Being obese or overweight is, for the overwhelming majority of such individuals, a choice. There is plenty of ink spilled over how hard or easy the choice of body weight is to make, but it is nonetheless a choice. Want to weigh less? Then persist in eating fewer calories in the context of a sanely balanced diet. It really is as simple as that. The only way to fail is to fail to eat fewer calories. That this is eternally a challenge, and that obesity is increasingly prevalent in an environment of cheap calories, tells us more about human nature than it does about our biology.
The present consensus on the effects of excess visceral fat tissue is that it increases incidence of near all age-related disease, shortens life expectancy, and raises overall lifetime medical expenditure. Raised levels of chronic inflammation produced by fat tissue are an important mediating mechanism in this outcome, regardless of whether they are produced by greater numbers of senescent cells in fat, immune cells infiltrating fat tissue, inappropriate interactions with cell debris, inflammatory signaling from adipose cells, or other fat-associated mechanisms.
This is a graded effect. Even more modest levels of excess fat tissue, additional weight that in this age of obesity wouldn't merit a second glance when seen on the street, produce significant increases in the risk of age-related disease and later life mortality. The more fat tissue, and the longer that fat tissue is retained, the worse the prognosis. Fat accelerates the damage and dysfunction of aging. On this topic, the publicity materials here note a couple of recent papers that reinforce the message: early life obesity leads to a shorter life expectancy, and fat tissue greatly increases chronic inflammation, exacerbating the serious downstream consequences that inflammation causes.
Young adults classified as obese in Australia can expect to lose up to 10 years in life expectancy, according to a new study. The model used by the researchers calculates the expected amount of weight that adults put on every year depending on their age, sex, and current weight. It also takes into account current life expectancy in Australia and higher mortality of people with excess weight. The model predicted remaining life expectancy for people in their 20s, 30s, 40, 50s and 60s in healthy, overweight, obese and severely obese weight categories. It also calculated the number of years lost over the lifetime for people with excess weight in each age group, compared to those with a healthy weight.
On average, healthy weight men and women in their 20s can expect to live another 57 and 60 years, respectively. But, if they are already in an obese weight category in early adulthood, women will lose 6 of these years and men will lose 8. If they are in a severely obese weight category, women will lose 8 years and men will lose 10. The risks of early death associated with excess weight were apparent at every age group but decreased with age. Obese women in their 40s will experience a reduction of 4.1 years, whilst obese men stand to lose 5.1 years. For individuals in their 60s, this reduction in life expectancy is estimated at 2.3 years for women and 2.7 years for men.
Studies in mice have demonstrated that obesity-induced inflammation contributes to the risk of colorectal cancer, but evidence in humans has been scarce. A new study shows that two inflammatory proteins in the colon increase in parallel with increasing weight in humans. An incremental rise in these pro-inflammatory proteins (called cytokines) was observed along the entire spectrum of subjects' weights, which extended from lean to obese individuals. In participants with obesity, there was evidence that two pre-cancerous cellular pathways known to be triggered by these cytokines were also activated.
Sixteen research participants were lean, with a BMI between 18.1 and 24.9, while 26 participants with obesity had a BMI ranging from 30.0 to 45.7. The participants were between the ages of 45 and 70 years of age and were undergoing routine screening colonoscopies. Using blood samples and colonic biopsies, the researchers determined that the concentrations of two major cytokines rose in parallel with BMI. Cytokines are proteins that mediate and regulate immunity and inflammation, among other things. In addition to evidence that they can promote cancer risk in certain tissues, pro-inflammatory cytokines have been identified as actors in insulin resistance and diabetes, as well as inflammatory disorders such as arthritis.
In an effort to identify potential confounding factors, the research team determined that thirteen of the 42 study participants were also regular users of NSAIDs, such as aspirin and ibuprofen. The research team discovered that participants who took NSAIDs at least once per week, compared to those who did not, had lower levels of pro-inflammatory proteins in the colon. This pattern was consistent across the two BMI groups.