‘Inflammation, interfering with cellular energy production, is probably the essential feature of the things called diabetes.’ Ray Peat PhD
Even though sugar consumption gets popularly believed to be responsible for the onset of type 2 diabetes and related illnesses, experiments suggest otherwise. Instead, they point to inflammation and associated factors. It includes insulin resistance, blood sugar dysregulation, and high blood fat levels, particularly polyunsaturated fats.
Dietary measures, including limiting fat intake and increasing consumption of easy-to-digest sugars, have been shown to help lower cortisol and release polyunsaturated fats (PUFAs) out of storage.
Both of these stress metabolism signs (rising cortisol and exposure to PUFAs) are known to be involved in promoting the symptoms of diabetes, and there is science showing that aspirin can be an effective and safe therapy.
‘We found that a 2-week trial of high-dose aspirin treatment (∼7 g/d) was accompanied by significant decreases in hepatic glucose production (22%), fasting plasma glucose…about 40 mg/d…(24%), fatty acids (50%)…and a 19% increase in peripheral glucose disposal…
…despite similar plasma insulin concentrations, aspirin treatment still resulted in a higher…rate of insulin-stimulated glucose disposal…reflecting increased…insulin responsiveness…
…Aspirin therapy also resulted in significant reductions in…plasma fatty acid concentration, and such reductions can also contribute to enhanced insulin action…
…There was no significant change in body weight…All the patients completed the study with no major side effects…
…There were also significant decreases in concentrations of…C-reactive protein (17%)’ (Hundal RS,, et al., 2002)
The above quotations got taken from one study. It showed that aspirin treatment, via mechanisms decreasing inflammation and free fatty acid release, improved all measures of hyperglycemia. And it caused an appreciable increase in insulin sensitivity and glucose oxidation and vastly improved symptoms in patients with type 2 diabetes without any noticeable severe or long-term side effects.
Similarly, sufficient consumption of sugar from sweet, ripe, juicy fruits, fruit juices, honey and white sugar is understood by some to be able to promote improvements in thyroid function, limiting stress and the release of PUFAs out of storage.
It makes sense, from a biological perspective, that this might then be able to help reduce exposure to inflammatory stress substances. It includes cortisol, thereby lessening insulin resistance, protecting against hyperglycemia, increasing cellular energy production, and protecting against developing or worsening type 2 diabetes symptoms and related conditions, including obesity, cardiovascular disease, and cancer.
Read through the above study and the other studies attached below, and make up your mind.
I’m not a doctor, and this is not a prescription or health advice, but information like this is available for all to go through, and I think it’s a good idea to at least have a look.
Copyright 2021, by Dan M @ CowsEatGrass. All rights reserved (except for quotations and images having their own protected copyrights). This copyright protects author-publisher Dan M’s right to future publication of his work in any manner, in any and all media — utilizing technology now known or hereafter devised — throughout the world in perpetuity. Everything described in this publication is for information purposes only. The author-publisher, Dan M, is not directly or indirectly presenting or recommending any part of this publication’s data as a diagnosis or prescription for any ailment of any reader. If anyone uses this information without the advice of their professional health adviser, they are prescribing for themselves, and the author- publisher assumes no responsibility or liability. Persons using any of this data do so at their own risk and must take personal responsibility for what they don’t know as well as for what they do know.
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Diabetes Care. 2015 Oct;38(10):1820-6. Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial. Jakubowicz D, Wainstein J, Ahren B, Landau Z, Bar-Dayan Y, Froy O.
J Clin Invest. 2001 Aug 1; 108(3): 437–446. Prevention of fat-induced insulin resistance by salicylate. J K Kim, Y J Kim, J J Fillmore, Y Chen, I Moore, J Lee, M Yuan, Z W Li, M Karin, P Perret, S E Shoelson, G I Shulman.
Diabetes. 2012 Apr; 61(4): 790–796. Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and in humans, mediating insulin sensitization. Mark Nixon, Deborah J. Wake, Dawn E. Livingstone, Roland H. Stimson, Cristina L. Esteves, Jonathan R. Seckl, Karen E. Chapman, Ruth Andrew, and Brian R. Walker.
Journal of Diabetes & Metabolism 02(04) January 2011 Mechanisms of Fatty Acid-Induced Insulin Resistance in Muscle and Liver. Rafik Ragheb, Amina Medhat.
J Clin Invest. 2002 May 15; 109(10): 1321–1326. Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes. Ripudaman S Hundal, Kitt F Petersen, Adam B Mayerson, Pritpal S Randhawa, Silvio Inzucchi, Steven E Shoelson, Gerald I Shulman.
J Clin Invest. 1996 Jun 15; 97(12): 2859–2865. Mechanism of free fatty acid-induced insulin resistance in humans. M Roden, T B Price, G Perseghin, K F Petersen, D L Rothman, G W Cline, and G I Shulman.
Science. 2001 Aug 31;293(5535):1673-7. Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta. M Yuan, N Konstantopoulos, J Lee, L Hansen, Z W Li, M Karin, S E Shoelson.
Image: ACP InternistWeekly: Artist Unknown
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