The lipid paradox may also extend to the location of excess body fat. Fat cells are not created equally. Researchers are beginning to embrace the concept of good fat and bad fat. Although the release of inflammatory molecules from visceral fat is considered to be a key factor in the development of the metabolic syndrome, these adverse effects are either not observed or are much less pronounced in adults with only excess subcutaneous fat.11 When it comes to inflicting havoc on our health, what seems to matter most is whether fat cells are taking up residence in visceral organs, such as the liver, or merely depositing themselves under the skin. For example, the relatively rapid metabolic improvement noted following bariatric surgery likely reflects the post-operative loss of visceral fat, because in most cases, it occurs prior to any significant loss of subcutaneous fat and body weight.
A Final Paradox
From an evolutionary standpoint, is there any advantage for a host to be afflicted with the metabolic syndrome? Perhaps.
In one study, a high-fat diet induced the metabolic syndrome, but also protected the CD-1 mouse strain from the lethality associated with Trypanosoma cruzi infection, dramatically decreasing mortality by 65%.12 It is conceivable that at an earlier point in evolution, the metabolic syndrome conferred a substantial benefit to our survival as a species, as our early ancestors warded off a raft of infectious challenges. Over time, this benefit has been far overshadowed by the syndrome’s downsides.
But all may not be lost. There may be one more lipid paradox to consider. Despite meeting clinical criteria for type 2 diabetes and metabolic syndrome, hibernating animals demonstrate no pathologic consequences of their brief bout with obesity. After shedding their extra fat during the winter fast, animals are able to immediately enter into the reproductive cycle. Nor are the ill effects of circumannual obesity transient; in one Swedish study, atherosclerotic lesions were entirely absent from the major vessels of obese, insulin-resistant hibernators despite marked hyperlipidemia.13 Similarly, obese hibernators fail to develop the smoldering inflammation that characterizes human obesity, despite similar metabolic parameters. The absence of pathology despite remarkably similar metabolic states suggests that transient obesity and insulin resistance are not necessarily pathologic and may, in fact, be part of an adaptive, evolutionarily conserved response to excess nutrient storage.
That may be the solution! Consider the option of hibernating this fall. With the anticipated pandemonium of the upcoming U.S. general election, imagine if we could hibernate just like our ursine cousins. Pack in those calories, party like it’s 1999, and then take a nap. A very long nap. Yes, you can have your cake and eat it, too.
