Spermidine, also called monoaminopropylputrescine, is a biogenic polyamine and thus an intermediate product in the formation of spermine from putrescine and decarboxylated S-adenosylmethionine.
Spermidine occurs in all living organisms, plays an important role in cell growth and is involved in various processes. However, the exact physiological function of spermidine in growing cells, e.g. in the production of nucleic acids and proteins or in membrane stabilisation, has not yet been fully clarified. The amount of spermidine in the organism increases when metabolism accelerates. When metabolism slows down, the production of spermidine decreases. The concentration and production of the body’s own spermidine also decline with ageing.
Natural circumstances that raise spermidine levels are growth, pregnancy, repair of muscle cells after strenuous exercise and regeneration of red blood cells after blood loss or anaemia or after prolonged stays at altitude. Various diseases are also signalled by raised spermidine levels, e.g. chronic inflammation of the joints in rheumatic diseases, of the liver in hepatitis, of the bowel in colitis and of the skin in eczema and psoriasis.
Spermidine enhances autophagy, a cellular process that is crucial for general cellular protein activity and for the function of mitochondria and cardiomyocytes (heart muscle cells). Animal experiments on fruit flies showed that dietary spermidine counteracts age-related dementia in these insects. A research group led by the Graz biochemist Frank Madeo demonstrated in laboratory mice that spermidine protects against cardiovascular disease and can thus contribute to extending lifespan. It delays cardiac ageing by improving diastolic function. Animal experiments demonstrated that hypertension (high blood pressure), a major cause of heart failure, is lowered by spermidine. Spermidine reduced the pulmonary and systemic fluid accumulation characteristic of heart failure. Dietary intake of spermidine correlated inversely with the occurrence of heart failure. Between the study groups (high and low intake), the risk of disease in the high-intake group was reduced by 40 per cent. A protective effect on kidney function was also observed in the experiments.
In August 2018, Austrian, French and British clinicians and researchers published the results of a study in which the spermidine intake in the diet of a group of people had been recorded regularly. The study covered a twenty-year clinical observation period from 1995 to 2015. 829 participants aged between 45 and 84 (49 per cent men) took part in the study. During this period, 341 of them died: 40.5 per cent of those in the lowest third of spermidine intake, 24 per cent in the middle third and 15 per cent in the highest third. The difference in mortality risk between people in the highest third and those in the lowest third corresponded to an age 5 to 7 years younger.
Literature
- J. Kim: Spermidine rescues proximal tubular cells from oxidative stress and necrosis after ischemic acute kidney injury. In: Archives of pharmacal research. (Arch Pharm Res.) October 2017, Vol. 40, No. 10, pp. 1197–1208, doi:10.1007/s12272-017-0957-3
- Occurrence of putrescine, spermidine and spermine in foods: M. Atiya Ali, E. Poortvliet, R. Strömberg, A. Yngve: Polyamines in foods: development of a food database. In: Food & nutrition research. Vol. 55, 2011, doi:10.3402/fnr.v55i0.5572. PMID 21249159. PMC 3022763 (free full text).
- Further studies on spermidine on PubMed.
