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Op donderdag 29 maart 2007 16:21 schreef Marloes het volgende:Even een vraagje, misschien dat één van jullie het weet!!
Je hoort vaak van mensen dat ze aankomen als ze gestopt zijn met roken. Maar ligt dat er dan aan omdat ze ipv roken meer gaan eten, of omdat je stofwisseling sneller wordt als je rookt??
Want ik rook de laatste tijd meer, en val ook wat sneller af. Ik hoop niet dat als ik weer ga minderen, ik dan weer aankom
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(ook al blijf ik gezond eten)
Over stoppen met roken en aankomen kwam ik wel een paar interessante samenvattingen op pubmed tegen:
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Int J Obes Relat Metab Disord. 2001 Sep;25(9):1322-6.
Weight gain and adipose tissue metabolism after smoking cessation in women.
Ferrara CM, Kumar M, Nicklas B, McCrone S, Goldberg AP.
Department of Medicine, Division of Gerontology, University of Maryland, Baltimore School of Medicine, USA. cindy@grecc.umaryland.edu
BACKGROUND: Cigarette smoking increases the risk of cardiovascular disease, and is an important preventable cause of death and illness. One major deterrent to smoking cessation is a gain in body weight. Understanding the mechanisms that contribute to this weight gain may maximize the success of long-term smoking cessation. We hypothesized that smoking cessation is associated with an increase in adipose tissue lipoprotein lipase (AT-LPL) activity and/or a decrease in lipolysis, two metabolic factors that determine the balance between fat storage and fat utilization, and thus affect the propensity for weight gain.
MATERIALS AND METHODS: Ten premenopausal women (37.1+/-6.2 y, 31.7+/-6.4 kg/m(2) body mass index (BMI), mean+/-s.d.) participated in a 4 week smoking cessation program. Measurements of body weight, waist and hip circumferences, adipose cell metabolism and resting metabolic rate were obtained at baseline and after 4 weeks of smoking cessation.
RESULTS: Of the 10 women who began the intervention, five successfully completed the smoking cessation intervention. After 4 weeks of smoking cessation, there were significant increases in body weight (95.1+/-13.9-97.7+/-14.4 kg, P<0.05), with no change in waist and hip circumferences or resting energy expenditure. Gluteal AT-LPL activity significantly increased in all women by 2.8-fold (1.65+/-1.30-4.72+/-3.34 nmol/g/min, P<0.05). Abdominal AT-LPL activity increased in four out of the five women, but did not reach statistical significance (1.14+/-0.88-3.50+/-3.76 nmol/g/min, P=0.14). The increase in body weight correlated with the increase in gluteal AT-LPL activity (r=0.89, P<0.05), as well as the baseline activity of gluteal AT-LPL (r=0.86, P=0.06). There were no changes in basal or stimulated lipolysis in the gluteal or abdominal fat depots.
CONCLUSIONS: These results suggest that smoking cessation is associated with significant increases in body weight, as well as changes in adipose cell metabolism, in particular increases in AT-LPL activity. This increase in LPL activity may contribute to the increase in body weight associated with smoking cessation.
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: Obes Rev. 2004 May;5(2):95-103. Links
Smoking cessation and weight gain.
Filozof C, Fernandez Pinilla MC, Fernandez-Cruz A.
Unidad de Tabaquismo, Area de Prevencion y Rehabilitacion Cardiaca, Instituto Cardiovascular, Hospital Clinico San Carlos, Universidad Complutense, Madrid, Spain. clfilozof@yahoo.es
Cigarette smoking is the single most important preventable cause of death and illness. Smoking cessation is associated with substantial health benefits. Weight gain is cited as a primary reason for not trying to quit smoking. There is a great variability in the amount of weight gain but younger ages, lower socio-economic status and heavier smoking are predictors of higher weight gain. Weight change after smoking cessation appears to be influenced by underlying genetic factors. Besides, weight gain after smoking cessation is largely because of increased body fat and some studies suggest that it mostly occurs in the subcutaneous region of the body. The mechanism of weight gain includes increased energy intake, decreased resting metabolic rate, decreased physical activity and increased lipoprotein lipase activity. Although there is convincing evidence for the association between smoking cessation and weight gain, the molecular mechanisms underlying this relationship are not well understood. This review summarizes current information of the effects of nicotine on peptides involved in feeding behaviour. Smoking was shown to impair glucose tolerance and insulin sensitivity and cross-sectional studies have demonstrated that smokers are insulin-resistant and hyperinsulinaemic, as compared with non-smokers. Smoking cessation seems to improve insulin sensitivity in spite of the weight gain. Nicotine replacement - in particular nicotine gum - appears to be effective in delaying post-cessation weight gain. In a group of women who failed to quit smoking because of weight gain, a dietary intervention (intermittent very-low-calorie diet) plus nicotine gum showed to both increase success rate in terms of smoking cessation and prevent weight gain. On the other hand, body weight gain at the end of treatment was significantly lower in the patients receiving bupropion or bupropion plus nicotine patch, compared with placebo. Studies with new drugs available for the treatment of obesity - sibutramine and orlistat - are warranted.
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J Appl Physiol. 1992 Feb;72(2):401-9.
Metabolic effects of cigarette smoking.
Perkins KA.
Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, Pennsylvania 15213.
The inverse relationship between cigarette smoking and body weight, a potent obstacle to stopping smoking, may be due in part to effects of smoking on increasing whole body metabolism. Studies examining chronic and acute metabolic effects of smoking, as well as its constituent nicotine, are reviewed. Evidence suggests the absence of a chronic effect; most studies indicate that smokers and nonsmokers have similar resting metabolic rates (RMR) and that RMR declines very little after smoking cessation. Although an acute effect due to smoking is apparent, its magnitude is inconsistent across studies, possibly because of variability in smoke exposure or nicotine intake. In smokers at rest, the acute effect of smoking (and nicotine intake) appears to be significant but small (less than 10% of RMR) and transient (less than or equal to 30 min). However, the specific situations in which smokers tend to smoke may mediate the magnitude of this effect, inasmuch as smoking during casual physical activity may enhance it while smoking after eating may reduce it. Sympathoadrenal activation by nicotine appears to be primarily responsible for the metabolic effect of smoking, but possible contributions from nonnicotine constituents of tobacco smoke and behavioral effects of inhaling may also be important. Improved understanding of these metabolic effects may lead to better prediction and control of weight gain after smoking cessation, thus increasing the likelihood of maintaining abstinence.
Hier haal ik oa uit dat een sigaret het rustmetabolisme met minder dan 10% verhoogt gedurende een korte tijd (een half uur en minder dan een half uur) na het roken, dit is verder nog afhankelijk van het moment van roken. Echt harde getallen kwam ik zo snel niet tegen.
Het was dus niet de 10 van minuten die ik had onthouden, maar de 10 van 10%
"Dear life, When I said "can my day get any worse?" it was a rhetorical question, not a challenge."