Lamarckism — Agential Biology Institute
A note from Charlie Munford, President, ABI

Lamarck did not "propose" Lamarckism actually, he was one of the main inventors of the theory of evolution, totally different idea. It was argued in the early 1800s whether there was any change in species over history at all, and Lamarck said Yes when others said No. Most biologists throughout the 19th century assumed that organisms, if they did change, changed at least in part according to "use and disuse" INCLUDING DARWIN! This later came to be called "Lamarckism" and it is still called that, even though that moniker would have made no sense to Lamarck, who didn't invent the idea and wasn't known for it or anything like it in his day. It's basically taken to mean pre-Darwinian thinking. But the true and useful fact that Darwin was a Lamarckist has been completely erased from the story, even though Denis Noble counts eight places in The Origin of Species where Darwin references "use and disuse" as a source of variation. I only counted five, but the point stands. I think very few of the people who talk about "Darwinian" this and that today have read much Darwin. Darwin had no "Darwinian" genetic theory, he had a Lamarckian theory that included natural selection (basically very much like epistolution.)

The actual situation is even more interesting. "Lamarckism" came to be so toxic as a slur that modern Lamarckists are at pains to be known as "neo-Lamarckists." (This is funny because "Darwinist" isn't a slur but "neo-Darwinist" might actually be one.) They do this because, I assume, they want to distinguish between the foolish Lamarckism which asserts that giraffes evolve long necks because of their conscious intentions to try to eat from higher branches. It's considered silly to think that organisms change because they want to change. This is distinguished from more specific, limited examples of "neo-Lamarckism" like the very carefully mechanistically documented ones we have cited, which are more like physiological "use and disuse" which is thought to be independent of the animals' intentions. But there are two problems with thinking this way. 1) there is absolutely no reason why the molecular mechanism has to be specified for an example to be valid, the results of heritable variation are evident whether we know the mechanism of transmission or not. And the silliness goes even deeper. 2) As far back as the 1950s, the biologist Conrad Waddington pointed out, and proved very convincingly with experiments in fruit flies, that as soon as you have any adaptive plasticity at all, you can expose a new trait by stressing a phenotype and then select for that trait, causing the trait to become genetically encoded over several generations. This is termed "genetic assimilation."

This means that the adaptive plasticity that giraffes exhibit, including of course their conscious intentions, are exactly the sort of trait exposure that results in genetic assimilation by shifting the landscape of selection. If you do something sensible with your plasticity, then selection can "canalize" that sensible trait over many generations until it becomes genetically encoded. So in other words, it is not only reasonable to think that conscious intentions of organisms actually result in evolutionary change, it is already a standard normative feature of textbook genes-based evolutionary biology. What I'm saying is that conscious intentions are actually part of standard evolutionary mechanisms, setting Lamarckism completely aside. People are just allergic to being attached to the name because they haven't thought seriously about the integration of the mind and the body into one system. It's quite embarrassing.

01 — Introduction

What Is
Lamarckism?

Your father's diet shapes your status as an embryo, and nobody knows why.

Well, someone predicted it: Jean-Baptiste Lamarck — but he's been dead for nearly 200 years, and his ideas were buried almost as long.

His* theories of inheritance were rejected and squashed under the heel of modern genetic theory. The thing is, he wasn't completely wrong, and common genetic phenomena we can only describe as "Lamarckian" are poised to break foundational assumptions about how we think about life.

Some background: Lamarck assumed, two centuries ago, that organisms could pass on traits they acquired during their own lifetimes — that experience could shape inheritance. Darwin's later theory, and especially the 20th-century "Modern Synthesis" that merged Darwin with genetics, largely displaced this idea. The consensus became: inherited change happens only through random mutation filtered by natural selection. The genome changes by accident and by culling, never by design. Organisms do not rewrite their own programs in response to what happens to them during their lifetimes.

That consensus is now under pressure. A growing body of evidence shows that organisms — from bacteria to mammals — possess mechanisms that produce heritable changes in direct response to environmental stress. These are not random mutations that happened to be useful. They are directed, repeatable, and often reversible responses. If that is what is happening, the question is not whether Lamarck had a point. The question is: what is the mechanism of this directed and heritable change, and what does it tell us about how life actually works?

Lamarckism is not saying:
  • That all acquired changes are inherited
  • That all conscious intentions affect evolution
  • That all physical changes are heritable — mutilations are not
In each case, it only happens sometimes.
Modern Synthesis Heritable change is random — organisms cannot direct changes to what they pass on
Lamarckism The idea that acquired experience can shape inheritance — discarded by modern genetic theory, but increasingly hard to dismiss
The exceptions Many well-documented phenomena appear to violate the Modern Synthesis, and they are not rare edge cases — they span the tree of life
Why it matters Understanding the mechanism represents a missing causal layer in biology — and would trigger a complete re-evaluation of foundational assumptions about life
02 — Example One

Bacteria:
The Genome
That Rewrites
Itself

Bacteria are the most abundant organisms on Earth, and they reproduce asexually — the daughter cells inherit everything the parent cell carried. When bacteria encounter stress, such as exposure to an antibiotic, they do something the Modern Synthesis would not predict: they actively exchange genetic material with neighboring cells. This process, called horizontal gene transfer, allows resistance to spread rapidly through a population — not by waiting for a lucky random mutation, but through a coordinated sharing of functional genetic information. Recent estimates suggest that 81% of cumulative genetic change in prokaryotic genomes is attributable to horizontal gene transfer. This is not an anomaly at the margins. It is the dominant mode of genetic change in the most numerous organisms on the planet, and it can be triggered by environmental challenge.

Asexual reproduction Bacteria reproduce by dividing in two — offspring inherit every change the parent carried
Stress response Under pressure (e.g., antibiotic exposure), bacteria can actively exchange DNA with neighboring cells
Horizontal gene transfer The name for this process — and the mechanism by which resistance spreads through a population
Dominant, not marginal Estimated to account for ~81% of cumulative genetic change in prokaryotic genomes
Triggered, not accidental The response can be activated by environmental challenge — it is not a random mutation that happened to be useful
03 — Example Two

Worms:
Stress Responses
That Outlast
the Individual

Caenorhabditis elegans is a millimeter-long roundworm that has become one of biology's most important model organisms. Research from Oded Rechavi's lab at Tel Aviv University has shown that when these worms are exposed to viruses or starvation, they produce small RNA molecules that silence specific genes — and then pass those silencing signals on to their offspring, for multiple generations. Crucially, the longer a response has already persisted across generations, the more likely it is to continue — a kind of epigenetic momentum. Rechavi's lab also demonstrated that the cytoplasm alone, without the nucleus, is sufficient to carry the inherited signal. The worm is not passing on a random mutation. It is passing on a functional, calibrated response to a specific environmental threat — one that its offspring have not themselves encountered.

Small RNAs When exposed to viruses or starvation, C. elegans produce small RNA molecules that silence specific genes
Inherited response These silencing signals are passed to offspring — for multiple generations — without further exposure to the original threat
Epigenetic momentum The longer a heritable response has already persisted, the more likely it is to continue into the next generation
No nucleus required The cytoplasm alone is sufficient to carry the inherited signal
Pre-loaded immunity Offspring inherit a calibrated stress response to threats they have never themselves faced
04 — Example Three

Mice
& Men:
Diet, Sperm,
and Inherited
Metabolism

The same phenomenon is now being documented in mammals. Research from the Rando lab showed that male mice fed low-protein diets produced sperm carrying specific small RNA molecules — and that their offspring showed measurable differences in how their livers synthesized cholesterol, despite never being on a restricted diet themselves. In humans, multiple labs have found that sperm contains abundant small RNAs produced in the epididymis — the tissue through which sperm mature — and that the composition of these RNAs correlates with the father's diet, his metabolic state, and even with IVF embryo quality. What a father eats, and how his metabolism is functioning, appears to influence what his children inherit. This is not a statistical artifact. It is a repeatable, mechanistically grounded finding in our own species.

Diet-shaped sperm Male mice on low-protein diets produce sperm with altered small RNA profiles
Inherited metabolism Their offspring show different liver cholesterol synthesis — without ever being on a restricted diet themselves
Human sperm RNAs Human sperm contains abundant small RNAs produced in the epididymis, the tissue where sperm mature
Father's state, child's blueprint These RNAs correlate with the father's diet and metabolic condition
Clinical relevance They also correlate with IVF embryo quality — this is not a laboratory abstraction
05 — ABI's Question

What This
Means

These three examples — drawn from bacteria, roundworms, and mammals including humans — share a common structure. In each case, an organism detects an environmental challenge, produces a heritable molecular response, and passes that response to offspring who have not themselves encountered the challenge. This is not what a purely random-mutation-plus-selection framework predicts. The genome is not a passive recipient of accidental change. It is, in some meaningful sense, a system that can read its environment and write back to its own inheritance.

The Agential Biology Institute was founded on the proposition that the Modern Synthesis may have the causal arrow backwards — it treats agency as something evolution produced, when the evidence suggests agency is what makes evolution possible in the first place. Agency — the capacity to sense, respond, and direct — is not a late product of evolution but a foundational feature of living systems.

The examples above are not curiosities to be explained away. They are evidence that the question of how organisms direct heritable change is one of the most important open problems in biology. ABI exists to pursue that question. Getting the mechanism right doesn't just correct the textbooks — it opens entirely new approaches to disease, development, and the nature of intelligence itself.

Shared pattern Across the tree of life, organisms detect environmental challenges and produce directed, heritable responses
Inconsistent with current theory This pattern cannot be explained by a strictly genes-first, random-mutation framework
The mechanism is unknown How organisms read their environment and write to their inheritance remains poorly understood — and underinvestigated
An inversion, not a refinement ABI's hypothesis: agency is not a product of biological complexity but a precondition for it — the causal arrow in the Modern Synthesis points the wrong way
The stakes If organisms are active participants in their own heredity, then medicine, evolutionary theory, developmental biology, and our models of intelligence itself all need revisiting — and new foundations become possible
References
Horizontal gene transfer in prokaryotes

Dagan, T., Artzy-Randrup, Y., & Martin, W. (2008). Modular networks and cumulative impact of lateral transfer in prokaryote genome evolution. Proceedings of the National Academy of Sciences, 105(29), 10039–10044. https://doi.org/10.1073/pnas.0800679105

RNA-based inheritance in C. elegans worms

Rechavi, O., Minevich, G., & Hobert, O. (2011). Transgenerational inheritance of an acquired small RNA-based antiviral response in C. elegans. Cell, 147(6), 1248–1256. https://doi.org/10.1016/j.cell.2011.10.042

Rechavi, O., Houri-Ze'evi, L., Anava, S., Goh, W.S.S., Kerk, S.Y., Hannon, G.J., & Hobert, O. (2014). Starvation-induced transgenerational inheritance of small RNAs in C. elegans. Cell, 158(2), 277–287. https://doi.org/10.1016/j.cell.2014.06.020

Houri-Zeevi, L., Korem Kohanim, Y., Antonova, O., & Rechavi, O. (2020). Three rules explain transgenerational small RNA inheritance in C. elegans. Cell, 182(5), 1186–1197. https://doi.org/10.1016/j.cell.2020.07.022

Rieger, I., Weintraub, G., Lev, I., Goldstein, K., Bar-Zvi, D., Anava, S., Gingold, H., Shaham, S., & Rechavi, O. (2024). Nucleus-independent transgenerational small RNA inheritance in Caenorhabditis elegans. Science Advances, 10, eadj8618. https://doi.org/10.1126/sciadv.adj8618

RNA-based inheritance in mice and humans

Carone, B.R., Fauquier, L., Habib, N., Shea, J.M., Hart, C.E., Li, R., Bock, C., Li, C., Gu, H., Zamore, P.D., Meissner, A., Weng, Z., Hofmann, H.A., Friedman, N., & Rando, O.J. (2010). Paternally induced transgenerational environmental reprogramming of metabolic gene expression in mammals. Cell, 143(7), 1084–1096. https://doi.org/10.1016/j.cell.2010.12.008

Sharma, U., Conine, C.C., Shea, J.M., Boskovic, A., Derr, A.G., Bing, X.Y., Belleannée, C., Kucukural, A., Serra, R.W., Sun, F., Song, L., Carone, B.R., Ricci, E.P., Li, X.Z., Fauquier, L., Moore, M.J., Sullivan, R., Mello, C.C., Garber, M., & Rando, O.J. (2016). Biogenesis and function of tRNA fragments during sperm maturation and fertilization in mammals. Science, 351(6271), 391–396. https://doi.org/10.1126/science.aad6780

Lismer, A., et al. (2024). Epigenetic inheritance of diet-induced and sperm-borne mitochondrial RNAs. Nature, 630, 720–727. https://doi.org/10.1038/s41586-024-07472-3