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Tags: diabetes, fat, inflammation, obesity, type 2
I believe the inflammation hypothesis is in some ways meant to supersede the insulin hypothesis, however, it’s quite possible that excess insulin is a significant contributor to inflammation, by both inhibiting prostaglandin production, and by activating delta 5 desaturase, which would increase the proportion of inflammation-causing prostaglandins — at least that’s how I understand it.
Of course I read it. I ought to have started my comment with more acknowledgement. Your analysis and insights, as I have come to expect from you, are careful, relevant, and reflect the most recent advances in our knowledge. You did discuss insulin resistance as both a cause and effect of diabesity. I was just mentioning another possible mechanism, that comes from the prolonged presence of insulin itself. It may be a minor point.
I definately think that there is something to the Inflamation and insulin resistance connection. But I wonder if there is even more.
I would love to know how to reverse insulin resistence. I know what most recommendations are….exercise. But if exercise was the key to reversing it then why isn’t it the key to preventing it. What does one do when one reaches a pain threshold that prevents them from exercise? Particularly when it affects every major muscle group and every major joint.
Chris, I see now how my comment looks like I am asserting they work together as if you hadn’t already asserted it, and could even be construed as implying you are proposing inflammation as an alternative mechanism to insulin, which you are obviously not. Sorry for the sloppiness.
Yippee skippy!! Finally seems as if, after searching everywhere on the web, there might, just might be a ray of hope and answers to “questions no one wants to hear” – never mind find a solution to — like: why do my joints hurt? why can’t I eat wheat without getting sick? why do I have little patches of eczema? whence the peripheral neuropathy? and are all these ailments related?” Most are greeted with the equaivalent of <SHRUG>.
Great post. Has some ideas in common with some other blog posts I’ve come across recently on Carb-Sane Asylum and Adipo Insights and maybe a few others that have overturned my previous notions on insulin resistance. The idea that was overturned is that obesity results from insulin resistance of muscle cells. The idea was that muscle cells become insulin resistant which forces blood glucose to be taken up by fat cells and then converted to fat. Now this blog post reinforces the new interpretation that it is only after the fat cells are overfilled and hence insulin-resistant (not accepting any more glucose) that blood sugar can no longer be adequately controlled and diabetes develops. In other words the fat cells protect against diabetes up until they can’t accept enough glucose anymore. What the heck is my point?
Well considering all this, it seems to me that insulin resistance is in large part due to over-consumption of calories. Even of fat calories. Excess fat is taken up by fat cells which can fill them up and lead to the point where they won’t accept any more glucose. So I really believe that overeating is one of the main contributors to insulin resistance and that is regardless of the macro-nutrient composition of the diet and regardless of the quality of the diet. I’m just wondering what you think Chris.
@Taylor - Your theory that IR is due to over consumption of calories doesn’t explain all of the skinny T2 diabetics out there. Like one of my grandmothers. She was always tiny and yet lost her eyesight and legs to a raging case of T2.
Regarding inflammation – mine is sky high and I’m always looking for supplements to help bring it down. I’m taking a baby aspirin every day along with krill oil and turmeric. Anything else that would help?
@Chris - My omega-6 consumption is very low for past couple years, I eat grass-fed beef, take fermented cod liver oil, drink raw milk from pastured cows. Only oils at home are olive & coconut.
I do have some tomato and potato, but I can eliminate them. Also, legumes I eat rarely. Wheat I do have small amounts of daily. I’ll eliminate them, too.
However I have a lot of weight to lose, but could that cause my C-reactive protein to be 20+ instead of 2? Oh, also my fasting insulin is always high and insulin is inflammatory, yes? Recently started on Metformin. Thanks!
Thanks for informative post, Chris. You took quite a big bite with this one. I totally agree with importance of the inflammation in the diabesity. Couple of things I’d like to comment.
You wrote that expanding of the fat cells leads to the inflammation of the adipose tissue. I have to disagree with that. It seems that the size of the fat cells is a driving force for adipose tissue inflammation not the fat mass. PPARg agonists are meds that are used against the malfunction of the fat storage seen in diabesity or metabolic syndrome.
Another thing is that inflammation is something that is made by our own cells. It is highly dependent on the state of our immune cells. The responce to the inflammatory stimuli like LPS can differ markedly in different situations. High omega-6 for example blunts the immune responce and that leads to higher mortality for infections and cancer. Dietary saturated fatty acids have opposite effect on immune system.
I have to ask because I don’t understand what you just wrote. If serum FFA (which are mainly SAFA) increase the macrophage related inflammation through TLR-4 why it is opposite with dietary SAFA? Saturated FFA directly bond and activate TLRs and/or they increase the responce of macrophages to acivation made by LPS.
In either way SAFA seems to increase inflammation.
I ment something like this:
A high fat meal (even dairy fat) can increase inflammation like high BS. Also SOCS-3 is increased and that is related to leptin resistance:
I mentioned this researsch because this kind of research is growing atleast in Europe. We have to know how to deal with it. For example this type single high fat meal worsens the symptoms of asthma. I think these results fit to the picture but I think we have to be more clever than those low fat high fibre proponents. We do have advantage because we know that for example dairy fat is very good in healing or atleast relieving inflammatory diseases like asthma.
I think this all is understandable if we truly understand how innate immunity works and how its responce can be modified towards more tolerant phenotype. If you have no idea what I mean I think there could be much more interesting reading. Problem is that I don’t think that answer can be found in any written book so far. It hasn’t been done yet.
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