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Biomedical subjects

P R Burch

Publications and source records attributed to P R Burch.

At least 37 records · Page 2Linked to original sources
PubMed1984

Esophageal cancer in relation to cigarette and alcohol consumption.

Cigarette smoking and alcohol consumption both associate, at the individual level, with esophageal cancer; the basis of these associations is explored. Secular (temporal) trends in England and Wales, from 1911 to 1980, show that death rates from esophageal cancer correlate positively with alcohol consumption but negatively with average rates of cigarette smoking. The details suggest that alcohol helps to cause esophageal cancer through an indirect precipitating action. This hypothesis is tested, and loosely corroborated, by using the sex- and age-patterns of esophageal cancer in England and Wales and in U.S. Whites to infer the sex- and age-patterns of alcohol consumption by the victims of the disease. Genetic predisposition, alcohol consumption around 2-3 years before death and a proximal precipitator all appear to have a causal role.

Adolescent↗
PubMed1984

The surgeon general's "epidemiologic criteria for causality". Reply to Lilienfeld.

I argued in my Critique [6] that the Surgeon General's five epidemiologic criteria for causality are not given adequate definition, and that, unless they are so lax as to be meaningless, not even one of them is indisputably satisfied by the evidence relating to smoking and lung cancer. Lilienfeld concedes that "It is tactically unfortunate that the 1982 Report used the same criteria that were adopted in the original 1964 Report" [4], but he is unable to demonstrate that the available evidence, interpreted according to the accepted canons of scientific inference, is consistent either with the original or the "more detailed criteria". He makes no acknowledgement of the principle that valid inferences about cause cannot be drawn from epidemiologic comparisons between selected, non-randomized groups; he actually violates that principle in his defence of the Report by deploying conclusions from such evidence. As to the vexed 85% of lung cancer cases and the 30% of all cancer deaths in the U.S. attributed to smoking [5], no justification is offered for assigning the entire "relative risk" to a (smoking) causal relation; indeed at one point, and perhaps inadvertently, Lilienfeld repudiates that practice. I know of no valid arguments from reliable evidence that justify such precise estimates of attributable risk and if Lilienfeld cannot supply them who can? If specific claims about the hazards of any agent cannot be sustained by scientifically rigorous methods they should never be made publicly in the first place but, once having been made and exposed, they should then be retracted with as much grace and dignity as possible.

Animals↗
PubMed1984

Cancer and senescence: is there a biological link?

It is shown that sex- and age-specific death rates from all causes of death other than neoplasms have features that resemble those of corresponding rates for all neoplasms. The same generalization holds in connexion with specific neoplastic and non-neoplastic disorders. In both categories of disease many age-patterns suggest that the rate-governing mechanism for their occurrence is stochastic in character; a rather small number of random events, generally fewer than ten, suffice for their initiation. It is not immediately obvious how a widespread degenerative disorder, sometimes involving an astronomical number of target cells, can be initiated by only a few random events. We infer that all such disorders, together with natural cancers, are autoaggressive in nature. They are initiated by random somatic mutations in comparator stem cells of the central system of growth control. Mutant stem cells propagate forbidden clones of cells that attack target cells at one or multiple sites. (In certain disorders, the presence of an extrinsic precipitator in the host in essential to the propagation of forbidden clones). Autoaggressive attacks have consequences that range from the destruction of target cells to their transformation with invasive proliferation. Senescence can be regarded as the cumulative effect of predominantly late-onset autoaggressive disorders. The relevance of studies of twins to this unified theory is discussed.

Aged↗
PubMed1983

The surgeon general's "epidemiologic criteria for causality." A critique.

The methodology of the 1982 Report of the Surgeon General is examined with special reference to smoking and lung cancer. Part II of the Report describes the five criteria for causality that have guided the judgment of committees since 1964. I show that not one of the criteria, plausibly interpreted, is satisfied by the epidemiologic evidence for lung cancer. A weakness underlying all the Reports is a prior failure to recognize all the logical possibilities inherent in an association between smoking and a disease. The five criteria and the subjective method of "judgment" are inappropriate to a scientific analysis; they should be replaced by the objective testing of hypotheses. Limitations in the evidence and in concepts about tobacco carcinogenesis preclude definitive conclusions. Nevertheless, the entire association between cigarette smoking and lung cancer--at least in male Caucasoid populations--is unlikely to be explained by causation.

Adult↗
PubMed1982

Cigarette smoking and lung cancer: a continuing controversy.

During the late 1950s Sir Ronald Fisher questioned the already popular, but in his view precipitate, causal interpretation of the association between smoking and lung cancer. His pungently expressed views began a controversy that has smouldered and sometimes flared ever since. The most recent attack on Fisher's constitutional hypothesis was launched by Reif and in this paper I consider the validity of his criticisms. A range of evidence shows that it is not yet possible to distinguish between constitutional and causal-plus-constitutional interpretations although recent studies indicate that a pure causal hypothesis is incapable of explaining the full association as observed in Western populations. Unfortunately, errors of diagnosis and death certification still impede the rigorous testing of adequately formulated hypotheses.

Adult↗