
Sugar overflow into urine (seen in big SGLT-2 doses or frank hyperÂglycaemia) | Glucose 355 mg dL-š in a dilute sample. When we scale to a typical creatinine it shrinks to â90 mg dL-šâstill unusual, but compatible with a sweet coffee just before the test HAL-Genova-Diagnostic 2025.pdf](file-service://file-G3N327fubLTMQt2dUnHoLW) | Isolated finding; not enough to call habitual caloric excess. Repeat in a fasting, morning void. |
Citric-acid-cycle congestion (citrate, cis-aconitate, isocitrate all high) | All three sit mid-range (Citrate 265 mmol /mol Cr on a 40-520 ref band) CHAL-Genova-Diagnostic 2025.pdf](file-service://file-G3N327fubLTMQt2dUnHoLW) | No sign of âmetabolic backlogâ typical of chronic over-feeding or insulin resistance. |
Chronically suppressed ketones (β-HB <0.2 mmol /mol Cr) | Even after correction youâre at 0.8âsquarely in ânutritional ketosisâ | Suggests at least intermittent carbohydrate restriction or caloric dips. |
RBC fatty-acid excess signals (very high palmitic/stearic, elevated Ί-6:Ί-3) | Palmitic & stearic on the high edge; Ί-6:Ί-3 ratio 11.3 H but Omega-3 index 1.8 L CHAL-Genova-Diagnostic 2025.pdf](file-service://file-G3N327fubLTMQt2dUnHoLW) | Tells us what you eat (lots of MUFA/SFA, scant EPA/DHA), not how many kcal. |
Hyper-insulinaemia / high C-peptide | Not measured in this panel | Need fasting insulin/HOMA-IR to judge. |
Adiposity hormones (leptin, adiponectin) | Not measured | â |
Net read-out:
Your organic-acid and ketone pattern is more compatible with under-fuelled periods (low-carb or time-restricted eating) than with chronic caloric excess. Isolated glucosuria could be beverage sugar or a transient blood-glucose peak, not proof of habitual over-eating.
Where lab blind-spots remain
Missing piece | Why it matters |
---|---|
Body-weight / body-fat trend | Scale or DEXA is still the most direct âcaloric scoreboard.â |
Fasting insulin Âą HOMA-IR | Elevated insulin precedes weight gain and is a sharper caloric-excess biomarker than glucose alone. |
Serum triglycerides & ALT | Climb when liver is chronically flooded with surplus calories. |
Leptin & adiponectin | Reflect longer-term fat-mass signalling and caloric status. |
Add those on your next venepuncture if you want a definitive metabolic-energy picture.
Quick self-check until the next blood draw
- Weight log: if weekly morning weight is flat or slowly down, net calories are at or below maintenance.
- CGM or glucometer: if 2-h post-prandial glucose < 120 mg/dL most days, youâre unlikely to be chronically over-eating carbs.
- Food diary reality check: one week in â track everything, including the coffee extras. Compare to estimated TDEE.
Take-home
Your IONÂŽ data show some nutrient imbalances (low omega-3, low Îł-tocopherol, high coffee polyphenol load) but no metabolic smoke-signals of a sustained caloric surplus. To answer the calorie question with high confidence, layer in body-composition tracking and a basic metabolic panel (fasting insulin, lipids, ALT). For now, your mild ketosis and balanced citric-acid intermediates suggest youâre more likely hovering at maintenance or on the lean side of the ledger.
Iâm getting a retest of my urine sample b/c the first sample was too low due to creatinine dilution, preventing measurement of lipid pexoxides and distorting 8oxoG and phenylacetateâŚ
[maybe this time im gonna load on both rapamycin and NAC shortly before just to see if the values can change that much]
getting my next test tomorrow! Which means I canât drink too much today (otherwise it will wreck my per creatinine test). [it recommends 1.41953 Liters max in 24 hours beforeâŚ] and one sparkling water is 0.615 L. and 18.3 oz jovial diced tomatoes⌠+ coffee⌠this can get slightly toughâŚ
Iâm gonna take lots of TMG, tocotrienols, metformin, NAC Ethyl ester, whatever. It means I canât single out anything that will change everything, but any existence proof will help. But Iâm also going to hold off on the taurine.
[and maybe 1-2 nicotine lozenges to replace the coffee]
500 mg melatonin too
Ion Panels are far far higher ROI than almost any of the tests people currently takeâŚ
later I ate more diced tomatoes
but I did have 6 orders of salad (with croutons, with toasted tempeh => and while it didnât feel like much, I really hope the toasted tempeh wonât end up wrecking my readings today).
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thereâs an issue tho⌠and itâs this
Yes â but mostly by dilution, not by changing how much creatinine your body makes.
1. What canagliflozin does to urine volume
Osmotic diuresis. Blocking SGLT-2 makes 60-100 g of glucose spill into the urine each day. Glucose drags water with it, so 24-h urine volume rises by â0.3â0.5 L after the first dose. In most people the kidney partly adapts, but a persisting extra 200-300 mL /day is common. (PubMed Central, AHA Journals)
Transient natriuresis. Sodium excretion and atrialânatriuretic-peptide rise for a day or two, then return toward baseline, while the extra water loss continues. (insight.jci.org)
2. Consequence for urinary creatinine concentration
Parameter Typical baseline After âĽ4 wk of Cana 100â300 mg 24-h urine volume ~1.5 L â 0.2â0.5 L 24-h creatinine excretion (reflects muscle mass) unchanged unchanged Creatinine concentration (spot sample) e.g. 120 mg/dL â 5â15 % Class data: In a mechanistic study, empagliflozin (another SGLT-2i) lowered 24-h urinary creatinine concentration by â1.66 mmol /L (~-9 %), matching the rise in urine volume. (AHA Journals)
Canagliflozinâspecific: A pooled analysis found both urine creatinine and albumin-to-creatinine ratio (UACR) fell significantly versus placebo after 12 weeks of canagliflozin. (Diabetes Journals)
3. Why total creatinine excretion stays the same
Creatinine production depends on muscle mass, not the kidney. Because canagliflozin does not alter creatine breakdown, the amount excreted in 24 h is stable; it is simply diluted into a slightly larger urine volume.
4. Practical implications
Albumin- or protein-to-creatinine ratios (ACR / PCR).
Part of the 20-30 % fall in UACR seen with canagliflozin is due to lower albumin leakage (real renoprotection); a small part is dilution from lower urinary creatinine concentration. Clinically, the total drop is still accepted as beneficial.Spot-urine drug screens & research samples.
Very low creatinine (<20 mg/dL) can invalidate some assays. If you need concentration-independent data, use a 24-h collection or correct for specific gravity rather than creatinine.Serum creatinine / eGFR.
Serum creatinine may rise a little in the first 2â4 weeks (hemodynamic effect on the glomerulus) before returning toward baseline; this is unrelated to the dilution seen in urine.Hydration status matters more than the drug.
A large glass of water will change urine creatinine far more than the extra 250â300 mL attributable to canagliflozin.
5. Bottom line
Canagliflozinâs mild, chronic osmotic diuresis spreads the same daily creatinine load over a bigger urine volume, so spot urinary creatinine concentration typically falls by roughly one-tenth. That can slightly exaggerate drops in UACR or PCR but does not mask kidney injury, and it has no bearing on serum creatinine or true renal function.
2:55AM I gave it. Meh. the draw is scheduled at 8AM to 10AM and Iâm not sure Iâm going to be able to really sleep⌠But I prepared hard in some ways to not drink TOO much
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AND⌠rescheduled⌠unfortunatelyâŚ
got blood drawn today, this was way smoother. i did drink 2 1-liter tetrapaks of almond milk yesterday but spaced far apart and this was not a high level of fluid consumption for me in a day.
[i had a small amt of roasted chickpeas and vegetables for dinner, did not eat much other than shirataki before dinner]. i later took A LOT of melatonin.
my sleep was disrupted, but i at least dreamed. fitbit doesnt record anything yet⌠but i could wake up for 5AM
they have metabolomix+
im gonna send in sample for tasoo imyoo later today