Full NAD+/NADPH blood panels

#1

I got one from biotek (2 dried blood spots), this is way more informative than jinfinit’s

NAMPH would be helpful too

INTEGRATIVE MEDICINE
BLOOD SPOT Result Range Units
NAD/NADH Profile
NAD (NAD+) 27.9 10.0 - 50.0 nmol/ml 
NADH 1.83 0.50 - 4.00 nmol/ml 
NAD/NADH Ratio 15.3 5.0 - 50.0 RATIO 
NADP 15.53 5.00 - 50.00 nmol/ml 
NADPH 17.2 4.0 - 25.0 nmol/ml 
NADP/NADPH Ratio 0.9 0.5 - 4.0 RATIO 
NAD/NADP Index ([NAD/NADP] x 100) 179.6 100.0 - 700.0 
Nicotinamide (NAM) 13.91 *H 0.60 - 5.80 nmol/ml 
Nicotinic Acid (NA) 0.46 0.06 - 1.04 nmol/ml 
NAD Comment
NICOTINAMIDE ELEVATED:
Elevated levels of nicotinamide can exert negative effects through multiple routes;
high-level nicotinamide may alter cellular methyl metabolism and affect methylation of
DNA and proteins.
Consider:
Decrease/cease nicotinamide supplementation.

NADP/NADPH RATIO LOW NORMAL:
The redox theory of aging suggests that lifespan is regulated by redox changes,
including alterations in the NADP+/NADPH ratios. Manipulations that lead to a reduction
of the NADP+/NADPH in the cytoplasm are especially linked with increased longevity.

PractitionerName

seems like there’s a bias towards both reduced forms in my system…+

NAD+ in BLOOD triggers inflammatory response!!

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and NR/NMN can build up and cause methylation problems
Niacinamide causes greater methylation problems than NR/NMN, rite?

#2

You’re talking about this company, is that correct?

#3

Yes

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Yes, if “complex II + III” function is genuinely restored, your NAD⁺/NADH ratio would be expected to go up (more NAD⁺ relative to NADH). That’s basically what the ETC is for: turning NADH back into NAD⁺ by letting electrons keep flowing.

Why “unblocking II + III” should raise NAD⁺/NADH

  • Complex I oxidizes NADH → NAD⁺ by handing electrons to ubiquinone (CoQ) .
  • Complex III is what helps re-oxidize the CoQ pool downstream (via the Q cycle), so electrons can keep moving.
  • When Complex I/III are inhibited , cells can’t convert NADH back to NAD⁺ efficiently , and the NAD⁺/NADH ratio can drop dramatically (reported >10-fold in some contexts).

So if you remove a real downstream bottleneck, NADH stops backing up, and NAD⁺ regenerates. Ratio rises.

But your specific pattern matters

You’ve got:

  • Complex I: 136% (normal/high)
  • Complex II: 107% (normal)
  • Complex II + III: 23% (low)
  • Complex IV: 80% (normal-ish)
  • Citrate synthase: 171% (high-normal)

That “II+III” test is usually succinate:cytochrome c reductase, meaning it’s a combined functional readout across II → CoQ → III.

A key point: low complex I-III and/or II-III activity is classically used as a clue for CoQ10 deficiency , because those linked assays depend on endogenous CoQ.

So your 23% could mean:

  1. CoQ pool problem (quantity/availability/oxidation state), or
  2. Complex III impairment/inhibition , or
  3. assay/sample issues (these tests are famously sensitive to handling and what tissue/cell type was used).

How this ties to your blood-spot NAD panel

Your blood-spot NAD⁺/NADH ratio was normal-ish (15.3). That doesn’t rule out a mitochondrial bottleneck in some tissues (muscle/brain) because your blood spot is mostly measuring blood-cell compartment behavior, not necessarily your “whole body ATP grid.”

So: unblocking II+III could raise NAD⁺/NADH in the affected cells , but your DBS ratio might barely move if the defect isn’t dominant in the blood compartment.

About the supplement advice you were given (quick sanity filter)

Some of it is plausible, some of it is “wellness fanfiction”:

  • CoQ10: makes sense if this is CoQ-related (linked complex II+III is a known indicator).
  • Vitamin K2 (MK-4) “bypass”: controversial. There’s evidence vitamin K2 cannot substitute for CoQ10 to restore electron flow/ATP in CoQ-deficient models.
  • Methylene blue: has real redox activity, but also real risk. It can precipitate serotonin toxicity in people on SSRIs/SNRIs and other serotonergic meds, and the FDA has warned about serious CNS reactions with interacting psych meds.
  • “Remove complex III inhibitors from diet/lifestyle”: outside of actual drugs/toxins, this is often just spooky phrasing. True complex III inhibitors are things like antimycin A in labs, not “seed oils.”

Practical conclusion

Yes, restoring II+III throughput (whether by fixing CoQ availability or resolving a real complex III impairment) should increase your NAD⁺/NADH ratio in the affected mitochondria.

But don’t expect your dried blood spot ratio to perfectly track that , and don’t treat “23%” as a diagnosis by itself.

If you want this to be more than expensive speculation, the next useful steps are:

  • confirm what tissue/cell type this assay used and whether they normalized to citrate synthase,
  • consider a direct CoQ10 status evaluation (the linked-enzyme clue is suggestive but not definitive),
  • review meds that can lower CoQ (statins are the classic example),
  • and be extremely cautious with anything like methylene blue if you take serotonergic meds.

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niacin =>NPY (no ideal)

#4

I asked OpenEvidence.com if there are studies demonstrating benefit to Nuchido Time+ in increasing intracellular levels of NAD+

Finished thinking

No published studies demonstrate benefit of Nuchido Time+ specifically for increasing cellular NAD+ levels. Nuchido Time+ is not mentioned in the medical literature provided, and no recognized clinical trials or peer-reviewed research on this specific product could be identified.

The available evidence focuses on established NAD+ precursors such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (NAM), and nicotinic acid (NA).[1-3] These compounds have been studied in both preclinical and clinical settings and have demonstrated the ability to safely raise NAD+ levels in humans.[1-3] Early clinical trials show these precursors can increase NAD+ in blood and some tissues, with some studies suggesting modest benefits for blood pressure, lipid profiles, and inflammatory markers.[1][4]

However, the efficacy of these established NAD+ precursors in humans has been lower than expected from preclinical studies, and questions remain about optimal dosing, treatment duration, and long-term safety.[2-3][5] The field lacks adequately powered randomized trials to definitively establish clinical benefits.[1]

If considering NAD+ supplementation, the focus should be on compounds with published safety and efficacy data—primarily NR and NMN—rather than proprietary formulations lacking peer-reviewed evidence.

References:

Nicotinamide Adenine Dinucleotide in Aging Biology: Potential Applications and Many Unknowns.

Endocrine Reviews. 2023. Bhasin S, Seals D, Migaud M, Musi N, Baur JA.

NAD+ Precursors in Human Health and Disease: Current Status and Future Prospects.

Antioxidants & Redox Signaling. 2023. Yaku K, Nakagawa T.

Dietary Supplementation With NAD±Boosting Compounds in Humans: Current Knowledge and Future Directions.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2023. Freeberg KA, Udovich CC, Martens CR, Seals DR, Craighead DH.

Impact of Geroscience on Therapeutic Strategies for Older Adults With Cardiovascular Disease: JACC Scientific Statement.

Journal of the American College of Cardiology. 2023. Forman DE, Kuchel GA, Newman JC, et al.

Current Uncertainties and Future Challenges Regarding NAD+ Boosting Strategies.

Antioxidants. 2022. Poljšak B, Kovač V, Milisav I.