Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study
BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.38779.584028.55 (Published 04 May 2006) Cite this as: BMJ 2006;332:1064
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A causal pathway linking tobacco exposure to glucose intolerance,
diabetes and coronary heart disease (1) is that of the
catecholamines. Nicotine is known to cause a rise in the secretion of
catecholamines (2), which in turn inhibit the cell-mediated uptake of glucose by
insulin and suppress the secretion of insulin by the pancreas (3).
This process also provides an explanation for the finding that
glucose intolerance associated with tobacco exposure was greater in men
than women and greater in white people than black people.(1). Secretion of
catecholamines has been found to be higher in males than females(4), and
greater in whites than blacks (5).
Finally, diabetes and excess activity of the catecholamines are known
to predispose to coronary heart disease.
References.
1. Thomas K. Houston, Sharina D. Person, Mark J Pletcher, Kiang Liu,
Carlos Iribarren, Catarina I Kiefe. Active and passive smoking and
development of glucose intolerance among young adults in a prospective
cohort: CARDIA study. BMJ. 2006. 332: 1064-1067.(6 May ).
2. Report of a Joint Working Party of the Royal College of Physicians of
London and the British Cardiac Society. Prevention of Coronary Heart
Disease. Journal of the Royal College of Physicians 1976. Vol 10, 214-275.
3.David S. Goldstein. Stress, Catecholamines and Cardiovascular Disease.
Oxford University Press. (1995)
4. Bergman, L.R. Magnusson, D. Over-achievement and catecholamine
excretion in an achievement-demanding situation. Psychosomatic Medicine.
Vol 41, 181-188.(1979)
5.Voors, A.W., Berenson, S.S, Dalferes.E.R.Webber L.S., Shuler, S.E.
Racial differences in blood pressure control. Science 1979, Vol. 204, 1091
-1094.
Competing interests:
None declared
Competing interests: No competing interests
Mr. Alastair G Browne asserts that "the fabled cotinine test for use
as a measure of the amount of tobacco smoke that an individual is subject
to ... is not a proven method and is therefore unreliable ... has not been
properly proven beyond doubt and therefore should never be used within a
scientific environment."
Apparently Mr. Browne is unfamiliar with the scientific literature of
which the following is just a small sample:
1. Benowitz NL, Jacob III P. Metabolism of nicotine to cotinine
studied by a dual stable isotope method. Clin Pharmacol Ther 56:483-93
(1994).
2. Benowitz NL. Biomarkers of Environmental tobacco smoke exposure.
Environ Health Perspect 107 (suppl 2):349-355 (1999).
3. Jarvis MJ. Application of biochemical intake markers to passive
smoking measurement and risk estimation, Mutation Res 222:101-110
(1989).
4. Repace JL, Jinot J, Bayard S, Emmons K, and Hammond SK. Air
nicotine and saliva cotinine as indicators of passive smoking exposure and
risk. Risk Analysis 18: 71-83 (1998).
5. Repace JL, Lowrey AH. An enforceable indoor air quality standard
for environmental tobacco smoke in the workplace. Risk Analysis, 13:463-
475 (1993).
6. Repace JL, Al-Delaimy WK, Bernert JT. Correlating Atmospheric and
Biological Markers in Studies of Secondhand Tobacco Smoke Exposure and
Dose in Children and Adults. JOEM 48: 181 194 (2006).
Competing interests:
None declared
Competing interests: No competing interests
Fully agree with clinical results in abnormal GTT due to smoking,
this has been substantiated by affecting mutants in several genome parts
and insulin response element.
Triglicerides & CAD are increased by smoking due to genetic effects in
allele Sst l3238C>G present mutations in 5%-12.5% of the population
Differences in response of insulin and glucose post OGT in young healthy
men predispose to abnormal OGT and DM 2 in smokers due to genetic effects
in allele 482C>T present mutations in 25%-40% of the population.
Smoking directly affects Insulin Response Element: abolition of insulin
responsiveness of APO CIII promoter strongly affecting glucose metabolism
by effect in allele 455T>C that affects 40-55% of the population.
Li WW, et al.: Common genetic variation in the promoter of the human
apo CIII gene abolishes regulation by insulin and may contribute to
hypertriglycerdemia. J Clin Invest 1995, 96:2601-2605.
Waterworth DM, et al.: ApoCIII gene variants modulate postprandial
response to both glucose and fat tolerance tests. Circulation 1999,
99:1875-1877.
Eliasson B, et al.: The insulin resistance synfrome and posprandial lipid
intolerance in smokers. Atherosclerosis 1997, 129:79-88.
Waterworth DM, et al.: The contribution of apoCIII gene variants to the
determination of triglyceride levels and interaction with smoking in
middle-aged men. Arterioscler Thromb Vasc Biol 2000, 20:2663-2669.(2.)
Rees A, et al.: DNA polymorphism hypertriglyceridaemia. Lancet 1983,
1:444-446.
Talmud PJ, et al: Apoliprotein C-III gene variation and
dyslipidaemia. Curr Opin Lipidol 1997, 8:154-158.
Waterworth DM, et al.: The contribution of apoCIII gene variants to the
determination of triglyceride levels and interaction with smoking in
middle-aged men. Arterioscler Thromb Vasc Biol 2000, 20:2663-2669.
Dammerman M, et al: An apolipoprotein CIII haplotype protective against
hypertriglyceridemia is specified by promoter and 3’ unstranlated region
polymorphisms. Proc Natl Acad Sci USA 1993, 90:4562-4566.
Competing interests:
None declared
Competing interests: No competing interests
There are several parts of the paper by Houston et al (BMJ,
doi:10.1136/bmj.38779.584028.55 (April 7 2006) that are inaccurate,
contradictory or complete supposition.
The article cites the fabled cotinine test for use as a measure of
the amount of tobacco smoke that an individual is subject to. This is not
a proven method and is therefore unreliable. It is widely assumed that the
production of cotinine by the human body is a direct indication of the
amount of tobacco smoke ingested. This has not been properly proven beyond
doubt and therefore should never be used within a scientific environment.
The authors then go on to add a hypothesis to the experiment which is
subsequently applied to the null hypothesis and then used as a basis upon
which to conduct the experiment. This is invalid scientific practice. The
hypothesis in question concerns the effect of varying degrees of exposure
to tobacco smoke and their effect on the likelyhood of diabetes. Once one
makes assumptions like this, the whole experiment cannot help but be
conducted with this assumption in mind.
Later on in the paper, under the section on methods, another wild
assumption is made. The inconvenient fact that some subjects' cotinine
levels didn't tally with what was expected at baseline is simply brushed
aside and the subjects are effectively made out to be giving false
information to the scientists. No justification whatsoever is given for
this and it appears that no attempt was made to investigate this matter.
This involved 85 people out of an initial 1390---not a significant number
but it does raise the question of how many other "awkward" problems were
simply swept under the carpet in this manner, during the course of the
experiment.
Moving on the results of the experiment, and specifically table four
which details glucose intolerance by category. Looking particularly at the
incidence precentages, in one case the incidence percentage works out
higher for "never" smokers with passive smoke exposure than it does for
current smokers. It would be reasonable to expect that current smokers are
subject to greater levels of tobacco smoke than non-smokers of whatever
category. The results do not reflect this and there is no attempt at
explaining this within the text. Additionally, the majority of the figures
do not show a deviation of greater than 10% between smoker categories.
Such a deviation is considered the minimum acceptable in order to give
meaning to experimental results. Accordingly, this paper appears to be
inconclusive.
There has been no attempt made to split the "previous smoker" group
into passive smoke and non-passive smoke categories, as has been done with
non-smokers. Therefore any comparison made with this group is unreliable
and should be ignored.
Moving back to table one in the results. Three factors are listed
without justification for their inclusion. These are to do with high
school education, income and health insurance. How these factors affect
the outcome is not made clear in the text.
To summarise, this paper is currently being cited as definitive
evidence that environmental tobacco smoke increases the chance of
contracting diabetes. Due to the reasons above, this paper most certainly
does not prove this to be so. The authors should therefore make it clear
to the world's media that there has been some misunderstanding regarding
the interpretation of this document and also should modify the synopsis at
the end to delete the reference to passive tobacco smoke.
Alastair G. Browne MSc, BEng(Hons)
Competing interests:
None declared
Competing interests: No competing interests
Passive smoking and glucose intolerance
EDITOR - Dr Houston et al present interesting results on passive
inhalation of environmental tobacco smoke (ETS) to be a new risk factor
for glucose intolerance (1). However, their finding was inconsistent
between whites and African-Americans; no association of ETS with glucose
intolerance was found in the latter group (half of the study population).
The combined data analysis gave the overall significant association, but
probably made the conclusion overstated.
Whites with ETS had as high a risk of glucose intolerance as smokers,
which did not follow a dose-response effect. It seemed not to be explained
by that some toxic substances in ETS could be even more concentrated due
to different temperature compared to active smoking and contributed to
such a high risk; otherwise the data on the African-Americans should show
a similar pattern on the risk. Further examination is necessary to
identify why those ETS whites, particularly women, had such a high risk of
glucose intolerance. Low socio-economic status (SES) is related to stress,
depression and other unmeasured factors, increasing the risk of type 2
diabetes (2,3). Stress could result in the young non-smokers to starting
to smoke. It would be of interest to investigate differences in
psychosocial characteristics and the rates of starting smoking over follow
up between ETS and non-ETS groups by ethnicity and sex.
Defining non-ETS by negative report and undetected cotinine was an
advantage, but among three ETS groups (positive report but cotinine
undetected, negative but detected, positive and detected) there may be
differences in the risk factors and outcomes. We previously reported a
poor agreement between the two levels in each of self report and serum
cotinine (4). The combined use of different levels of self report
(including ETS duration) and cotinine concentrations could test a dose-
response effect (5). Further analysis, including adjustment for the
psychosocial factors and restricting never-smokers through follow up would
clarify the issues and help campaign against smoking in public areas.
References
1. Houston TK, Kiefe CI, Person SD, Pletcher MJ,Liu K, Iribarren C.
Active and passive smoking and development of glucose intolerance among
young adults in a prospective cohort: CARDIA study. BMJ 2006; 332: 1064-9.
2. Chandola T, Brunner E, Marmot M. Chronic stress at work and the
metabolic syndrome: prospective study. BMJ 2006; 332:521-5.
3. Knol MJ, Twisk JW, Beekman AT, Heine RJ, Snoek FJ, Pouwer F. Depression
as a risk factor for the onset of type 2 diabetes mellitus. A meta-
analysis. Diabetologia 2006;49:837-45.
4. Chen R, Tavendale R, Tunstall-Pedoe H. Measurement of passive
smoking in adults: self-reported questionnaire or serum cotinine? J Cancer
Epidemiol & Prev 2002; 7:85-95.
5. Chen R, Tavendale R, Tunstall-Pedoe H. Coronary heart disease in
relation to passive smoking by self report, serum cotinine and their
combination: Scottish MONICA study. Occup Environ Med 2004; 61:790-2.
Competing interests:
None declared
Competing interests: No competing interests