Gerontology as a Science of Ontogeny in The Past and Present Time

The overview is presented of historical aspects and our own studies that justify the consideration of gerontology as a science of whole ontogeny. Such consideration allows for gerontology to serve as umbrella for various biomedical investigations performed in the paradigm of Developmental Origins of Health and Disease (DOHaD).

“If a person does not know a history, then he (or she) will hardly have a solid future…” Therefore, at first we shall observe, how gerontology as a science emerged. We need to do such an observation, since at present time gerontology is assuming the degree of extreme importance, because of rapid population aging even in developing countries, i.e. an increase in the fraction of elderly people in the population of almost every country, thus elevating the burdens on financial systems of retirement payments and on health care system. And the focus of present-time gerontology is not simply in increasing the lifespan, but first of all, in elevating the health span. Let’s return now to historical aspects. The term “gerontology” was used for the first time by Russian researcher Elie I. Metchnikoff, Nobel prize laureate, at the beginning of 20th century in his book “Essays on human nature” published at first in French and thereafter in Russian. But this term came to English-language literature, thus spreading to international level due to Moscow psychologist Nikolai A. Rybnikov who used it in his article “To the question on psychology of senescence” published in Russian journal “Psychology Questions”, because the abstract of this article was republished in the journal “Psychological Abstracts” [1,2]. By the way, the context of using the term “gerontology” by these two researchers was not the same: if Elie I. Metchnikoff put it together with thanatology, the science on death mechanisms, Nikolai A. Rybnikov used it in the row of sciences studying other stages of ontogeny. And this is not surprising, since N.A. Rybnikov was interested not only in psychology of elderly people, but also in studying children and adolescents. On the other hand, one cannot consider the psychology of an elderly person, without knowing the biography of this person, beginning, at least, from the moment of birth. And in fact, N.A. Rybnikov was the creator of so-called biographical method in psychology.

Finally, another researcher of Russian origin, Vladimir G. Korenchevsky may be considered as one of the most active founders of International Association of Gerontology and Geriatrics (IAGG) during the decades of thirties and forties of the last century [3]. Here we should discuss also the origins of the term “gerontology”. Usually, it may be explained that this term is derived from the combination of Greek words “gerontos” and “logos” that mean “old person” and “science” respectively. But in this case, it is not clear why the science of medical treatment of elderly people is called “geriatrics” (and not “gerontoatrics”), whereas a new, relatively recently organized journal has the name “GeroScience” (and not “GerontoScience”). On our opinion, such circumstances allow us to have another interpretation: from the very beginning of its creation, gerontology is a science not only about senescence but also on the whole ontogeny including both pre- and postnatal development, intermediate age categories and senescent period. And such interpretation may be justified also by the following opinion: gerontology is a science not only about senescence, but first of all, on aging that is considered as ontogenetic process from zygote formation till the final stages of an organismic life [4]. Here we should remember that from the end of eighties of the last century, a new paradigm emerged, on Developmental Origins of Health and Disease (DOHaD) [5]. One of the main founders of this new paradigm, English epidemiologist David J.P. Barker was the first to establish in his retrospective studies that lower birth weight probably caused by intrauterine growth restriction, can provoke higher risk of chronic non-infectious disorders, such as metabolic syndrome including systemic arterial hypertension and type 2 diabetes mellitus.

We became more involved in this paradigm from the beginning of current century, performing a series of epidemiological studies on age-related dynamics and sexual differences of morbidity and mortality, at first in the Southern region of Brazil, thereafter in Argentina and Chile and finally in several European countries [6,7]. And in fact, DOHaD paradigm has two main branches: epidemiological and biomedical. But whereas the first one has already its proper name, life-course epidemiology, another, biomedical part is multidisciplinary, including physiology, biochemistry and other biomedical sciences studying the mechanisms of the phenomena of programming / imprinting, when adverse events in perinatal period have long-term consequences till adult state and even senescence [8]. Considering the above-mentioned historical aspects of gerontology, we can propose that exactly this science may serve as umbrella for biomedical branch of DOHaD paradigm [9]. And indeed, at present time the most numerous parts of studies concerning this paradigm is performed from prenatal period till adult state. Of course, such a situation is explained simply by the lack of sufficient resources for studying the whole ontogeny including intermediate age categories and senescent period. On the other hand, “classical” gerontology usually studies the processes from adult state till the senescence. On our opinion, here is the essence of general problem, since it is important also to study the periodization of ontogeny and transformation from development to aging. In order to fill this lacune, from the nineties of 20th century, we studied not only traditional curves of somatic growth, but also the growth plots obtained by means of linearization in mono- and bilogarithmic coordinates [10,11]. This procedure has allowed us to show ontogenetic transitions, as revealed by the breaks in straight lines on linearized growth plots.

In humans at least wo types of ontogenetic transitions were observed: juvenile, during the age of 6-8 yr and pubertal one at the age of 12-14 yr. The corresponding transitions in rats occur approximately at the ages of 3 and 5 weeks respectively. Moreover, only in humans one more ontogenetic transition, the infantile one was revealed at the age of 1-2 yr. Since the programming / imprinting phenomena can be initiated not only in antenatal, but also in early postnatal development, we have suggested that infantile transition can separate programming / imprinting phenomena occurring before it and biological embedding taking place later on, being characterized also by cumulative manner [12]. Moreover, we have offered a hypothesis of metamorphosis, in accord to which juvenile transition marks principal transformation from development to aging, because of its proximity to the minimal value of mortality in humans at the age of 9-10 yr in both genders [13]. In this case our consideration is based on definition of aging as biological process that leads to increases in morbidity and mortality. As the next step in our theoretical endeavor, we suggested that three ontogenetic transitions, at least in humans, correspond to 3 stages in adenohypophyseal differ one including 3 main bioregulatory axes: corticotropic, thyrotropic and gonadotropic [14]. It is interesting that 50 yr ago W.D. Denckla has shown the existence in anterior pituitary of an unidentified metabolic inhibitor, capable of diminishing the stimulatory influence of thyroid hormones on tissue oxygen consumption [15]. Apparently, the pituitary content of this substance begins to increase since the prepubertal phase, i.e. close to juvenile ontogenetic transition. Just recently we have suggested that such substance may be similar to chromogranin- or secretogranin-like pro-hormone protein, together with its peptide derivatives [16].

Another important part of our theoretical studies concerns with the onto- and phylopathogeny [17]. Ontopathogenic model considers the establishment of etiopathogenic mechanisms along the whole ontogeny beginning from pre- and postnatal development till adult state and continuing during intermediate age categories and senescent period, whereas phylopathogenic model considers the transfer of pathogenic risk in the inter-, multi- and transgenerational mode, i.e. across generations. It is pertinent to outline here that the ontopathogenic model is in fact a particular case of phylopathogenic one, at least in mammals, due to interactions of maternal body with the embryo and fetus, resulting in pathogenic risk transfer from the founder generation (F0) to its offspring (F1), such as in gestational diabetes. Apparently, in much less extent such transfer may occur also in paternal manner. In order to differentiate onto- and phylopathogenic models, we can presume that transgenerational mode begins from considering the generation F2, i.e. the transfer between grandmothers and grandfathers to grandchildren (F0à F2). In any case, phylopathogenic model at present is much less elaborated, as compared to the ontopathogenic, since the last one is based already on more than 3 decades of intense studies related to DOHaD paradigm. In conclusion, gerontology considered as a science of whole ontogeny may serve quite well for studies in the ontopathogenic model, whereas developmental biology, embryology, perinatology and pediatrics are much less suited for this aim, exactly since they are not able to consider ontogenetic stages after sexual maturation. Our main intention continues to be the same, as for David Barker and many other researchers of DOHaD paradigm: to think not about immediate consequences of health care interventions, but as referred to long-term impacts in next generations.