Don’t think YOU have it? Think again. Most people who have chronic inflammation
don’t know it. There is a full spectrum of problems caused by chronic inflammation –
from fatigue, hormone imbalance and reduced immunity, to osteoporosis, Alzheimer’s heart disease and cancer.
Inflammation is typically thought of as a swelling, painful or otherwise uncomfortable situation – perhaps in your joints, sinus or intestine. But for most people, inflammation occurs without any symptoms. Inflammation is defined classically as a protective reaction by the body, in response to some physical or chemical injury. Acute inflammation is typically accompanied by pain, swelling, redness, and heat. A closer look at the area of inflammation reveals that the small blood vessels are dilated, which brings in more blood and warmth, and other fluid, which causes swelling of the area.
Anyway, here is another paper that points to overeating as a source of inflammation which then promotes obesity. The idea is that obesity is in some ways a by-product of inflammation.
While chronic inflammation is generally considered a consequence of obesity, the new results suggest the inflammatory reaction might also be a cause of the imbalance that leads to obesity and associated diseases, including diabetes. As Cai says, it appears that inflammation and obesity are "quite intertwined." An abundance of calories itself promotes inflammation, while obesity also feeds back to the neurons to further promote inflammation in a kind of vicious cycle.from this release
This idea that too much food promotes inflammation is of course one of the reasons that intermittent fasting can be a good idea. IF can limit inflammation as pointed out here. If you are interested in IF I would recommend Eat Stop Eat as a great introduction.
Of course a low carb diet might also be antiinflammatory.
There is further discussion of the paper at NHS Choices
While the researchers are optimistic that their “results suggest a novel therapeutic strategy for combating the ever-increasing spread of obesity and associated diseases”, it will be some time before we see the application of these findings in humans. It will be difficult, for example, to develop anti-inflammatory drugs that specifically target the brain. The study was also conducted in mice in a disease model that was similar to obesity. But there are likely to be huge metabolic differences between mice and humans, so it is not clear whether the exact same reactions happen in response to over-nutrition in the human brain. Human research, which is the only way to establish this, is still a long way off.
Anyway, here is the abstract
Hypothalamic IKKβ/NF-κB and ER Stress Link Overnutrition to Energy Imbalance and Obesity
Overnutrition is associated with chronic inflammation in metabolic tissues. Whether metabolic inflammation compromises the neural regulatory systems and therefore promotes overnutrition-associated diseases remains unexplored. Here we show that a mediator of metabolic inflammation, IKKβ/NF-κB, normally remains inactive although enriched in hypothalamic neurons. Overnutrition atypically activates hypothalamic IKKβ/NF-κB at least in part through elevated endoplasmic reticulum stress in the hypothalamus. While forced activation of hypothalamic IKKβ/NF-κB interrupts central insulin/leptin signaling and actions, site- or cell-specific suppression of IKKβ either broadly across the brain or locally within the mediobasal hypothalamus, or specifically in hypothalamic AGRP neurons significantly protects against obesity and glucose intolerance. The molecular mechanisms involved include regulation by IKKβ/NF-κB of SOCS3, a core inhibitor of insulin and leptin signaling. Our results show that the hypothalamic IKKβ/NF-κB program is a general neural mechanism for energy imbalance underlying obesity and suggest that suppressing hypothalamic IKKβ/NF-κB may represent a strategy to combat obesity and related diseases.