> “A fat cell is almost like a primitive immune cell,” says Hotamisligil. “It can request the assistance of immune cells when in trouble, but if the stress continues, and the immune cells remain, they start changing their character and behavior from helpful to harmful.”
...
> When overloaded with stored lipid, fat cells begin to lose their functional and structural integrity and may start spilling their toxic cargo. When cells fail like this, the immune system kicks in, initially to assist in clean-up. Macrophages engorge themselves on the leaking fuel, and may die themselves during this process. But in the long run, what is meant to be a mutually beneficial interaction between the metabolic and immune systems turns into a very dangerous and harmful relationship. Obese individuals thus live in a state of chronic stress and inflammation; in fact, many people do, because their energy intake vastly exceeds their needs. Hotamisligil calls this chronic energy overload, and the resulting abnormal immune response, metaflammation: metabolic inflammation.
This article brings together a whole host of different areas of research about human inflammation. I would recommend reading it, but it isn't an article you can skim and there's no big bang conclusions, just more areas of keen research and exploration.
> Critics might suggest that inflammation is just a symptom in these diseases, rather than a cause. But Hotamisligil says, unequivocally, “Chronic inflammation is uniformly damaging and is absolutely causal to the process, because if you interfere with it, you can reverse the pathology.” And this ability to control such diseases simply by reversing inflammation is a biological response, dating far back to the time of a common ancestor, that has been retained across diverse species of animals to the present day, he says, pointing to experimental evidence: “If you can make Drosophila [fruit fly] diabetic, and then block the inflammatory response systems, you can cure diabetes in Drosophila, the same way you can reverse it in the mouse, in primates, and in humans, provided that you do it with the right tools. Of course, the higher the organism, the more complex these pathways are, so it takes more effort to define the precise mechanisms to manipulate.”
For type 2, more, longer and more frequent fasting. Stopping most carbs and all refined sugar. Reducing calories (through fasting or general reduction) so that weight can normalize. Hormones are overriding in this, and elevated blood glucose generally also means elevated insulin which will reduce the effectiveness of any approach to weight loss.
Extended fasting is the most assured way to help normalize glucose. Some, and expecialy over time (I'm one of these) show elevated gluconeogenesis response and will take longer to normalize under a fasting focused or very low carb (aka keto diet). Once glucose is normalized (without supplemental insulin) the weight is easier to manage/normalize as well.
It's not easy, and the longer you are diabetic (type 2) the harder it is. Supplemental insulin works against you in a lot of ways. Time restricted eating, generally, and more specifically very low carb (not overdoing protein) are good approaches.
There's a lot of supporting articles and reference linked data on dietdoctor.com and elsewhere. First, and foremost, stop all refined sugars. Second, avoid refined carbs. Third, reduce refined seed oils. Eat clean and get some fatty fish 3-4x a week. And imho clean can mean red meat from naturally fed sources, likewise eggs and fish.
Im pretty sure this is for type 2 diabetes. To reverse, you have to loose significant weight which is at least -20%, sleep well, exercise regularly, and eliminate stress
> you have to loose significant weight which is at least -20%
I think that's an oversimplification. Roughly a third of people with T2D have a normal BMI, and most obese people don't have T2D. I mean, sure, lose the weight if you can afford it, but that's attacking an exacerbating factor rather than the root causes (which are not really understood yet).
Huh? Losing weight requires less resources (money) than maintaining it, you just simply stop eating and fast. Proper nutrition and hormone regulation to maintain your lower body weight is a different question, but even that should be cheaper or the same amount of money given that you're reducing your overall caloric intake, even though the food you purchase may be slightly more expensive.
Also, the root causes are fairly well understood at this point. Yes, genetics play a role (sometimes a large on), but if an individual eats a balanced mostly plant based diet, exercises, and gets enough sleep (minimum 8 hours), then the likelihood of getting T2D reduces significantly. If someone has T2D, they are almost assuredly lacking in one of those three areas.
Parent wrote “Roughly a third of people with T2D have a normal BMI.” Those people can’t “afford” to lose weight not in the dollar sense, but because they have no weight to lose.
I slipped and wrote "higher eukaryotes" in relation to yeast and this is my post-doc's comments:
"that broke my heart :(
other eukaryotes? multicellular eukaryotes? animals? Whatever you like, but please, no "higher", the poor yeast have been evolving for a long time and are much better than us at fermenting beers..."
Book recommendation - "Toxic Fat" by Barry Sears (disclosure - the father of a friend of mine). Its thesis is in line with much of the research in this article.
> “A fat cell is almost like a primitive immune cell,” says Hotamisligil. “It can request the assistance of immune cells when in trouble, but if the stress continues, and the immune cells remain, they start changing their character and behavior from helpful to harmful.”
...
> When overloaded with stored lipid, fat cells begin to lose their functional and structural integrity and may start spilling their toxic cargo. When cells fail like this, the immune system kicks in, initially to assist in clean-up. Macrophages engorge themselves on the leaking fuel, and may die themselves during this process. But in the long run, what is meant to be a mutually beneficial interaction between the metabolic and immune systems turns into a very dangerous and harmful relationship. Obese individuals thus live in a state of chronic stress and inflammation; in fact, many people do, because their energy intake vastly exceeds their needs. Hotamisligil calls this chronic energy overload, and the resulting abnormal immune response, metaflammation: metabolic inflammation.
This article brings together a whole host of different areas of research about human inflammation. I would recommend reading it, but it isn't an article you can skim and there's no big bang conclusions, just more areas of keen research and exploration.