Friday 26
and Saturday 27 November 2021
Bern and
online
Registration:
“In what
circumstances can we pass from this observed association to a verdict of
causation?”
“The ’cause’
of illness may be immediate and direct, it may be remote and indirect
underlying the observed association.”
“…the
decisive question is whether the frequency of the undesirable event B will be
influenced by a change in the environmental feature A.”
“What
aspects of that association should we especially consider before deciding that
the most likely interpretation of it is causation?”
“In
occupational medicine our object is usually to take action. (…) we shall wish
to intervene to abolish or reduce death or disease.”
“All
scientific work is incomplete – whether it be observational or experimental.
All scientific work is liable to be upset or modified by advancing knowledge.
That does not confer upon us a freedom to ignore the knowledge we already have,
or to postpone the action that it appears to demand at a given time.”
A. Bradford Hill: “The
Environment and Disease: Association or Causation?”,
Proc. Royal Soc. Med., p. 295 –
300, 1965,
https://doi.org/10.1177/003591576505800503
Keywords: agnotology, ambiguity, causality, cause, co-causal, control,
determination, direct cause, effect, evidence, hubris, ignorance,
indeterminacy, indeterminism, indirect causes, multi-causality, non-target
effect, precaution, Precautionary Principle, precision, probability, risk
assessment, target effect, uncertainty
Content of the conference
The understanding of “causes” is at the core of
scientific investigations. It underlies all current efforts to face ecosystemic
challenges. Physics has framed causality within robust and unifying
“conservation principles” (energy, momentum etc.). But how can we
understand and verify supposed causal relations within the historicity and
diversity of life in a unified manner? How can we scientifically describe the
effects which appear to be caused by a chemical or physical event on an
ecosystem governed by reproduction and variation and on environments enabling
diversity?
A special influence on our notions of causality in biology and ecology
is exerted by our advanced reliance on automation, digitization, computers,
in-silico models, computational surrogates, artificial intelligence and machine
learning. If life-science phenomena are viewed as caused by one or a few
selected agents, how does this view align with what can be obtained from a
computerized output, with less and less reliance on hands-on experience and
human senses for verification?
A paradoxical situation seems to emerge, where this approach
appears to enable to flip cause and effect, as exemplified in synthetic
biology. Traditionally, say, cloning relied on the appropriate functioning of
an entire framework system (environment), such as E. coli, to express a
specific gene insert. With the advent of reverse genetics, the same technique
is now publicized as being “under the control of the gene” to be
expressed. It seems that modeling, and focusing on what one wants to obtain,
has shifted the comprehension and understanding of what is cause and effect,
demonstrating that the entire framework of causality is not only poorly
understood, but little investigated.
When approaching this question from another level, one may ask
what the biological influencers of causality are. Is it about material entities
(e.g. genes), or also about interactions, relationships, and context (from
sub-cellular to ecological)? A unique ability of life is to be able to adapt to
a changing environment. So one may ask: what causes habituation and learning,
and in which way do these influence the appearance of causality (in gene
expression, disease and other phenomena)?
“Science is the organised attempt to discover how things work
as causal systems.”[1]1 But in current biology and ecology every cause has
multiple effects and every effect has multiple causes. So at this conference we
study notions of multi-causality within complex systems that encompass many
variations, in time and space, of the “known” co-causal factors,
whilst acknowledging the existence of many other unknown, yet possibly influential
variables.
There are some current attempts
to re-introduce simple causality, for example, in searches for the particular
gene or environmental circumstances that are relevant to a specific biological
trait, via genetic modification which is claimed to be “precise“.
However, other approaches are
attempting to identify modifiable co-causal factors within context and time
dependent complex biological and ecological systems, factors which enable both
life and harms to emerge and which, if removed or reduced in a timely manner,
would result in less harm to people and environments.
Such approaches to identifying
robust causal inferences in biology, ecology, tort law and public policy on
health and environment eschew simplistic dichotomies (e.g. nature/nurture; gene/environment;
acute/chronic; effects/adverse effects; statistically significant/insignificant
effects; association/causation; valid/invalid arguments) in favour of
continuums, or spectrums, along which choices need to be made as to where and
when positions on such continuums justify robust causal inferences.
Current approaches to coaxing
causality from complexity also include systematic review methodologies;
systematic approaches to integrating different evidence streams; and “inferences to the best explanation”
used in tort law. There are also approaches that render explicit and
transparent the often implicit sources of divergent evaluations of the
“same” evidence, which can be illustrated historically with: leaded
petrol; low dose ionising radiations; and antibiotics as animal growth
promoters; and currently with: per- and polyfluoroalkyl substances (PFAS);
glyphosate; neonicotinoid insecticides; and electromagnetic fields (EMFs).
These sources of divergent
evaluations include (1) different types of paradigms, assumptions and
argumentation used; (2) the diverse disciplinary conventions of toxicologists,
endocrinologists, epidemiologists, biologists, ecologists, and lawyers; and (3)
their value based choices.
Public and stakeholder
involvement in helping to identify robust causal inferences for public policy
interventions have also been used, sometimes including communities affected by
harms. The value of these approaches will be reviewed.
Programme
Friday 26 November 2021
8:30 Registration
9:00 Welcome / Introduction – Diederick Sprangers, ENSSER
9:30 Prof. Giuseppe Longo, Centre Cavaillès (République des
Savoirs), CNRS and Ecole Normale
Supérieure, Paris
Causality
and novelty production in biology
10:15 Discussion
11:00 Coffee break
11:30 Prof. Denis Noble, University of Oxford
20th century
biology got causation in living systems the wrong way round
12:15 Discussion
13:00 Lunch
Moderator: Prof. Giuseppe Longo
14:30 Dr. Siguna Müller, Kärnten, Austria
Causality and
SARS-CoV-2 – new findings that mandate a broader perspective
15:15 Discussion
16:00 Tea break
16:30 Dr. Thierry Paul, National Centre for Scientific Research
(CNRS) and Sorbonne University,
Paris
Causality, indeterminism and all
that: a quantum entanglement
17:15 Discussion
18:00 End
Saturday 27 November 2021
Moderator: Dr. Ricarda
Steinbrecher, EcoNexus, Oxford
9:00 Dr. Maël Montévil, French National Centre for Scientific
Research (CNRS)
Organization,
historicity and causality
9:45 Discussion
10:30 Coffee break
11:00 Dr. Elena Rocca, Centre for Applied Philosophy of
Science, Norwegian University of Life Sciences
Difference-maker, mechanism or disposition? How explicating and
critically discussing basic assumptions about causality improves scientific
evaluations of risk
11:45 Discussion
12:30 Lunch
Moderator: Dr. Angelika Hilbeck,
Swiss Federal Institute of Technology
14:00 Prof. Ana Soto, Tufts University School of Medicine (Boston),
Centre Cavaillès, Ecole Normale
Supérieure (Paris) and Institute for Advanced Studies of Nantes
Towards the
understanding of biological causality and its application to endocrine
disruption
14:45 Discussion
15:30 Tea break
16:00 Prof. Thomas Vondriska, David Geffen School of Medicine, University of California, Los
Angeles
Genomes, epigenomes and causal
inference in multicellularity and human disease
16:45 Discussion
17:30 Final discussion
18:00 Closing words: NN
Please note the conferences fees:
Online participation: voluntary fee: Please consider making a
donation towards covering the considerable costs of this conference, e.g.: € 10
(reduced), € 50 (regular), € 80 (solidary);
On site participation: registration fee: € 50 (reduced), € 150
(regular), € 250 (solidary). This includes lunch on both days.
The conference fee can be transferred to our bank account with reference “conference fee”
or to our paypal
account (when the page opens, click on the button
“Donate” in the top right corner and the paypal page will open).
If the reduced fee is still beyond your financial capacity, please
inform us: the fee should not stop anyone from attending.
Please contact us for onsite participation,
SOURCE: ARCHIVE of Culture, 16.11.2021.
[1] Waddington,
C.H. (1943), “The Scientific Attitude”, second revised edition,
Penguin
