In this modern age people tend to grow increasingly fat with advancing age. Near any given individual can choose not to do so, but considered in aggregate the masses tend to follow the available incentives more often than not: cheap food; cheap ways to get around without walking; lots of interesting activities that don't require you to move from your chair; and so forth. For your typical fellow in a developed country advancing age means more wealth, more calories, and less exercise, and this has the inevitable effect on waistline, metabolism, long-term health, and life expectancy. With more fat and more years spent fat, the costs pile up: more money spent on medical services, more disability, frailty, and age-related disease, and more years cut from your life expectancy.

So don't get fat, don't stay fat. The weight of evidence tells us that being fat isn't good for you - and for everyone in a developed region, excepting a tiny handful of people with profound genetic disorders, whether or not you are in fact fat is absolutely a choice.

Given the ready way in which we can alter the amount of fat in our bodies through diligence - or lack of same - and the way in which lifestyle choices change with age for most people, there is no desperate need for other explanations as to why people gather more fat with advancing years. Nonetheless, I'll point out a recent open access paper (the full text is PDF only): if I'm reading it right, the researchers here argue that one of the unfortunate low-level biochemical effects of the presence of advanced glycation endproducts (AGEs) in our tissues is that it encourages the growth of fat tissue, or adipose tissue to give it the more formal name - to be fat is to have adiposity, and growth of fat tissue is adipogenesis.

Since AGE levels rise with age, even if an individual doesn't increase their ingested levels of AGEs, this mechanism for AGEs to spur fat tissue growth leaves the door open for some interesting speculation. The researchers don't put any useful numbers to the putative effect, however, and thus I'm inclined to think it small in comparison to, say, how much a person eats or exercises:

An advanced glycation end products (AGEs)-the receptor for AGEs axis restores adipogenic potential of senescent preadipocytes through modulation of p53 function

Impaired adipogenic potential of senescent preadipocytes is a hallmark of adipose aging and aging-related adipose dysfunction. ... We show a novel pro-adipogenic function of AGEs in replicative senescent preadipocytes.

While our study is largely based on in vitro and ex vivo studies, we would predict that a chronic dietary intake of AGEs would positively contribute to adipose development during aging. ... To our knowledge, our study is the first report that AGEs are able to restore senescence-impaired adipogenic potential of aged preadipocytes. These findings implicate that AGEs-induced adipogenesis in senescent preadipocytes is likely to contribute to exacerbating aging-related adiposity.

If you look back in the Fight Aging! archives, you'll find much more information on AGEs and their role in degenerative aging - the established discussion of past years, rather than the new thoughts on fat tissue quoted above. The characteristic buildup of AGEs and similar compounds that occurs with age harms the integrity of tissue and biological systems in a number of ways:

• SENS5 Video: Talking About AGEs and Aging
• AGE Breakers Beyond Alagebrium
• A Raft of Papers on AGEs, ALEs, RAGE
• Commenting on the Utility of AGE-Breakers

Advanced glycation endproducts (AGEs) are a class of undesirable metabolic byproduct. The level of AGEs in the body rises with age and causes harm through a variety of mechanisms, such as by excessively triggering certain cellular receptors or gluing together pieces of protein machinery by forming crosslinks, thus preventing them from carrying out their proper function.

In past years a number of efforts were undertaken to develop drugs that can safely break down at least some forms of AGE. Early promising candidates in laboratory animals failed in humans because the most harmful forms of AGE are different for short-lived versus long-lived mammals - so what benefits a rat isn't of much utility for we humans. So far little progress has been made towards a therapy for the dominant type of AGE in humans, glucosepane, sad to say, as there is comparatively little interest in this field of research.

Source:
http://www.fightaging.org/archives/2012/11/arguing-that-ages-contribute-to-increased-fat-tissue-with-age.php