After sketching the state of the discussion, it is time to find a way out that allows us (i) to avoid the definitory vagueness of the notion of self and the historical ambiguity of the notion of personhood; (ii) to continue speaking of identity persistence also for demented individuals; (iii) to pave the way for potential solutions of the question concerning demented individuals’ moral status. These three outcomes will be achieved by introducing the WPA of identity, based on the notion of ‘the whole phenotype’, which, moreover, overcomes the problems both of the biological (even if WPA is grounded in biology) and of the psychological account.
The WPA of identity
Boniolo and Testa (2012) proposed an empirical account of identity based on the notion of ‘whole phenotype’. Borrowing from the evo-devo (evolutionary/developmental) line of thinking, by ‘whole phenotype’ I mean the set of all those strongly intertwined phenotypic modules (the metabolic phenotype, the immunological phenotype, the nervous phenotype, the somatic phenotype, the behavioral phenotype, etc.)Footnote 17 that render an individual what they are at a given time of their development. Here the notion of ‘phenotype’ deserves to be clarified, since, over the decades, many different definitions have been proposed. I use it in the contemporary biological meaning, that is, as something referring both to gene expression and regulation as a consequence of (internal and external) signals (also due to the environment in which one lives and to its life style), and to DNA methylation and selected histone post-translational modifications, that are persistent over many cellular generations independently of the underlying DNA sequence. That is, the phenotype we have at a certain time of our life is the product of all the genetic and epigenetic processes happened since the moment of fecundation. Moreover, always following an evo-devo perspective, it should be emphasized that ‘development’ regards all the processes and changes occurring in an individual over his or her lifespan and then affecting different phenotypic modules (and, as a result, his or her whole phenotype). In this way, ‘development’ is a process occurring all through life and, thus, a continuous move from a past whole phenotype (for example, the embryo whole phenotype) to the current whole phenotype (for example, the newborn whole phenotype, or the adult whole phenotype).Footnote 18
Now, we could claim that a human individual in any instant of their life, is nothing but the result of all the genetic and epigenetic processes that, in the course of time, have causally shaped all of their intertwined phenotypic modules (be they metabolic, somatic, immunological, nervous, behavioral, etc.), that is, an individual, in any instant of their life, is nothing but their whole phenotype. This means, coming to the persistence problem, that an individual’s identity through time is given by the continuity of their whole phenotype.
It is not necessary now to go through all the technical details and the justification of the proposal (for more detail, see Boniolo and Testa 2012). Nevertheless, for the sake of current discourse, among the many phenotypic modules composing the whole phenotype, it is worth dwelling upon the central nervous phenotype, which allows lower and higher mental functions.
To be scientifically sound, we should affirm that an individual’s higher mental functions are what they are because of a particular instantiation of their central nervous phenotype, which is, in turn, the result of all the genetic and epigenetic processes occurred until that moment of their development. That is, no individual can have the higher mental functions they have without the suitable central nervous phenotype, as, for example, the extreme cases of the anencephalic infants, patients in persistent vegetative state, or demented individuals show.
To sum up, the higher mental functions possessed by a given individual are the result of their central nervous phenotype and this is, in turn, the result of their genetic and epigenetic history. Needless to say, by taking into consideration that we are moving along a purely empirical approach, we are implicitly affirming that possessing particular higher mental functions without the suitable nervous phenotype is impossible.Footnote 19
Accepting this scientific perspective means overcoming the mentioned difficulties affecting both the biological account and the psychological account of identity. Concerning the former, according the WPA we are not only our organism, but also (i) the allowed and correlated central nervous phenotype, and therefore the allowed and correlated higher mental functions (memory, consciousness and self-consciousness), and (ii) the allowed and correlated behavioral phenotype. Concerning the latter, the WPA allows us to positively cope with the identity of embryos, fetuses, patients in persistent vegetative states and demented individuals, because we are not only our mind, in particular our higher mental functions, but also all the other phenotypic modules composing our whole phenotype. It is to note that the WPA is surely grounded in biology: it speaks in terms of phenotypes due to genetic and epigenetics processes. Nevertheless, since it considers the nervous phenotype and the correlated higher mental functions, it goes beyond a purely organismic account and regards also the aspects characterizing the psychological account. In different terms, WPA should be thought of as a bridge between the organismic account and the psychological account; in particular it is an account that takes into consideration the relevant aspects of both these accounts, without having their weaknesses.
Concerning our central question, that is, the link between identity and dementia, if we accept the WPA we can continue speaking about the persistence of demented individuals’ identity. They can have a brain pathology, and this could be called ‘dementia’ or ‘major neurocognitive disorder’, but this does not imply that they have lost their identity over time. They could have lost some higher mental functions, due to some brain damages, but this does not affect their identity over time, since this is guaranteed by the continuity of their whole phenotype, even if a phenotypic module (in particular, the central nervous phenotype) is changed in a pathological manner. There is no reason—and this is my main point—to privilege a particular phenotypic module over the others. No one, I suppose, would claim that we are not the same individual if we had a severe cardiac disease, or a severe immunological disease. The cardiac phenotypic module or the immunological phenotypic module would be, respectively, changed in a pathological way; some of the original functions would be lost; but this would not imply the loss of the identity as a whole. The same considerations should be applied to the nervous phenotype: it can be damaged by a disease, but this does not mean that we have lost our identity over time.
At this point we have the possibility to speak about individuals with dementia without speaking about their loss of identity, unless we prefer to embrace a particular theory of identity based only on the higher mental functions. But, as seen, there is no necessity to adhere to such a position. There is no need to claim that if an individual has lost the memory of who they were, they are no longer the same. Actually, they are the same from the WPA point of view, even if they do not know who they were. Memory is one of the functions of a non-pathological central nervous phenotype, which, in turn, is one of the many phenotypic modules composing the whole phenotype. An analogous discourse could be constructed for behavior. Individuals with some level of behavioral impairment could have totally different conducts from those ones they had before the pathology. But, again, this does not mean they are different individuals. The behavioral phenotype has changed (and of course the social relationships, as a consequence), but this is one of the many phenotypic modules composing the whole phenotype. Both in the former and in the latter case we have moved continuously from a (pre-dementia) whole phenotype to a (early, middle or severe dementia) whole phenotype.
We could speak in terms of identity of single phenotypic modules: we could say that there is the question of the identity of central nervous system, as there could be the question of the identity of the immunologic system, of the metabolic system, etc. Nevertheless, none of them implies the identity of the individual as a whole, since their identity has to be given in terms of their whole phenotype and there is no reason at all for choosing a particular phenotypic module over the others. We speak in terms of identity of higher mental functions, but we should recall that they are an expression of the brain we have, that is, of the central nervous system we have. The higher mental functions are not the individual as a whole.
Up to this point, I have introduced the notion of whole phenotype and argued for a theory of identity based on its continuity. Accepting this account means accepting that a demented individual has not had any break in their identity, even if they have lost their cognitive capacities, in particular the decision-making capacities. It means accepting that they have a peculiar disease and not that they are something else from what they were before.Footnote 20