Once contributors have been discovered…

You can forget about illusory causes. If there are contributors, then there cannot possibly be a cause. There may be a driver if less than 50% of the observed effect has been accounted for by the known contributors. Generally, however, being more obvious (harder to conceal), drivers are discovered before contributors.

Advertisements

Thanks to the imperfections of scientists, even science is mostly rubbish

Rule: as practiced by scientists, words (terms) have ambiguous meanings.

Exception: a handful of rigorously defined terms.

Consider that in science (genuine knowledge) a word (a term) must have the same meaning. Not true in art – art thrives on ambiguity.

Consider the word “cause.”

In these two statements it must mean the same thing.

1. The motion of the cue ball causes the motion of the 8 ball.
2. The cause of death was Salmonella food poisoning.

In statement 1, the word “causes” is close to “completely responsible for.”
It conveys the notions of sufficiency(S), immediacy(I), and necessity(N), SIN for short. This is close to being true: transfer of momentum is not quite instantaneous. Air resistance and the friction of the billiard table contribute to the observed motion. The term “drives” is better – the driver of the effect is primarily responsible for the effect. There cannot be two drivers – if neither is primarily responsible, then they are both contributors to the effect. A contributor is NOT primarily responsible for the effect.

In statement 2, the word cause has a different meaning. It cannot mean what it does in statement 1. Death from Salmonella food poisoning is not even close to immediate. Death is not necessary, as the majority of people survive bouts of Salmonella food poisoning. The Salmonella food poisoning is not sufficient to cause death. The Salmonella challenges our defenses, and those people whose defenses were not up to the challenge succumb. Their weaknesses drive their own deaths. Salmonella was a challenge, a contributor. Personal weaknesses drove the death, and nothing, and I mean nothing, caused their deaths.

The logic of science

If any assertion of any kind is contradicted by reliable data, it is wrong.

The assertion must be corrected, unless the data are subsequently corrected.

If the assertion fits ALL of the available data, it might be right.

Tentative acceptance.

As time passes, if the assertion continues to fit all of the available data, and makes useful predictions, there is greater acceptance.

In no case is their blind faith in the truth of the assertion, unless, in the meantime, the assertion is shown to be true by definition.

 

The most important terms are the ones we leave undefined

Neither scientists nor philosophers define important terms adequately.

For example, Aristotle never defined the term “cause” adequately before launching into categorizing all of the different ways the term is used, in a way enshrining all of the intellectual confusions people have with this term. What we needed from Aristotle was criticism of the superficiality of all of this nonsense. A poet making fun of all of this self-important nonsense re Causation would have been more informative. Aristotle’s “four causes” multiplies confusion. There are likely no causes in nature, not four every time we think we have identified one.

Thinkers are sloppy by nature; so this is expected.

But it may also be deliberate – it allows them to claim more for their discoveries, and in some cases get away with it.

“HIV causes AIDS” – millions of research dollars would never have been given to “HIV initiates immunodeficiency in the immunocompetent and it exacerbates immunodeficiency in those already immuno-deficient.” – the latter view of HIV and AIDS being my modest attempt to get at the plain truth.

There is no cause of sickle cell anemia

By definition, the cause of an effect is completely responsible for it. Thus, there cannot be two or more causes. The phrase “a cause” is a contradiction in terms. Removal of the cause of a malady cures ALL people of ALL aspects of the condition.

By definition, the driver of an effect is predominately responsible for it. Thus, there cannot possibly be two drivers of an effect, although when apparent drivers interact, and when each is studied independently, each can appear to be predominately responsible for the effect. In reality, both apparent drivers are contributors. With the exception of interacting “drivers”, the phrase “a driver” is a contradiction in terms. Removal of the driver of a medical condition approaches a cure of the condition.

By definition, a contributor to some effect is partly responsible for it. Removal of a contributor alleviates the condition.

There can be only one cause and only one driver. If there is a driver, there must also be at least one contributor. There can be any number of contributors along with one driver, and there must be two or more contributors when there is no driver and no cause.

Statistics and common sense tell us that in nature there are many more correlates than contributors and many more contributors than drivers, and many more drivers than causes.

The genetic mutation in the Beta globin gene is the driver of sickle cell anemia, not the cause of sickle cell anemia.

The mere existence of a wide range of phenotypes of those who suffer from the disease says that there is more to this disease than this genetic mutation, this driver, this common denominator, this defining characteristic, this challenge, the mutation being the challenging problem that sets up a whole lot of other problems.

The fact that there are mild cases of sickle cell anemia says either that the genetic lesion itself -the driver- is not so bad as imagined or that other things can ameliorate the condition.

If those suffering the worst cases of the disease were cured of the driver, they would not be restored to ordinary levels of health. They have other maladies that make their disease so much worse than average.

“The cause of sickle cell anemia” is a phrase that approaches reality only in those with the mildest forms of the disease. If this one malady were reversed, their health would be much, much better, though never perfect. Perfect health does not exist.

An anecdote that says that vitamin C deficiency does not cause scurvy

High dose vitamin C is a therapy for scurvy precisely because vitamin C deficiency is NOT the cause of scurvy.

What? Huh?

Some background:

By definition, the cause of something is completely responsible for it. There can be only one cause of something.

By definition, the driver of something is predominately responsible for it. There can be only one driver of something and there must also be at least one contributor.

By definition, a contributor to some effect is partly responsible for it. There can never be one contributor if there is no driver and no cause.

Statistics and common sense tell us that in nature there are many more contributors than drivers, and many more drivers than causes.

If vitamin C deficiency is the cause of scurvy, then only vitamin C can cure scurvy.

If vitamin C deficiency is a contributor to scurvy or a correlate of scurvy, and not the cause, or even the driver of scurvy, then a therapeutic dose of vitamin C might cure scurvy.

If vitamin C deficiency is a correlate of scurvy, not a cause, then simply increasing bodily pools of vitamin C to above the level seen in scurvy will not cure scurvy.

On the contrary, it will take quite a bit higher doses to do that. This is what is observed and was in fact the second thing that made me suspicious of the one-hit causal model of scurvy. The anecdote below, while not reliable, would disprove conventional wisdom, if the anecdote could be verified and established by rigorous experimentation.

If scurvy is a multi-hit a-causal disease, as I believe is the rule for diseases, then any number of things might cure it, including large doses of a single agent, vitamin C – because even single agents are multifactorial in their actions.

Scurvy could also be an exceptional one-hit causal disease or it could be a case of medical gerrymandering, making the statement somewhat trivial, as being true by definition. Gerrymandering means that only those symptoms attributable to vitamin C deficiency are included within the scope of the disease known as scurvy. Yet those who suffer from scurvy have more things wrong with them than that definition allows, including more deficiencies than just one vitamin.

As scientific evidence goes, anecdotes are weak, really weak. But they are not NOTHING. They are not controlled experiments and those reporting the anecdotes may even lack credibility. The anecdotes need to be investigated and the work repeated, scientifically. Most scientists just ignore anecdotes and go on about their business, but they do so at their own peril, the peril of the scientific error of promulgating and perpetuating overly simplistic univariate models.

Many an underpowered model, one that is too causal, too univariate, has arisen by ignoring anecdotes.

Here is a widely ignored anecdote about scurvy that if it is true, blows the theory that vitamin C deficiency is the cause of scurvy right out of the water because scurvy was cured rapidly without vitamin C. The two keys, which dispute scientists claims to the contrary, are the rapidity of the effect and the heat stability of the factor(s) responsible.

Reference:

J Ethnobiol Ethnomed. 2009; 5: 5.  Published online 2009 Feb 2. doi:  10.1186/1746-4269-5-5 PMCID: PMC2647905.  Arginine, scurvy and Cartier’s “tree of life”

“One of the first documented uses of indigenous medicine in North America was the cure in the winter of 1536 of Jacques Cartier’s crew from a disease he called “Scorbut”(scurvy) [1,2]. Cartier’s second voyage (1535–1536) was undertaken at the command of King François 1er to complete the discovery of the western lands under the same climate and parallels as in France. At Stadaconna, now Quebec City, Cartier’s crew was cured from scurvy by ascorbic acid (vitamin C) obtained as a decoction from the Iroquois. It was prepared by boiling winter leaves and the bark from an evergreen tree. The tree, identified as “Annedda”, became known as the “tree of life” or “arbre de vie” because of its remarkable curative effects. In the winter, scurvy was the most prevalent disease among the Iroquois. This was due to the lack of food and vitamin C [3].

The cure for scurvy was significant for future naval explorations and for the introduction of the tree into France during the Reformation when the Age of Reason began (1558–1648) [4]. The medicinal value of the tree of life contributed to the resurrection of botany, which at that time struggled to free itself from pharmacy when medical men were still its masters. By the eighteenth century, the French naturalists at the Jardin du Roi in Paris knew of Thuja occidentalis as the tree of life and planted an avenue of it in the Jardin itself [5].

The Iroquois referred to the tree as Annedda (l’Annedda, Aneda, Anneda, Hanneda) [2]. Other tribal names for conifers were “ohnehta” for white pine, “onita” and “onnetta” for white spruce (Mohawk, Onandaga). These names represent the evergreen nature characteristic of coniferous trees. Regarding the transmission of the tree of life to France, the earlier one goes, the sparser are the available manuscripts. The pre-Linnaeus terminology for conifers made their precise identity impossible to make. Based on collections by French explorers and the ethnomedicine of indigenous peoples in eastern Canada, the true identity of the tree of life became controversial [2]. The identity of Anneda was narrowed down to eastern white cedar or arborvitae (Thuja occidentalis L.), white spruce (Picea glauca (Moench) Voss), black spruce (Picea mariana (Mill.)), eastern white pine (Pinus strobus L.), red pine (Pinus resinosa Aiton), balsam fir (Abies balsamea (L.) Mill.), eastern hemlock (Tsuga canadensis (L.)), and juniper (Juniperus communis L.) [2,6].

We now know that during late a severe winter and at a similar latitude to Quebec City, the candidate trees of life are a rich nutritional source of arginine, proline and other amino acids [79]. Their physiological fluids and proteins contain amino acids which are essential in the human diet because the body does not synthesize them (viz., phenylalanine, valine, threonine, tryptophan, isoleucine, methionine, leucine, and lysine). Arginine, cysteine, glycine, glutamine, histidine, proline, serine and tyrosine are conditionally essential, meaning they are not normally required in the diet, but must be supplied to specific populations that do not synthesize these amino acids in adequate amounts [10]. Today, these amino acids are used as nutritional support for the recovery of critically ill patients [1114]. In the recovery from scurvy they would help to promote vitamin C-dependent collagen biosynthesis, promote wound healing, reduce susceptibility to sepsis, and contribute to weight gain [10,1517].”

He declares, I believe wrongly, in view of the trivial amount of vitamin C present in heat-treated extracts of Thuja occidentalis bark and needles, the rapidity of the cure, and the heat-stability of the curative agent(s):

“Several conifers have been considered as candidates for “Annedda”, which was the source for a miraculous cure for scurvy in Jacques Cartier’s critically ill crew in 1536. Vitamin C was responsible for the cure of scurvy [emphasis mine] and was obtained as an Iroquois decoction from the bark and leaves from this “tree of life”, now commonly referred to as arborvitae. Based on seasonal and diurnal amino acid analyses of candidate “trees of life”, high levels of arginine, proline, and guanidino compounds were also probably present in decoctions prepared in the severe winter.”

In spite of declaring vitamin C deficiency to be the cause of cancer, this author concludes more sensibly, more multifactorially:

“The history of medicine and clinical practice has involved a succession of blind alleys and detours, mountains of often uninterpretable observations, and a great leap forward as in the discovery of vitamin C as a cure for scurvy. This review takes us centuries back, and turns our attention to the combined values of arginine, NO, proline, other conditionally and essential amino acids, guanidino compounds, and antioxidants as added factors in the food and medicines of indigenous Canadian peoples.”

It’s not them – it is us

The multi-hit a-causal model of disease says that the problem, the enemy, is us, more specifically, our weaknesses.

Koch’s postulates have the wrong emphasis – it is them, not us. They cause disease and we suffer the consequences.

Our defenses, both specific and non-specific, should be the focus of research.

Pathogens are challenges, and little more, but they evolve. What works today against these pathogens will probably not be adequate in time.