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'Anti-aging' medicine has become a popular topic, in the lay press, the (semi-) scientific literature and the Internet.(1) In almost all instances, claims of drugs, health supplements and other types of intervention are not based on any evidence supported by sound scientific knowledge. Specifically, the aging process itself, in contrast to age-related diseases, has so far neither been fully understood, nor significantly influenced in higher species, notably humans. In addition to the ill-defined effects, claims of anti-aging medicine also pose a considerable economic burden on the usually poorly informed older segment of the population. The present paper is based on a recent report by the United States General Accounting Office (GAO) on the questionable and even harmful effects of anti-aging health products for seniors.

The Pathobiological Determinants of Atherosclerosis in Youth (PDAY)-study gave insight into the correlation between the classical risk factors for atherosclerosis development, such as hypercholesterolemia, hyperglycemia, high blood pressure and smoking in young Americans. We now present immunohistochemical data showing that immunological-inflammatory signs represent the first step towards atherosclerosis development in the arteries of young adults. In previous publications, we coined the term 'vascular-associated lymphoid tissue' (VALT) for the accumulation of mononuclear cells at regions of the arterial wall in healthy children and adolescents that are predisposed to the development of atherosclerotic lesions later in life if risk factors are present. In the present communication, we intended to close the gap between data from atherosclerotic arteries and those of healthy young children studied previously by our group. The PDAY-study comprising 15-34-year-old Americans who had no clinical symptoms of cardiovascular diseases offered a good basis for our intention. We document that inflammatory activity was found in all specimens, represented by activated T-lymphocytes, dendritic cells, macrophages and aberrant MHC class II expression in the intima. We therefore demonstrated that immunological-inflammatory cells are present in the earliest stages of atherogenesis in 15-34-year-old subjects, arguing in favour of an initiating role of the immune system in atherosclerosis development.