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Research papers: M S Mähönen, P McElduff, A J Dobson, K A Kuulasmaa, and A E Evans Current smoking and the risk of non-fatal myocardial infarction in the WHO MONICA Project populations Tob Control 2004; 13: 244-250 [Abstract] [Full text] [PDF]

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Might smoking compromise the capacity for metabolic compensation in acute reductive stress?

Richard G Fiddian-Green   (28 August 2004)

Might smoking compromise the capacity for metabolic compensation in acute reductive stress? 28 August 2004
Richard G Fiddian-Green, FRCS, FACS None Send letter to journal: Re: Might smoking compromise the capacity for metabolic compensation in acute reductive stress? richardfg{at}hotmail.com Richard G Fiddian-Green	If blood lipid profile improves and weight increases with smoking cessation (1) smoking might be causally related to both the development of an abnormal blood lipid profile and the avoidance of weight gain or even weight loss. How then might smoking have increased the risk of non-fatal myocardial infarction in this study (2)? By reducing the capacity to respond to reductive stress with a further increase in the degree of blood lipid shift (3)? The answer may lie in the next step in respoding to a progressive increase in the degree of reductive stress. If this is reverting to glucose as the preferred substrate for anaerobic glycolysis that would mean reversing the increase in nutrient energy density achieved by the antecedent lipid shift. In the case of an acute reductive stress equivalent to 25% of dysoxia that could mean having to increase a cardiac output of 4.7L/min that had been able to meet the tissues needs to as much as 16.2 L/min to achieve the same objective. A cardiac output of that magnitude is far in excess of the cardiovascular capacity of even a healthy fit athlete. There is another possibility. Anaerobic glycolysis might be averted after the capacity for increasing nutrient energy density per unit volume of flowing blood had plateaued by using amino acids for acetyl coenzyme A synthesis in providing the substrate needed for oxidative phosphorylation to proceed at the rate needed to meet the tissues needs for ATP resynthesis at the time(4). But if NH3 is produced in the process the pH could rise inhibitng oxidative phosphorylation and stimulating anaerobic glycolysis and with it the demand of glucose(5). This too could incease the demand for ATP resynthesis far in excess of the cardiovascular capacity to meet the tissues energy needs. Smoking might, therefore, have increased the risk of non-fatal myocardial infarction in this study by limiting the capacity for accommodating an acute reductive stress with a blood lipid shift and increasing the likelihood of acute cardiovascular decompensation. In which case smoking cessation can be expected to eliminate that risk once the blood lipid profile had been restored to normality even though weight was gained. What is more the gain in weight might be a compensatory response that enhanced the capacity to mount a lipid response to acute reductive stress. In other words a blood lipid shift revealed in blood lipid profiles may conceal the real capacity for mounting a fatty acid response to acute reductive stress. If it is the capacity for mounting a fatty acid rsponse rather than a shift in blood lipid profile per se that is the primary determinant in meeting the metabolic demands of an acute reductive stress within cardiovascular capacity then it may be compromised by the administration of statins. Not only might the size of the mobile pool of fatty acids be reduced by statins by the ability to release it in a timely manner in acute reductive stress might be reduced by an accompanying reduction in the capacity for steroid hormone synthesis. In which case the risk of non- fatal acute myocardial infarction might be greatest in smokers taking statins or even confined to them. 1. Botella-Carretero JI, Escobar-Morreale HF, Martin I, Valero AM, Alvarez F, Garcia G, Varela C, Cantarero M. Weight gain and cardiovascular risk factors during smoking cessation with bupropion or nicotine. Horm Metab Res. 2004 Mar;36(3):178-82. 2. M S Mähönen, P McElduff, A J Dobson, K A Kuulasmaa, and A E Evans Current smoking and the risk of non-fatal myocardial infarction in the WHO MONICA Project populations Tob Control 2004; 13: 244-250 3. Successful evolutionary adaptation to environmental stress? Richard G Fiddian-Green Heart Online, 14 Jul 2004 eLetter re: D A Lawlor, G Davey Smith, R Mitchell, and S Ebrahim Temperature at birth, coronary heart disease, and insulin resistance: cross sectional analyses of the British women’s heart and health study Heart 2004; 90: 381-388 4. Might biochemical fermionic complexities be dictated by antecedent bosonic simplicities? Richard G Fiddian-Green (26 August 2004) eLetter re: Rodrigo B. Cavalcanti Does perioperative lipid-lowering therapy reduce in-hospital mortality after major noncardiac surgery? CMAJ 2004; 171: 328 5. pNH3: a relevant pulmonary variable? Richard G Fiddian-Green Chest Online, 11 Aug 2004 eLetter re: pNH3: a relevant pulmonary variable? Richard G Fiddian-Green Chest Online, 11 Aug 2004