Total mortality and cause-specific mortality of Swedish shift- and dayworkers in the pulp and paper industry in 1952-2001

Karlsson, Berndt; Alfredsson, Lars; Knutsson, Anders; Andersson, Eva; Torén, Kjell

doi:10.5271/sjweh.845

Cited by 127 publications

(115 citation statements)

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“…Lund et al [40] reported that maladaption of endogenous circadian rhythms in shift workers was associated with increased insulin resistance and elevated postprandial triglyceride levels, findings consistent with other studies in this field [44][45][46][47]. In addition, shift work is associated with an increased risk of cardiovascular disease [46,47], reported in one study as conveying a 1.6-and 3.0-fold increased risk for men and women, respectively, in the 45-55 year age group [46,48]. As noted earlier in this article, it is particularly interesting to note that, in some mammals, migration north is accompanied by a chronic retention of circannual photoperiodicity appropriate for the region from which the animal is derived, rather than that in which it has settled [36].…”

Section: Man Diabetes and Cardiovascular Diseasesupporting

confidence: 63%

“…Disruption of these processes is exemplified by the extreme circumstances of reversal of day/night working patterns seen in some shift workers. Lund et al [40] reported that maladaption of endogenous circadian rhythms in shift workers was associated with increased insulin resistance and elevated postprandial triglyceride levels, findings consistent with other studies in this field [44][45][46][47]. In addition, shift work is associated with an increased risk of cardiovascular disease [46,47], reported in one study as conveying a 1.6-and 3.0-fold increased risk for men and women, respectively, in the 45-55 year age group [46,48].…”

Section: Man Diabetes and Cardiovascular Diseasementioning

confidence: 55%

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Neel revisited: the adipocyte, seasonality and type 2 diabetes

Scott

Grant

2006

Diabetologia

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The modern epidemic of obesity and insulin resistance with cardiovascular risk factor clustering is related to the development of type 2 diabetes and cardiovascular disease. Over 40 years ago, Neel postulated that insulin resistance should confer survival benefit. Extrapolating Neel's hypothesis, we propose that the cluster of associated abnormalities also confers survival benefit and is related to metabolic responses seen in seasonally responsive animals. Weight gain in preparation for winter is accompanied by a range of acute metabolic changes virtually identical to the long-term changes seen in type 2 diabetes. In seasonal animals the responses are acute, physiological and protective. In man, similar responses that would once have conferred survival benefit have become chronic, pathological and harmful in modern life. We hypothesise that type 2 diabetes and cardiovascular disease in man are the result of chronic and inappropriate pinealhypothalamic-adipocyte interactions biologically related to seasonal change.Keywords Adipocyte . Cardiovascular disease . Circadian and circannual rhythm . Clock genes . Hypothalamus . Inflammation . Insulin resistance . Melatonin . Metabolic syndrome . Seasonality . Type 2 diabetes Neel revisitedThe world is currently in the midst of an epidemic of type 2 diabetes, and around 300 million individuals are predicted to develop this disorder by the year 2025 [1]. The close biological relationship between diabetes and cardiovascular disease has focused attention on the common genetic and environmental antecedents of these conditions-the common soil hypothesis [2]-but the pathophysiological basis of these associations remains obscure. In 1962, Neel proposed the thrifty genotype hypothesis, which postulated that insulin overproduction must at one time have had a beneficial effect, in that it would provide 'an important energy conserving mechanism when food intake was irregular and obesity rare' [3]. Although Neel recognised insulin antagonism rather than insulin resistance, he hypothesised that the combination of obesity with increased insulin (or the presence of insulin antagonists) would lead to the development of diabetes. With hindsight, Neel was essentially speculating on the potential metabolic benefits of insulin resistance. The recognition in the last 20 years of an insulin resistance risk cluster [4] indicates that, under certain circumstances, elements of the risk cluster should also be beneficial to the survival of the organism, a response that, by analogy with Neel's original hypothesis, may coincidentally lead to the development of cardiovascular disease in times of plenty. The development of both insulin resistance and inflammation are physiological responses to increasing adiposity that, by definition, should be beneficial to the survival of the organism. The observation that the chronic metabolic milieu associated with type 2 diabetes is harmful raises the possibility that the adipocyte response to fat loading is beneficial when acute and short-lived, as is o...

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Section: Man Diabetes and Cardiovascular Diseasesupporting

confidence: 63%

Section: Man Diabetes and Cardiovascular Diseasementioning

confidence: 55%

Neel revisited: the adipocyte, seasonality and type 2 diabetes

Scott

Grant

2006

Diabetologia

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“…In mice, shifting food availability to the usual rest phase results in desynchrony between the master SCN clock and peripheral clocks, leading to metabolic syndrome (86) . Similarly, chronic exposure to shift work increases risk of metabolic syndrome (87) , as well as CHD, stroke and stroke-related mortality, and type 2 diabetes (88)(89)(90)(91) . Laboratory studies in human subjects have shown that consumption of meals during the biological night results in increased postprandial glucose, insulin and TAG relative to daytime meals (92)(93)(94) .…”

Section: Circadian Misalignment and Metabolic Dysfunctionmentioning

confidence: 99%

Circadian regulation of lipid metabolism

Gooley

2016

Proc. Nutr. Soc.

144

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The circadian system temporally coordinates daily rhythms in feeding behaviour and energy metabolism. The objective of the present paper is to review the mechanisms that underlie circadian regulation of lipid metabolic pathways. Circadian rhythms in behaviour and physiology are generated by master clock neurons in the suprachiasmatic nucleus (SCN). The SCN and its efferent targets in the hypothalamus integrate light and feeding signals to entrain behavioural rhythms as well as clock cells located in peripheral tissues, including the liver, adipose tissue and muscle. Circadian rhythms in gene expression are regulated at the cellular level by a molecular clock comprising a core set of clock genes/proteins. In peripheral tissues, hundreds of genes involved in lipid biosynthesis and fatty acid oxidation are rhythmically activated and repressed by clock proteins, hence providing a direct mechanism for circadian regulation of lipids. Disruption of clock gene function results in abnormal metabolic phenotypes and impaired lipid absorption, demonstrating that the circadian system is essential for normal energy metabolism. The composition and timing of meals influence diurnal regulation of metabolic pathways, with food intake during the usual rest phase associated with dysregulation of lipid metabolism. Recent studies using metabolomics and lipidomics platforms have shown that hundreds of lipid species are circadian-regulated in human plasma, including but not limited to fatty acids, TAG, glycerophospholipids, sterol lipids and sphingolipids. In future work, these lipid profiling approaches can be used to understand better the interaction between diet, mealtimes and circadian rhythms on lipid metabolism and risk for obesity and metabolic diseases.

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“…Non-traditional working hours has been linked to several metabolic and immune related disorders, including obesity [42], diabetes [43,44] stroke [44], atherosclerosis [45] and coronary heart disease [46]. Various cancers have been linked to disrupted circadian cycles, such as lymphatic [47], prostate [48,49] and breast cancer [50].…”

Section: Circadian Disruption and Diseasementioning

confidence: 99%