Ion panel tests and how to order them

#1

Geneva forces you to go through a doctor

#2

But can you get that much data on so many metabolites just via blood drops?

#3

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)

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#4

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 they’re a good way to test for rare nutritional deficiencies

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#5

I wonder if the test result ranges are simply the US normal range, the generally accepted as “healthy” range, or the optimal for longevity range… Do you have any idea?

#6

I found someone who ordered an ion panel for me thru https://www.evexiadirect.com at last

#7

Google Photos

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 thought…

  • 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.​’

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there are CENTRIFUGES at biomakerspaces!! [but they often have limited hours…]

LOOKS LIKE ARCPOINT LABS CAN DO THE CENTRIFUGE

#8

wow, mobile phblebotomist from getlabs.com came over and made it all super-easy (they’ll take care of the centrifuge and shipping), I really got lucky b/c I wasn’t compared for the complexity but they’ve done it before!

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#9

Got my report… Some parts are really scary. Trying to run thru o3.

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#10

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 don’t think it was the life altering accident, but it could have contributed…inasmuch as it increased appetite

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#11

Oxidative vs Reductive stress ― a side-by-side read of your ION ® panel

(all values already corrected for the very low urine creatinine, i.e. á 4)

“Stress dial” Key lab pointers from your report Net push
Oxidising-side drivers • Pyroglutamate = 9.5 mmol / mol Cr (high-normal) → glutathione is being spent faster than average• 8-OH-dG ≈ 3–4 µg / g Cr after dilution correction → some DNA oxidation, albeit mild• Orotate ≈ 0.27 mmol / mol Cr → nucleotide “repair debris”• Low γ-tocopherol and low ω-3 index → fewer lipid-phase antioxidants Moderately ↑
Reducing-side drivers • Whole-blood GSH = 786 µmol L⁻¹ → 60-ish percentile; plenty of reducing buffer• β-Hydroxybutyrate = 0.8 mmol / mol Cr (after correction) → fasting/ketosis raises the NADH:NAD⁺ ratio (“reductive push”)• Serine ↑, Taurine ↑ – both sulphur-rich, antioxidant amino acids • Riboflavin-FAD demand (borderline glutarate) suggests parts of the ETC want more oxidising power Mild ↑
Neutral / missing • Lipid peroxides not reportable (Cr too low) — would have sharpened the oxidation picture• No oxidised : reduced glutathione ratio (GSSG/GSH) in this panel —

Quick index:

Think of oxidative-stress “pressure” as how hard your antioxidant bank account is being tapped; reductive-stress “pressure” as how over-stuffed that bank is with reducing equivalents.

  • Withdrawal rate (oxidative): mild-to-moderate – enough to lift pyroglutamate and flirt with the 8-OH-dG cut-off, but not deplete glutathione.
  • Deposit rate (reductive): low-to-mild – 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 you’re using it; DNA-oxidation debris is detectable; lipid-phase defences are under-supplied. Reductive stress does not appear dominant—there’s a gentle reductive push from fasting/ketones, but nowhere near the “stuck in over-reduction” profile seen in heart-failure or chronic hyper-NADH states.

Tightening the redox balance

Goal Practical lever Expected shift
Lower oxidative withdrawals • 2–4 g EPA + DHA/d• 100 IU mixed tocopherols• NAC 600 mg × 2 + glycine 3 g at night• Polyphenol-rich plants (berries, cocoa, green tea)• Normal-volume morning urine on next lab → lipid-peroxide data ↓ 8-OH-dG, normalise pyroglutamate
Avoid over-reduction • Keep β-hydroxybutyrate in nutritional-ketosis range only when intended (≤ 1.0 mmol / mol Cr)• Riboflavin-5′-phosphate 20 mg for FAD enzymes Keeps NADH:NAD⁺ 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, you’ll 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 we’d revisit reductive stress—but at present your profile is “mild oxidative > mild reductive.”

What a lab panel

can

—and can’t—tell 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.

“Calorie-surplus flags” 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-hydroxy­butyrate 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 hyper­glycaemia) Glucose 355 mg dL-¹ in a dilute sample. When we scale to a typical creatinine it shrinks to ≈90 mg dL-¹—still 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 “metabolic backlog” typical of chronic over-feeding or insulin resistance.
Chronically suppressed ketones (β-HB <0.2 mmol /mol Cr) Even after correction you’re at 0.8—squarely in “nutritional ketosis” 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 —

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 “caloric scoreboard.”
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

  1. Weight log: if weekly morning weight is flat or slowly down, net calories are at or below maintenance.
  2. CGM or glucometer: if 2-h post-prandial glucose < 120 mg/dL most days, you’re unlikely to be chronically over-eating carbs.
  3. Food diary reality check: one week in — track everything, including the coffee extras. Compare to estimated TDEE.

Take-home

Your ION® data show some nutrient imbalances (low omega-3, low γ-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 you’re more likely hovering at maintenance or on the lean side of the ledger.

#12

I’m 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 phenylacetate…

[maybe this time im gonna load on both rapamycin and NAC shortly before just to see if the values can change that much]

#13

getting my next test tomorrow! Which means I can’t drink too much today (otherwise it will wreck my per creatinine test). [it recommends 1.41953 Liters max in 24 hours before…] and one sparkling water is 0.615 L. and 18.3 oz jovial diced tomatoes… + coffee… this can get slightly tough…

I’m gonna take lots of TMG, tocotrienols, metformin, NAC Ethyl ester, whatever. It means I can’t single out anything that will change everything, but any existence proof will help. But I’m 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 take…

later I ate more diced tomatoes
but I did have 6 orders of salad (with croutons, with toasted tempeh => and while it didn’t feel like much, I really hope the toasted tempeh won’t end up wrecking my readings today).

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there’s an issue tho… and it’s this

Yes — 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 ≈0.3–0.5 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 atrial‐natriuretic-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 ≥4 wk of Cana 100–300 mg
24-h urine volume ~1.5 L ↑ 0.2–0.5 L
24-h creatinine excretion (reflects muscle mass) unchanged unchanged
Creatinine concentration (spot sample) e.g. 120 mg/dL ↓ 5–15 %

Class data: In a mechanistic study, empagliflozin (another SGLT-2i) lowered 24-h urinary creatinine concentration by −1.66 mmol /L (~-9 %), matching the rise in urine volume. (AHA Journals)
Canagliflozin‐specific: 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 2–4 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 250–300 mL attributable to canagliflozin.

5. Bottom line

Canagliflozin’s 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 I’m not sure I’m 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… unfortunately…

#14

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