In light of these findings the question naturally arose as to whether lead impregnation _per se_ could produce gout. It was then elicited that the association of lead with gout was noticeably less frequent in Scotland and in the North of England than in London. On this interesting point Dr. T. Oliver observes, “We do not see in the north that intimate relationship between gout and saturnine poisoning. Workmen from the south develop it in the North of England. The natives of the north, though equally exposed, seldom become gouty even when the kidneys are affected.” Again, Osler tells us that in America lead-gout is comparatively rare, though chronic lead poisoning is frequently met with in that country in association with arterio-sclerosis and contracted kidneys. Again, Frerichs, out of 163 cases of plumbism in the Berlin Hospital, found not a single case of true gout. Some remarkable instances illustrating the influence even of medicinal doses of lead in determining outbreaks of gout are on record. In a man aged 25-30, suffering from chronic diarrhœa, Sir Lauder Brunton prescribed lead and opium pills. In less than ten days he returned with gout in one of his joints, though he had never previously suffered from an attack. My colleague, Dr. Munro, tells me of an even more striking case. A lady under his care had used a hair wash, for many years, with apparently no ill effects. She recommended a friend of hers to try the same lotion, and within a few days she developed acute arthritic gout, though she had never previously experienced the disorder. Analysing the preparation, Dr. Munro found the clue in the contained lead. As to proffered explanations of lead-gout some have sought it in the production by this poison of _arterio-sclerosis_ and _chronic nephritis_. But this is scarcely satisfying when we contrast the frequency of chronic plumbism and associated arterio-sclerosis and contracted kidneys with the relative rarity of lead gout. The balance of evidence would appear to be in favour of the view that lead _per se_ cannot produce gout. For the incidence of lead-gout is scarcely appreciable, save in a population amongst whom from other causes gout is prevalent. In short, lead in the absence of an hereditary bias, is impotent to evoke gout. As to its _modus operandi_, I think it exerts its effect through derangement of the intestinal secretions, and so favours the migration inwards into the system of pathogenic _bacteria_. As for occupations other than those concerned with lead, it is certainly notorious that gout is extremely frequent in those that are rich in opportunities for overeating, overdrinking, and sluggish habits. This point has never been more clearly illustrated than by James Lindsay, whose analysis I take the liberty of transcribing.