Secondhand Smoke Exposure May Cause Weight Gain
One of the countless explanations smokers give for not quitting smoking is that they dread they might put on extra weight, as smoking plays its part in keeping them slim. However, the latest investigations confront their conviction by proposing that being exposed to cigarette smoke, in reality, causes weight gain and that secondhand smoke augments this effect for non-smokers.
The new study reveals that cigarette smoke exposure triggers weight gain by activating a mechanism that weakens the cells’ response to insulin. The research team at Brigham Young University (BYU) in Provo, UT, discloses their observations in the American Journal of Physiology: Endocrinology and Metabolism. By now, it is an established fact that smoking is seriously injurious to health, even for non-smokers who are subjected to secondhand smoke exposure—and even third-hand exposure.
The research also suggests that approximately 20 percent of young children living with smoking parents or relatives endure secondhand smoke exposure. Benjamin Bikman, the study author from BYU, believes that people sharing a home with a smoking individual, especially children, are more at risk to be affected, leading to cardiovascular or metabolic problems. Moreover, roughly 4,000 young American adults smoke their first cigarette each day, 1,000 of whom eventually turn out to be regular smokers.
Prof. Bikman and Paul Reynolds, his BYU colleague, were curious to know how cigarette smoke impacts the metabolic function. For discovering the mechanism responsible for smokers becoming insulin resistant, they performed an animal study in which two mice were exposed to secondhand smoke. Researchers analyzed their metabolic profiles throughout the process.
The researchers observed that the mice exposed to smoke gained weight, and when they scrutinized the process on a cellular level, they found out the smoke had triggered a lipid known as ceramide to alter the mitochondria in the cells, upsetting normal cell function and harming the cells’ reaction to insulin. This made the team deduce the key to reversing cigarette smoke’s effects is to restrain ceramide.
As soon as someone becomes resistant to insulin, the body requires more insulin. As insulin goes up, fat is produced in the body. After the mice were treated with myriocin, which acts as a ceramide blocker, the researchers discovered they did not put on weight or display metabolic disruptions, whether or not there was any smoke exposure.
Fascinatingly, when a diet rich in sugar was given to the mice exposed to smoke, myriocin could not play any role in fixing the metabolic disturbance. At present, the team is seeking a ceramide inhibitor secure for human use. It would be a positive step to be able to provide some therapy for bystanders to protect them for secondhand smoke exposure.