Dr. Martin Picard, a professor of behavioral medicine at Columbia University, recently appeared on the Huberman Lab podcast to discuss energy production, aging and metabolic health. During the conversation, Picard addressed the peptide SS31, also known as elamipretide, a compound that has attracted attention in longevity research and clinical settings.
Picard has followed SS31 since its earliest days and described being present around the time of its discovery, recalling the excitement that initially surrounded it.
“I was a student when SS31 was discovered and I remember the person who discovered Hazel Szeto who discovered SS31 she was presenting at meetings.”
Early on, the peptide was positioned as a potential breakthrough for mitochondrial disease because it was designed to target mitochondria directly and improve cellular energy handling. That optimism later carried into commercialization, with SS31 marketed as a so called stealth peptide and supported by a company that eventually went public.
Picard’s assessment of how SS31 performed across most clinical environments remains blunt. When asked about peptides people are using for mitochondrial support, he said the results did not match expectations.
“It’s not lived up to its expectation. It was supposed to be a treatment for mitochondrial disease and mostly the trials have been negative.”
The disconnect between theoretical appeal and real world outcomes has persisted. The peptide did not produce the broad mitochondrial improvements many anticipated when evaluated across diverse patient groups.
In September 2025, the U.S. Food and Drug Administration granted accelerated approval to elamipretide under the brand name Forzinity as the first approved treatment for Barth syndrome in patients weighing at least 66 lbs (30 kg). Barth syndrome is a rare and serious mitochondrial condition that primarily affects males and often presents with significant cardiac impairment early in life. Individuals who reach adolescence and adulthood frequently experience persistent low energy, reduced stamina and exercise intolerance that meaningfully affect daily life and overall wellbeing.
In the case of Forzinity, approval was based on improvements in knee extensor muscle strength, a measure the FDA considers reasonably likely to translate into functional benefits such as standing more easily or walking farther. As a condition of approval, the manufacturer is required to conduct a post approval randomized double blind placebo controlled trial to confirm that these strength improvements meaningfully benefit patients.
Forzinity is administered as a once daily subcutaneous injection. The most commonly reported side effects in trials were mild to moderate injection site reactions, although serious reactions have also been reported.
Picard’s skepticism does not directly conflict with the FDA’s decision but it does place it in context. He consistently framed SS31 as part of a broader pattern of attempts to fine tune mitochondrial function through targeted compounds. He described these efforts as attempts to “tweak the system” and “optimize tweak the circuitry” while arguing that this approach often overlooks a more basic reality.
“My sense is you know we’ve evolved over very long periods of time and we’re really well optimized.”
He acknowledged that supplements and targeted therapies can be appropriate when biological systems are genuinely impaired or when a specific disease process is present. Outside of those scenarios, he pointed to the fact that many people live long healthy lives without pharmaceutical optimization.
“I think there’s ways to optimize the system and there’s a lot of people who live long healthy fulfilling lives and they get sick once in a while but they recover without supplements and without medical intervention.”
The SS31 discussion also allowed Picard to clarify a common misunderstanding about mitochondria themselves. He noted that terms like mitochondrial function or mitochondrial dysfunction can be misleading because mitochondria perform many roles. Beyond ATP production, they participate in cellular signaling, hormone production and metabolic regulation across multiple pathways. Targeting a single mechanism does not ensure system wide benefits.
Mitochondrial health is shaped primarily by behavior over time rather than shortcuts. Exercise, nutrition, sleep and stress regulation continue to do most of the work, while experimental peptides like SS31 occupy a much narrower role.
