Today I'll point out a couple of recent studies covering some of the consequences that result from the long-term damage done by letting yourself become overweight. There are great many such studies, for all the good it seems to do in this era of cheap calories and diminished exercise. When talking about the harms done by excess visceral fat tissue, I'm sure I'm largely preaching to the choir. While I haven't checked, I'm fairly certain that the audience here is well aware of the ways in which we can sabotage our health. Based on the robust evidence from a small mountain of study data, if you want to struggle with illness in later life, spend more on medical services, and die sooner than you would otherwise have done, then the most effective way to engineer that outcome is to take up smoking, stop exercising, and put on weight. Smoking is probably the worst of those, taking everything into account, but when you look at the life expectancy numbers one of the more surprising results is that a sedentary lifestyle and obesity are each about as bad for you as a smoking habit.
How does being fat do enough damage to knock years from your life expectancy? The problems are largely caused by the visceral fat around the organs, rather than by subcutaneous fat deposits. Visceral fat cells are very active, sending all sorts of signals out into the body at large. Some of those trigger the immune system, which leads to raised levels of chronic inflammation. Further, given a high enough sustained intake of calorie and visceral fat deposition, fat cells start dying in large numbers, and this also attracts immune cells and creates inflammation. Recently researchers have noted that DNA fragments from dead fat cells grow in number in the bloodstream with age, again capable of producing inflammation, but also capable of causing abnormal behavior in other cells throughout the body. As you can probably tell, it has been clear for quite some time that inflammation is a primary connection between visceral fat tissue and ill health.
Chronic inflammation will occur in aging no matter how well we take care of our health, at least given the limited capabilities of medical technologies available today, none of which yet meaningfully address the underlying causes of aging. The immune system suffers structural issues after a lifetime of exposure to pathogens, and in addition its cells and sustaining tissues accumulate molecular damage just like all other portions of the body. The result is a weakened immune system that is constantly overactive, inflamed but doing little good in that active state. That is bad enough, but the extra inflammation that comes with excess fat tissue and other outcomes of poor lifestyle choices is a considerable and entirely avoidable additional burden. To be in a state of greater inflammation for years on end is very harmful. Inflammation is demonstrated to raise the risk of suffering all of the common fatal age-related conditions: it speeds progression of the underlying cell and tissue damage that gives rise to those conditions, and then continues to accelerates the pathology of a condition once established, for all the same reasons. This is why the relationships outlined below exist:
A body mass index (BMI) over 30 is considered obese, and the connection between obesity and the risk of heart failure has been established in several studies. Now, researchers have conducted a new meta-analysis that shows that a BMI between 25 and 30 kg/m2, which is considered overweight, is also associated with increased risk. "Overweight individuals had a 35 per cent increased risk of heart failure as compared with normal weight individuals, and our findings indicate that overweight should be considered a clear risk factor for heart failure."
Body mass index (BMI) shows the relationship between weight and height and is used internationally as a measure of body fat. The risk of heart failure rose on average by 41 per cent for an increase of five BMI units, and the increase in risk accelerated the further up on the BMI scale you scored. Obesity increased the risk two to three times compared with normal weight. The researchers found no differences between men and women in the analysis, which included 23 studies with a total of almost 650,000 participants. Four studies looked at the link between BMI and the risk of death from heart failure, and the results suggested a 26 per cent higher risk for an increase of 5 BMI units. Meanwhile, the researchers saw that every ten-centimeter increase in waist circumference was linked to a 29 per cent higher risk of heart failure. These analyses were based on twelve studies with a total of just over 360,000 participants.
Researchers found that abdominal obesity - or having an apple-shaped body - is a strong predictor of serious heart disease in patients who have type 1 or type 2 diabetes, and haven't displayed any symptoms of heart disease. Apple-shaped bodies are already associated with metabolic syndrome (which includes high blood pressure, high sugar levels and high cholesterol), as well as coronary artery disease and heart failure, but this new study found that waist circumference is also a strong predictor of left ventricular dysfunction in patients. Metabolic syndrome is often accompanied by excess body fat around the abdomen. "This study confirms that having an apple-shaped body - or a high waist circumference - can lead to heart disease, and that reducing your waist size can reduce your risks."
The results of the new research expands on the results of a previously published study called FaCTor-64, which showed that the greater a person's body mass index, the greater their risk of heart disease. FaCTor-64 enrolled patients with diabetes who were considered to be at high risk for heart attacks, strokes, or death but had no evidence of heart disease as of yet. Study participants completed randomized screening for coronary artery disease by CT coronary angiography, then received recommendations to change their care or their lifestyles, or continue routine standard diabetes care, based on their results. They were then followed to track future adverse heart events.