Turn off everything else, just for a couple of minutes if you can. An ideal time is after exercise, spend those few moments to center your self. It takes practice and isn’t all that easy. Your mind quickly is thinking through the next task or issue.
Don’t listen to the brain, listen to the breath.
Are you raising a family? If so you want them to grow strong and healthy. When you consider their growth, think of their blood vessels. I know that seems kind of out of the ordinary, but if we can work to keep not only ourselves healthy and consider those who we share our lives with. Their health is important! Encourage your family to adopt healthy lifestyles and prevent disease.
Fact: Every pound of fat gained causes your body to make 7 new miles of blood vessels.
Knowing this, it’s easy to see why obesity and heart disease often go together. Most of the new blood vessels are tiny capillaries, but also include small veins and arteries. This means if you are “only” 10 pounds overweight your heart has to pump blood through an extra 70 miles of blood vessels.The good news is that this also works in reverse. If you lose a pound of fat, your body will break down and reabsorb the no longer needed blood vessels. This is encouraging to dieters, as one pound does not seem like a lot to lose, but even that little bit of difference will result in a large benefit for your heart!
But nature and nurture rarely operate independently and this week it was published a large study that further contributes to our understanding of how the complex interplay between genes and lifestyle affect the risk of obesity. Over 12,000 American women and men participated in the study which is published in reputable Circulation. In these researchers identified the 32 so-called “obesity genes”, ie genetic variants that are known to predispose to obesity, and the calculated using these overall genetic risk profile for each participant. This was relatively normal genes that most of us carry to a greater or lesser extent, not rare mutations observed in some cases of morbid obesity. Participants were followed up for two years and as expected the weight proportional to how they were genetically predisposed.
When researchers went deeper in the material and examined the effects of physical activity and inactive time on obesity risk was discovered however, the interaction between genes and the activity level was significant. Silent Sitting, measured as the number of hours participants reported watching TV every day compounded effect of genetic predisposition to obesity significantly. The influence of genes alone were 50% higher for those who put four or more hours watching TV daily. The good news, however, was that a relatively moderate level of physical activity significantly reduced the effect of obesity genes.
The researchers estimated that the difference in weight gain between those who were lucky with maximum genes (no genetic predisposition to obesity) and those who were unfortunate maximum (had all known genetic dispositions) was halved for each hour daily walk, or every half hour of jogging. On the other hand, the difference of 25% for every two hours participants spent on the couch.
Thus, it is particularly important, how unfair it may seem, to reduce sedentary activities and increase physical activity for those that are inherited predisposition to obesity. Just how physical activity overcomes the effect of obesity genes is not known in detail, but there are indications that regular physical activity triggers changes in gene expression so that health becomes more active while suppressing those that are related to weight gain. It is also worth noting that the importance of sedentary TV time and physical activity were independent of each other, that was both influential factors.
Thus, we can not change our genes, but it appears that we can greatly influence the impact they have on us. Therefore, the best advice is still, whatever genetic basis, following the authorities’ recommendations for diet and physical activity and reduce time spent watching television.
Written by Bjarne Nes, Fellow CERG.