Super Panda Peptides, a new vendor selling on Discord and PeptideChat. $300 for 50 mg X 10. I have a vial being tested by Finnrick, but I was too impatient to wait for the results. I did filter the solution.
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I test my GFR every two or three months, always with creatinine, using both Labcorp and my local hospital. I donāt use creatine and Iām not a mesomorph.
GFR decreases with age, and the drop accelerates after age 70. Iām 78 and I have CKD, so this is not entirely unexpected.
Youāve never checked your GFR by cystatin C just to make sure itās consistent with the creatinine-based measurement? I certainly would, for something this important. My cyst C GFR tends to run 20+ points higher than my creatinine-based GFR, even when I completely stop creatine supplements for several weeks and avoid exercise for 3 days prior to creatinine measurement.
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Now that you mention it, I did have a strenuous workout on the day before the test, a day when it was 60 degrees, the first nice day in four or five months and so I really pushed it. I was sore when I had the blood draw. I bet my GFR would be 10 points higher if I took the same test tomorrow. Iām glad you brought it up.
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Where do you inject yourself, Beth?
Iāve tried stomach and thigh and prefer my stomach. Iām not sure if itās less sensitive or if itās just about itās a closer reach ?
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Beth, do you notice anything with regard to your energy levels when taking SS-31?
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Itās really hard to tease out.
Am I getting more things done now because itās tamping down my ADD or is some of it attributed to more energyā¦?
I do feel I can go off my t3 now, so there very well might be an energy component in there. I am just not sure about this one. My hunch is if there is more energy, itās not drastic enough for me to be sure about it.
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The ADD effect is interesting. That gives some weight to the theory of mitochondrial dysfunction being the root cause of many psychological conditions. Are you currently taking anything else for the ADD? How does SS-31 compare to other interventions youāve tried for the ADD?
@Beth , this is really interesting. I have never heard of this - it seems to suggest that there is a reasonable theoretical basis for it to be helpful:
Scientific and Clinical Evidence of Mitochondrial Dysfunction in ADHD
1. Clinical and Biomarker Evidence
Mitochondrial dysfunction (MD) is increasingly recognized as a foundational factor in the pathophysiology of attention-deficit/hyperactivity disorder (ADHD). Because direct brain biopsies are clinically prohibitive, evidence is primarily derived from peripheral biomarkers and ex vivo cellular models.
- Mitochondrial DNA Copy Number (mtDNA-cn): Clinical studies demonstrate that children diagnosed with ADHD exhibit significantly higher mtDNA-cn in peripheral blood compared to healthy controls (ĆÄĆ¼tlĆ¼, 2021). This elevation is generally interpreted as a cellular compensatory mechanism attempting to offset bioenergetic deficits and mitochondrial impairment (Almutairi, 2024). Notably, a one-year follow-up study observed that as ADHD symptom severity decreased in treated patients, mtDNA-cn also showed a correlated reduction, suggesting that ameliorating ADHD severity may coincide with normalized mitochondrial function (ĆÄĆ¼tlĆ¼, 2021).
- Cybrid Cell Models: To isolate mitochondrial pathology from nuclear DNA, researchers have utilized cybrid cell lines by fusing platelets from ADHD patients with neuroblastoma cells lacking mitochondrial DNA. ADHD cybrids demonstrate significantly reduced cellular and mitochondrial respiration, decreased ATPase 6/8 transcript levels, impaired complex V activity, and a loss of mitochondrial membrane potential (Verma, 2016). Because cybrids isolate the mitochondrial genomeās influence, these findings provide direct evidence of intrinsic mitochondrial bioenergetic failure in ADHD phenotypes (Verma, 2016).
Theoretical Basis for SS-31 (Elamipretide) in the Treatment of ADHD
Currently, there is no direct scientific research, clinical trial data, or specific in vivo animal modeling explicitly evaluating the peptide SS-31 (elamipretide) for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD).
However, there is a highly robust theoretical basis for its potential efficacy. This rationale is constructed by mapping the well-documented molecular mechanisms of SS-31 onto the established pathophysiological mitochondrial deficits observed in ADHD.
1. Mechanistic Overlap: Cardiolipin Stabilization
The core theoretical argument for SS-31 in ADHD rests on its highly specific mechanism of action. SS-31 is a cell-permeable, mitochondria-targeted tetrapeptide that selectively binds to cardiolipin , a unique phospholipid expressed almost exclusively on the inner mitochondrial membrane.
- The ADHD Deficit: As established by cybrid cell models of ADHD, patients exhibit impaired electron transport chain (ETC) function (specifically complex V), loss of mitochondrial membrane potential, and excessive reactive oxygen species (ROS) leakage.
- The SS-31 Mechanism: By binding to cardiolipin, SS-31 stabilizes the architecture of the inner mitochondrial membrane and the ETC complexes (particularly cytochrome c). This interaction prevents electron leakage, thereby reducing the generation of ROS at the source while simultaneously restoring ATP synthesis. This directly antagonizes the bioenergetic failure and redox imbalance hypothesized to drive ADHD neurobiology.
2. Evidence from Analogous Neurological Models
While unstudied in ADHD, SS-31 has demonstrated significant efficacy in preclinical models of cognitive impairment that share downstream pathologies with ADHD (neuroinflammation, oxidative stress, and synaptic dysfunction).
- Protection Against Neuroinflammation-Induced Cognitive Deficits: In mouse models injected with lipopolysaccharide (LPS) to induce severe neuroinflammation and oxidative stress, pretreatment with SS-31 prevented mitochondrial dysfunction, reversed the loss of dendritic spines, and preserved hippocampus-related learning and memory. It also facilitated the regulation of brain-derived neurotrophic factor (BDNF), a critical protein for synaptic plasticity that is frequently dysregulated in neurodevelopmental disorders.
- Reversal of Sleep Deprivation Deficits: Short-term sleep deprivation rapidly induces oxidative stress and cognitive/attention deficits. In aged mice, administration of SS-31 prevented sleep-deprivation-induced learning impairments, restored brain ATP levels, and decreased inflammatory cytokines. Given the high comorbidity of sleep disturbances and ADHD, this neuroprotective effect on executive function is highly relevant.
- Dopaminergic Protection: Preclinical studies in Parkinsonās disease models demonstrate that SS-31 protects dopaminergic neurons from oxidative damage. Because dopaminergic pathways in the prefrontal cortex and striatum are structurally energy-demanding and highly susceptible to oxidative stress, preserving their mitochondrial efficiency is theoretically beneficial for the dopamine dysregulation seen in ADHD.
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That is interesting. Itās worth nothing I know itās not placebo because I didnāt google until after I noticed my newly found consistent focus and mental clarity.
On that noteā¦ when I first started rapa and commented how my lifelong insomnia vanished (not that every night was perfect), @John_Hemming said rapa can fix mitochondria, so it made sense it could therefore fix my insomnia (of course he said it in a more scientific way!).
If I recall correctly, today I also noticed him say in another thread that spectrum conditions might be related to mitochondria.
(Iām tagging you John incase Iām saying of this incorrectly).
@fasterfour last night I was just addressing your question in another threadā¦ here is a cut and pasteā¦
I didnāt know I had ADD until I was aprox 40 (almost 20 years ago). My sister in law had a hunch and handed me an adderall. The clouds parted and the angels sang. Everything became crystal clear (focus, no fog) and I could get things done.
I was on it for probably 60-90 days, an incredible 60-90 days. Then, at a cardiologist appointment, he said ādo you know itās speed and causes vasoconstriction and will increase your risk for a heart attack?āā¦ I said, nope, no one told me. I never took it again.
Those glorious 60-90 daysā¦ that is exactly how I feel now.
Iād procrastinate and could never get myself do anything I didnāt want to (mostly admin things), but I could hyper focus on things that were in my wheelhouse.
Iām getting tons of things done all the time now. Nothing super human, but Iām just ānormalā. I also notice it a lot here too. The health/science topic has never come easily for me, not that itās easy now, but I used to torture myself trying read one of these threads in order to get it to register (and often would fail), but now I can focus on things and my mind wonāt wander.
Speaking of feeling great, I had a long meeting with my doc today to go over everything Iāve been doing and to discuss my resultsā¦ everything is so different now that we decided to do a trial of going off my T3 (staying on T4). I was always sluggish and foggy, but now that Iām not, we are seeing if I still need it (can be a net negative for bones and heart rate, so I thought Iād see).
It didnāt seem like this could be real, but it made sense after hearing @John_Hemming say ADD might be a mitochondrial issueā¦ TA DA!
Iāve never tried anything else for my ADD.
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I thought that just the muscle heads had residual creatinine, but after abstaining from sprinting for three days, I checked my GFR again and it went up by a third. I expect Iāll see another jump when I try Cystatin C. Iāve also learned that intervals will spike my PSA, alarming my urologist.
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