The HART group response to the ‘no-virus’ argument proposes a model of disease that is, in its simplest form, one of ‘bottom-up’ causality from RNA molecule up to systemic level. This page proposes an alternative ‘top-down’ model.

We will examine the idea of top-down causality and see how it compares with the HART group model in its ability to explain the evidence. This model will provide a credible alternative to the RNA replication model and explain the epidemiology of influenza to a more satisfactory degree.
It is not ‘complete’ by any means and some of the mechanisms are missing but the HART group have indicated that they are open to nuanced debate and are prepared to allow some ‘tolerance’ in the model. Many in the ‘no-virus’ group by contrast have declared an open hostility to any degree of uncertainty, to any form of ‘modelling’ and any evidence that cannot be directly observed.
Modelling, in brief: The idea is to construct a framework of central assertions within which measurements and other evidence can be interpreted as having some meaningful relationship towards other pieces of evidence and towards the model as a whole. The model is asserted at the outset and evidence is tested against it, with any contradictions requiring a review of the whole theory.
Making minor adjustments for each small anomaly leads to an integrity ‘creep’ whereby the structure of the model slowly degrades to a point whereby the initial foundations can become quite meaningless and actually unrelated to the evidence.
The Terrain Model proposed by the ‘Terrain theorists’ has always been one of top-down causality of disease states, with environmental factors such as toxicity leading somehow to actual disease. Lanka, Cowan and Kaufman have said from the beginning that the particles characterised as viruses are really exosomes and are produced as a result of disease rather than being a cause of it.
Similarly, activities of what is described as the ‘immune system’ are really productions of specific proteins to help resolve some sort of deterioration at the cellular level. They are produced by the body, not by the assumed virus.
How do environmental factors actually cause disease? This seems to be not talked about so much with Terrain theorists simply claiming that toxicity leads to a ‘detox’, the symptoms of which are misinterpreted as disease. No actual evidence of the expulsion of toxins has been put forward.
Claims such as “The body needs to expel toxins and so initiates a detox process” suggest an intelligent system that ‘knows what it needs to do’ and ‘initiates’ the appropriate protocol. This is an odd insertion of teleological language into a scientific framework, but not necessarily incorrect.
An extended version of the above model puts in a couple of ‘interpretive matrices’ to indicate what must be necessary to make sense of real world data and translate it to physical processes within the body.
Each matrix is effectively a ‘cognitive system’ in its own right, taking information from one ‘realm’ of reality and converting it to a form suitable for use in another.
Environmental influences impact the body from top down and information is funnelled from the outside macro world into meaningful structure in the micro world in the form of very precise and functional molecular organisation.
This then is the foundational structure of the proposed model:
- Top-down causality
- Coupling of organism and environment
- Information interpreted, translated and scaled downwards
- Disease as an altered state of regulation
- Altered molecular expression as a consequence of disease – not the cause
It is time to look at some of the questions raised by the HART team.
From the HART group: “First of all, given that all life is based on a system of encoded replication, it would be extraordinary for there not to be viruses that can hijack that system. They have been studied in plants and animals as well as humans.”
This is their foundational principle which forms a lens through which all other concerns are viewed.
Terrain response: The body forms an integrated whole that is organised, stable and robust to all manner of insults. Causality is top down and it would therefore be very surprising indeed if an organised disease state could be forcibly induced by a few complex bio-molecules. The foundation of life is ‘organisation’.
HART group: “An environmental exposure predicted an illness. Although a significant proportion of infections were not traceable to an outbreak, the majority were. Groups of people became ill with similar symptoms after having shared the same environment.”
The HART group claims that this supports their hypothesis of viral transmission but this is a flawed argument as explained here: The HART group. The top down model has environmental influence built in as a fundamental and so the fact that “Groups of people became ill with similar symptoms after having shared the same environment“, far from needing an explanation, now becomes actual evidence in favour of the Terrain Model.
From HART: “A unique RNA sequence was detected in these people.” Also unique protein coded for by RNA and matching antibodies.”
Within our top-down model this can be rephrased as ‘individuals in the same physiological state will produce similar if not identical bio-molecules’. This should come as no surprise as individuals regularly reproduce precisely the same molecules on a daily basis, most of them without the need for an RNA template.
The contentious part of the top-down idea then will be that it is the precise form of the molecules that is a function of the overall physiological state as opposed to the other way around. How can this be?
Information flow in biological systems can be thought of as consisting of bottom-up emergence combined with top down causality.
Molecular activity is coordinated to form translational structures (attractors) via the phenomenon of emergence. These attractors act as interpretive (cognitive) systems to effect meaningful action as a response to environmental input.

Information from the macro scale is received and interpreted according to the current attractor state before being merged into the active regulatory system, with the natural consequence that a specific stimulus may not necessarily result in the same disease state in all individuals. Variation within a norm is thus built into the system.
Contrast this with the viral model where the particle itself is claimed to produce precisely the same symptoms in everybody. This doesn’t happen and some extra addition to the model is required to explain it away.
Classical determinism formulates causality as proceeding from one event to another in a way that is precisely predictable from a theoretical point of view but which in practice will diverge considerably as time goes on owing to noise in the system leading to an accumulation of errors.
Attractor activity however behaves in the opposite manner, with long term stability that is robust to the input of noise. Errors do not accumulate and the result is a convergent causality that can produce a precise result even from differing starting points and despite considerable ‘noise’.
From this point of view then, it is not surprising that individuals could react to the same environmental stimulus with different symptoms and yet still produce precisely the same RNA sequence. This is a now a feature not a bug.
There are precursors to this idea even in mainstream biology today, where the study of epigenetics proposes that organised network activity is held to produce very precise molecular structures and moreover that such activity can be passed on to the next generation in the form of self-sustaining feedback loops (Wikipedia).
From HART: “Lab grown virus. Material thought to contain virus has been collected from patients and replicated in cell culture.”
There was no evidence supplied that such material was capable of causing a disease state. The Terrain model claims that these particles are a reflection of the experimental conditions and so identical lab conditions will result in near identical genome sequences.
Material is produced according to attractor activity which has the properties of convergence to the attractor but variation within the attractor leading to both stability and variation of genome and thereby giving the illusion of viral evolution described by the group themselves. (See Evolution and Inheritance).
Attractors exhibit long term stability with the occasional sudden phase change, possibly in response to a stimulus but not always. This is similar to the way viruses are said to mutate and produce variants which remain stable for a while before mutating suddenly again. This behaviour does not seem so consistent with the actual viral model which claims continuous mutation despite reproducible results. (Strange attractors)
The fact that seasonal influences can affect biological systems in has been demonstrated by Giorgio Piccardi, Vlial Kaznacheev and Simon Shnoll. Cell cultures, rabbits blood, enzyme reactions, precipitation rates and even atomic clock timings were found to have seasonal variations that were measurable and to some degree, predictable

From HART: “Finally, There was an illness which some people regard as both viral in nature, and also characteristic. This is of course subjective and opinions differ on this. Some claim it is unclear how different this actually was from the range of respiratory viral illnesses experienced before.”
Well, “viral in nature” is clearly circular reasoning. More interesting though is how one measures a difference between diseases. Geneticists might be tempted simply to count the differences in sequences, others might look at bio-metrics such as temperature or simple verbal descriptions of symptoms.
If attractors are involved however, we need to think somewhat differently. In this case we would expect difference between individuals but similarity of clusters within a population. Attractor phase shifts can be sudden and unpredictable, with cause and effect seemingly de-coupled. Dose-response relationships may be complex or even non-existent, with apparently large stimuli having no more effect than smaller ones.
It is entirely conceivable that individuals could have very different symptoms, yet generate identical RNA sequences and antibodies.
We see all these effects.
Attractors are characterised by their sub-states so some direct identification of these is necessary to obtain a classification of disease that corresponds to some sort of internal reality. Some progress has been made in this area with the identification of the Core Diseasome.
Summary:
- Seasonal variation clearly implies a seasonal cause
- The epidemiology favours environment over transmission as a cause
- Interesting genome sequences are a result of disease
- Attractors enable a direct causal pathway from environment to cell
- The claimed evolution of viruses shows attractor-like qualities
- The sudden onset and stability of disease state is typical of attractors
- Causality is top-down in biological systems
- The model described above is a better fit to the evidence than the viral model


