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Re: Cardiovascular mortality in the Glasgow Cohort: from the Great War to the United Nations

Dear Editor,

Yu-Kang Tu brilliant work investigated the complex emerging field of microbial risk factors and cardiovascular disease. The paper concluded that tooth loss (used as an index for poor oral health) is related to CVD mortality. However, a clear link between both conditions is missing in the study. This publication raised in our group many reflections. The related editorial published in the same issue of Heart only partially cover our questions.
A crucial point to reduce potential confounders in similar experiences deals with the socioeconomic status of the enrolled population.
Race/ethnicity, education, and socioeconomic environment are important for periodontal health. Poverty and residence in a disadvantaged environment are associated with higher risk of periodontitis as well. Moreover low socioeconomic status seems associated with progression of atherosclerosis.
Consistent data demonstrated also the association between adverse socioeconomic circumstances in childhood and both adult dental diseases and atherosclerosis. Children who grew up in low socioeconomic status families have poorer dental health including dental caries, plaque scores, gingival bleeding and periodontal diseases compared with those from high socioeconomic backgrounds.
This study offers a unique, at our knowledge, chance to understand the relationship between social aspects and oral disease leading to higher vascular risk.
We can’t forget how the birth time interval of the Glasgow Alumni study started right when the Great War came to an end until the United Nations headquarters officially open in New York City. This is a timeline of great changes in the western societies, where also UK specific socioeconomical features may have played a big role in the study.
British economic growth between 1950 and 1955, as measured by an average annual increase in gross national product of 2.9 per cent , has been the slowest: less than one-third that of Germany (9.8), half of Austria (6.9), and Italy (5.9), lower than France (4.2), Belgium (3.1), the Netherlands (4.9) or Norway (3.5). And this trend was similar according to the United Nation reports in the following years.
Postwar British society grew slowly until 1973 placed in comparison with international context. According to the British Nutrition Foundation the weekly intake of sugar in England and Wales in the decade 1942-1952 was below 300g, raising above 500g per week in 1962. Food rationing in UK ended around 1954. We can easily speculate on the large effect of sugar rationing measures, taken by British authorities, may have on the oral pathology of the study population. No comparable measures were taken in other western countries during postwar period.
Adverse socioeconomic circumstances in childhood confer a greater risk for adult-life vascular diseases. We should also take into account how the 1918-19 influenza epidemic killed at least 40 million people worldwide and 675,000 people in the United States, exceeding the US combat deaths in the two World Wars combined.
The first cases of the influenza epidemic in Britain appeared right in Glasgow in May, 1918. It soon spread to other towns and cities and during the next few months the virus killed 228,000 people in Britain. This was the highest mortality rate for any epidemic since the outbreak of cholera in 1849.
In UK desperate methods were used to prevent the spread of the disease. However, despite attempts, all treatments devised to cope with this new strain of influenza were completely ineffectual.
Besides its extraordinary virulence, the 1918-19 epidemic was also unique in that enormous number of its victims were men and women aged 15 and 44, giving the age profile of mortality a distinct ‘W’ shape rather than the customary ‘U’ shape, and leading to extremely high death rates in the working ages.
Infants and young children are traditionally a more vulnerable group, both to influenza and other forms of infectious disease, and their relative mortality was also increased dramatically. The dependence of the very young on their parents, particularly their mothers, however, suggests that high adult illness and mortality is likely to have an impact on infants and children, and this makes discussion on the effects of a similar infants selection on the Glasgow Alumni study population. Another possible confounder is connected to the possible variation in attributes of coronary heart disease cases suggesting a change in the primary source- subpopulation of cases over time. It was proposed that an early 20th- century expansion of a coronary heart disease–prone subpopulation, characterized by high serum-cholesterol phenotype and high case-fatality which contributed to most of the coronary heart disease cases and deaths during the 1960s may be a late result of the 1918 pandemia. The same abnormal immune response to infection that in 1918 killed mostly men, whites, and born from 1880 to 1900 (20–40 years old) may have “primed” survivors of those birth cohorts to late vascular mortality. The extinction of such birth cohorts would result in a relative increase in cases coming from a 2nd subpopulation, which was characterized by insulin resistance and chronic expression of low-grade inflammation markers and was comparatively less vulnerable to die acutely from coronary heart disease.
In conclusion the Glasgow Alumni experience may be biased by some global and local confounder that include: (i) a birth cohort selection bias: influenza survivors less vulnerable to vascular diseases; (ii) the study took place in a time span when UK may not represent the general socioeconomic trends in western countries and continental Europe: resulting in lower caloric and nutritional standards leading to peculiar patterns of dental status; (iii) no clear data regarding the familial income, and hygienic standards in the study population are available.

References

1. Tu YK, Galobardes B, Smith GD, McCarron P, Jeffreys M, Gilthorpe MS.
Associations between tooth loss and mortality patterns in the Glasgow Alumni Cohort.
Heart. 2007 Sep;93(9):1098-103. Epub 2006 Dec 12.

2. Samuel P. Perry, Jr
Economic Survey of Europe in 1956 by United Nations Economic Commission for Europe Annals of the American Academy of Political and Social Science
Vol. 313, (Sep., 1957), pp. 190-191

3. Abbas MA, Galantucci S, Parnetti L, Corea F.
Atherosclerosis assessment confounders in the Rancho Bernardo study.
Am J Cardiol. 2007 Mar 15;99(6):876.

4. Corea F, Kwan J, Abbas MA.
Predisposition to carotid atherosclerosis in ICARAS dental substudy.
Stroke. 2007 Jan;38(1):12; author reply 13. Epub 2006 Nov 16.

5. Abbas M, Sessa M, Corea F.
Asymptomatic carotid lesions: traditional vs. emerging risk factors.
Arch Med Res. 2006 Jul;37(5):687-8.

6. Abbas M, Bignamini V, Corea F.
Effects of chronic microbial infection on atherosclerosis.
Atherosclerosis. 2006 Aug;187(2):439-40.

7. Data downloaded from www.nutrition.org.uk on 30 August 2007