Water and arteriosclerosis

Rank, Peter

doi:10.1016/0306-9877(87)90050-8

Cited by 4 publications

(1 citation statement)

References 17 publications

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“…The author bases his theory on ecological data, examining the geographical, demographic and historical distribution of the disease. Routes of infection are posited to be ingestion of unfermented milk, public water supplies drawn from surface waters as distinct from groundwater [ 108 , 109 ], and earth-contaminated food and other objects [ 107 ]. The author also critiques the three theories of the pathogenesis of arteriosclerosis that were current at the time (response-to-injury, lipid hypothesis, and monoclonal hypothesis) and suggests laboratory studies to replicate and study the disease.…”

Section: Introductionmentioning

confidence: 99%

Cyanobacterial lipopolysaccharides and human health – a review

2006

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Cyanobacterial lipopolysaccharide/s (LPS) are frequently cited in the cyanobacteria literature as toxins responsible for a variety of heath effects in humans, from skin rashes to gastrointestinal, respiratory and allergic reactions. The attribution of toxic properties to cyanobacterial LPS dates from the 1970s, when it was thought that lipid A, the toxic moiety of LPS, was structurally and functionally conserved across all Gram-negative bacteria. However, more recent research has shown that this is not the case, and lipid A structures are now known to be very different, expressing properties ranging from LPS agonists, through weak endotoxicity to LPS antagonists. Although cyanobacterial LPS is widely cited as a putative toxin, most of the small number of formal research reports describe cyanobacterial LPS as weakly toxic compared to LPS from the Enterobacteriaceae.We systematically reviewed the literature on cyanobacterial LPS, and also examined the much lager body of literature relating to heterotrophic bacterial LPS and the atypical lipid A structures of some photosynthetic bacteria. While the literature on the biological activity of heterotrophic bacterial LPS is overwhelmingly large and therefore difficult to review for the purposes of exclusion, we were unable to find a convincing body of evidence to suggest that heterotrophic bacterial LPS, in the absence of other virulence factors, is responsible for acute gastrointestinal, dermatological or allergic reactions via natural exposure routes in humans.There is a danger that initial speculation about cyanobacterial LPS may evolve into orthodoxy without basis in research findings. No cyanobacterial lipid A structures have been described and published to date, so a recommendation is made that cyanobacteriologists should not continue to attribute such a diverse range of clinical symptoms to cyanobacterial LPS without research confirmation.

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Section: Introductionmentioning

confidence: 99%