Consider that this article is from 2011. So much more has been discovered since then.
Some sections from this article that were of particular interest to me:
" Although it is the obesogenic environment that has resulted in this major healthcare problem, it is acting by revealing a sub-population with a pre-existing genetic predisposition to excess adiposity. There is substantial evidence for the heritability of obesity, and research in both rare and common forms of obesity has identified genes with significant roles in its aetiology."
"obesity and its causes are still elusive.
In the 1960s, Neel (11) proposed the ‘thrifty gene’ hypothesis, whereby genes that predispose to obesity would have had a selective advantage in populations that frequently experienced starvation. People who possess these genes in today's obesogenic environment might be those that ‘overreact’— not just becoming slightly overweight, but extremely obese. Recent support for the thrifty gene hypothesis was provided by Pritchard and co-workers (13), who found that many genes involved in the glucose and lipid metabolism have been subject to positive selection in the last 10 000 years."
" research into monogenic or syndromic obesity resulted in the identification of many genes involved in the regulation of appetite via the leptin–melanocortin pathway"
"The Human Obesity Gene Map summarizes the present situation in the field of common polygenic obesity (31). There are currently 253 quantitative-trait loci (QTLs) identified in 61 genome-wide scans, and 52 genomic regions contain QTLs supported by two or more studies. As in any complex genetic disease, there are many unconfirmed genetic associations. There are currently 22 gene associations supported by at least five positive studies (summarized in Table 1). These genes include members of the leptin–melanocortin pathway, proinflammatory cytokines and uncoupling proteins."
It is also becoming clear, in both rare and common forms of obesity, that epigenetic influences, defined as any heritable influence on genes that occurs without a change in the DNA sequence, are also important. There is also an initial report of genomic imprinting, playing a role in common obesity at three different genomic loci, it would be highly surprising if epigenetics was not a significant contributor to the complexity of the genetics of common obesity."
" Altogether, these data suggest that obesity can be metabolically ‘neutral’ if there is an effectively unlimited availability of small insulin-sensitive subcutaneous adipocytes for fat storage. This appears to protect against the progressive development of fat-related chronic inflammatory disease. This protective pattern is, at least in part, genetically driven. In contrast, it has also been shown that in the context of obesity, carrying gene variants that worsen obesity-associated insulin resistance dramatically increases risk for diabesity and also for CHD "
OBESITY, HEALTH AND GENETICS
The controversy about the consequences of obesity on health was recently fuelled by two papers: a follow-up study of former obese subjects ‘cured’ by bariatric surgery found no beneficial effect on mortality (87), suggesting that losing weight, even for very obese people, does not always improve health. Furthermore, a large Scandinavian epidemiological study showed that overweight subjects with no associated co-morbidities (i.e. with no metabolic syndrome) who intended to lose weight, and succeeded in doing so, died earlier than those who maintained or increased their weight (88).
Thus, it seems that obesity is more phenotypically and genetically heterogeneous and more complex than previously thought. Genetics (and probably epigenetics) plays an important role in the energetic imbalance leading to fat accumulation, but being obese does not necessarily mean being ill and, indeed, it is likely that very good health is required to establish and to maintain extreme obesity. As demonstrated by the data on adiponectin, genetics also determines, at least in part, the extent to which the inflation of fat depots predisposes to dysmetabolism, eventually dramatically increasing morbidity and mortality risk. Unravelling the genetic background associated with every stage of obesity and its consequences for health is of paramount importance, as it may help to suggest less emotive and more efficient ways to manage the obesity phenomenon."