As a species we are presently succeeding ourselves into a harmful pit. We've succeeded in the goals of our ancestors (eat, feel good, evade pain, become wealthy) to the point at which we're breaking the evolved metabolic processes intended to deal with a short and brutish life of privation. We became fat and now surround ourselves with more food than we need, in other words - not a condition that our bodies respond well to, and so we suffer for it. The collection of symptoms suffered as a consequence of being fat, not exercising enough, and eating a lot is termed "metabolic syndrome." It's a step along the way to more serious failures of your organs and bodily systems, such as diabetes, that result from the damage being done by fat through the years.
Unfortunately, while we've succeeded enough to get into this hole, we've not yet succeeded enough to be able to dig our way out through medical science. Until that happens, indulgence will continue to have adverse consequences on your health and your longevity - lost years, lost money, sickness, and pain.
Here's an open access view of the processes that lead to the body's accelerated decay due to excess food, visceral fat, and the soft life of no exercise:
The nutritional milieu which modern humans have created for themselves is leading to rampant levels of obesity, type II diabetes (T2D) and insulin resistance. This is resulting in a reduction in life expectancy. The condition that precedes T2D, the ‘metabolic syndrome’, is currently defined as central obesity plus two factors: raised triglycerides (TGs), reduced HDL, hypertension and evidence of pathological insulin resistance
The metabolic syndrome is a continuum and may sit at the opposite end of the oxidative stress spectrum to the long-lived phenotype induced by calorie restriction. A common feature of these two phenotypes is the involvement of the insulin/insulin-like growth factor axis.
We believe that it is now possible to provide a basic hypothesis to explain insulin resistance and the metabolic syndrome by studying redox signalling. In short, insulin resistance is determined by the ability to resist oxidative stress (‘redox-thriftiness’), which is itself modulated by mitochondrial hormesis (‘preconditioning’) and thus, hormetic stimuli like physical activity and fasting. The development of the metabolic syndrome could then be defined by a "thrifty-inflammatory tipping point" - the point when insulin resistance goes from being thrifty (e.g. generally restricted to the musculature) to inflammatory (involving more tissues, such as adipose tissue).
We propose that temporal and tissue specific insulin resistance is a friend as long as you live within your hormetic zone, but it may become your enemy in a modern sedentary environment.
Ultimately, the term 'metabolic syndrome' is not truly descriptive of the condition now afflicting a large fraction of mankind. We propose a more appropriate term might be the 'Lifestyle-Induced Metabolic InflexibiliTy and accelerated AGEing’, or, ‘LIMIT-AGE’ syndrome. The ultimate conclusion from this may be that ‘thriftiness’ is only bad for us without hormetic stimuli; a situation that very rarely occurred in prehistoric times - until humans made their environment almost totally risk and hormetic stress free. It is likely that any level of hormesis is better than none: this may be critical in reintroducing ‘postive hormetic stressors’ into a modern lifestyle.