I was thinking about the difference between "studies" one often hears about in the mainstream media - studies that contradict each other (and therefore cannot be considered "factual") - and pieces of information that are more substantive. Rather than listen to one "expert" talk about how great red wine is while another drones on about the perils of alcohol consumption, which might be best described as "factoidal" (in a new, more apt, language designed to reconsider findings deemed "scientific"), my tentative opinion is that something like feeding an animal species (such as dogs) different diets and seeing if any was substantially better or worse than the rest (in terms of health, but mostly longevity) would be best thought of as "factual." Feeding dogs a diet no human would or has ever eaten, then looking for markers of this or that "disease" (even though dogs rarely die of it - unlike humans), and not determining whether the dogs live shorter and less healthy lives, is at best "factoidal" information. And yet this is what most "science" these days (on biomedical and nutritional issues, at least) amounts to for the most part.

This brings me to the subject of "epidemiololgy," which is a statistical study of "disease" that starts with all kinds of assumptions, one of which, in the "infectious disease" context, is that "germs" are the direct and sole cause of these kinds of "diseases." I have written about the problems and misleading advice that has been derived from epidemiology in some of the other essays, but here I want to turn my attention to a study that is very interesting, though most likely flawed. The question worth asking, after examining it, is: is it factual or factoidal? And in this case, I think the answer has to do with how wise the investigator is, rather than what is contained within the study itself.

The study in question is J.C. Annand's "Further evidence in the case against heated milk protein," published in Atherosclerosis journal; 1972 Jan-Feb;15(1):129-33. Annand points out that pasteurization, cooking, or improper storage can make make lactose much more allergenic. He then states that: "It seems possible therefore that this same response against denatured MP [milk protein] may be a factor in the development of atherosclerosis or of arterial thrombosis." After that, he talks about the correlations found or not found in the epdiemiological evidence: "...the dietary factor which seemed to correlate consistently throughout these surveys appeared to be MP which had received relatively prolonged heat treatment. Thus the consumption of flash-pasteurized milk, saturated fatty acids, milk fat and sugar all failed to correlate on this historical basis in the UK."

Now he may indeed be on to something here, but note that at this point he can only suggest a scientific hypothesis. In order to present a hypothesis like Annand's, at this point in history, one would need to do an experiment that controlled for oxidized cholesterol, since there is now a great deal of evidence, down to the molecular level, that this is the root cause of "heart disease." In 1972, this was not known, and so Annand's idea was reasonable. In fact, his point about milk protein is still worth considering, an should certainly be controlled for in relevant experiments. However, my point is that while Annand's investigations were thoughtful, one still needs to follow the scientific method to determine what the reality is. Unfortunately, in the case of various "diseases," it is now routine to take all kinds of "short cuts" that directly violate the scientific method, and the results of this are all too obvious. Also worthy of note, though in this the "mainstream media" is at least complicit, is the scant attention paid to results that contradict the simplistic and misleading notions that abound these days. For example, in the July 17, 2006 edition of Newsday (page 26), in an article entitled, "Midlife clues to dementia," we learn that after studying "cholesterol in a group of 1,027 men over three decades. Among many who developed dementia, records showed that their cholesterol levels had dropped about 15 years earlier, and had remained low." No explanation was offerred; the author merely characterized it as a "contradiction."

Now I'll discuss some problems with non-epidemiological "scientific" claims. Below are some citations that I will use in the remainder of this essay, when I have the time to finish it.

Genetic variation linked to age-related macular degeneration "The effect of CFH [a gene "turned on" by stressors] is significantly influenced by environmental and genetic factors that determine the inflammatory response and activate the complement pathway." (JAMA. 2006;296:301-309. Available pre-embargo to the media at www.jamamedia.org). http://www.eurekalert.org/pub_releases/2006-07/jaaj-gvl071306.php High-manganese, low-copper environments can create prion diseases without the organophosphate catalyst, as seen in deer and elk herds in Colorado who eat manganese-rich pine needles. http://madcow.pamrotella.com/ Cambridge University prion biochemist, David R. Brown is dismissive of the science behind the infectious model of BSE. He terms it "a very limited amount of science by a few assumed -- reputable scientists." He insists there is "no evidence an infectious agent is present in either meat or milk." "Simple tests on udder walls of cows -- which could easily detect an infectious prion -- have not been done, why I don't understand." A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same Dr. David Ray was appointed to the UK Veterinary Products Committee (VPC) -- a government body that licences animal medicines. Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey chemical poisoning model matches with the epidemiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither. The question is rhetorical, and Purdey has an eye-opening answer. He argues that the prion molecule acts as a shock-adsorber of damaging energy from ultraviolet rays and other oxidizing agents. Once this prion defence system is rendered ineffective by organophosphates, these oxidizing effects have an unmediated impact on tissues. http://www.cqs.com/opmadcow.htm IT HAS BEEN DEMONSTRATED HOWEVER THAT H5N1 kills hen embryos and can be cultivated in eggs. Where is the rat to be smelled in this? These experiments have been used already since over 100 years back, in order to "prove" the existence of several "viruses" quite different from each other, for instance also that of the purported smallpox virus. In these experiments, extracts are being injected through the eggshell into the embryo. Depending on how much is injected and where in the embryo the supposedly "virus-infected" extract is injected, the embryo dies faster or more slowly. It would die from such injections in precisely the same manner too if the extracts were sterilized in ad- vance. This killing then is presented by those virologists, firstly, as direct proof of the existence of the respective virus, secondly as proof of the possibility of multiplying the virus, and thirdly and simultaneously as proof of the isolation of the virus. From hen embryos killed in this way, millions of which are dying silently each year at the vaccine manufacturers', various vaccine substances are being produced. Besides hen embryos, also cells are being killed in test-tubes in order to present the dying of these cells as proof of the existence, the multiplying and the isolation of a disease- causing virus. Nowhere however is a virus being isolated in this manner, photographed in an electron microscope and its component parts described in processes of the type called electrophoresis. http://www.gatago.com/misc/health/aids/2472802.html and: http://www.gnn.tv/A02138 Several US trials failed to invoke BSE in cattle after feeding or injecting them with massive doses of scrapie-contaminated brain tissue. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass-and-silage system without any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding. http://www.ourcivilisation.com/madcow/madcow.htm