Humanin and age-related diseases: a new link?
Gong. Zhenwei Z; Tas. Emir E; Muzumdar. Radhika R
Key Findings
- Humanin is a 24‑amino‑acid mitochondrial peptide involved in cell survival, metabolism, and stress responses.
- Animal and cell studies show humanin can improve outcomes in many age‑related diseases (Alzheimer’s, stroke, diabetes, heart injury, atherosclerosis, ALS, certain cancers).
- Humanin levels are linked to the GH/IGF‑1 axis and lifespan in mouse models with altered GH/IGF signaling.
Practical Outcomes
- Humanin looks promising for longevity and disease protection, but there’s no clear guidance on how to use it safely in people yet. For now, it’s more of a research target than a ready‑to‑take supplement, so biohackers should wait for human trials before considering self‑experimentation.
Summary
Humanin is a tiny protein made in mitochondria that seems to help cells survive stress, control metabolism, and reduce inflammation. Studies in cells and animals suggest it could protect against diseases linked to aging like Alzheimer’s, stroke, diabetes, heart damage, and some cancers, and it may be tied to the growth hormone/IGF system that influences lifespan. However, the paper is a review and doesn’t give specific dosing or protocols for humans.
Abstract
Humanin (HN) is 24-amino acid mitochondria-associated peptide. Since its initial discovery over a decade ago, a role for HN has been reported in many biological processes such as apoptosis, cell survival, substrate metabolism, inflammatory response, and response to stressors such as oxidative stress, ischemia, and starvation. HN and its potent analogs have been shown to have beneficial effects in many age-related diseases including Alzheimer's disease, stroke, diabetes, myocardial ischemia and reperfusion, atherosclerosis, amyotrophic lateral sclerosis, and certain types of cancer both in vitro and in vivo. More recently, an association between HN levels, growth hormone/insulin-like growth factor-1 (GH/IGF axis), and life span was demonstrated using various mouse models with mutations in the GH/IGF axis. The goal of this review is to summarize the current understanding of the role of HN in aging and age-related diseases.
Study Information
pubmed
2014
2014-12-04T00:00:00.000Z
10.3389/fendo.2014.00210
97
111