Rapid fat loss can cause diabetes and liver disease, likely due to systemic exposure to free fatty acids
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When people asked Ray during interviews and in emails about weight loss, he always cautioned that rapid weight loss through fasting and/or exhaustive exercise is likely to be harmful due to increased lipolysis and thus PUFA flooding the bloodstream and literally poisoning the rest of the body. It seems that one of the main roles of adipose tissue is not only to store energy (in the form of fat) for use during emergencies (e.g. prolonged lack of food), but also to keep the evil PUFA away from other organs. Multiple studies have demonstrated that when a meal is consumed, the saturated fats are preferentially oxidized as fuel, while PUFA (and to a lesser degree, MUFA) are preferentially stored in adipose tissue in an inert (triglyceride) form. While in “storage”, PUFA is a lot less dangerous than when floating around the blood and while still subject to peroxidation the negative effects are largely contained to the adipose tissue. Said peroxidation can also be safely inhibited by taking antioxidants such as vitamin E, but that approach only works while PUFA is stored. When PUFA is released into the blood, it is released in the form of free fatty acids (NEFA), and the elevation of NEFA has been shown by countless studies to cause damage to virtually any organ exposed to NEFA. It is now known that the kidney damage seen in virtually all patients with diabetes II is due to chronic exposure to NEFA, and the same has been shown to be true for liver disease, and even neurodegenerative conditions such as Alzheimer’s. As such, keeping PUFA stored rather than floating around is perhaps the best approach while a person works on thyroid and eliminating PUFA from diet so that total PUFA stores are replaced slowly and with as little NEFA elevation as possible. So, it seems that carrying extra weight and working to slowly get rid of it while also changing its composition is preferable to the “shock and awe” approach we keep heating about from every doctor and fitness/exercise commercial on TV and social media.
https://doi.org/10.1172/JCI198387?utm_source=miragenews&utm_medium=miragenews&utm_campaign=news
https://www.miragenews.com/u-m-study-links-rare-fat-loss-disease-to-1616383/
“…Many people may have a dim view of their fat tissue, yet scientists have come to recognize adipose as a necessary and metabolically active organ, carrying out many vital functions within the body. In the case of obesity, too much fat can contribute to conditions such as diabetes and heart disease. Intriguingly, for people with certain rare genetic and autoimmune disorders, such as familial partial lipodystrophy type 2 (FPLD2), the abnormal loss and distribution of adipose tissue can also lead to diabetes and metabolic disease.”
“…A simple explanation is that all of the fat cells (adipocytes) have really catastrophic things happening in them,” said Maung. The team created a mouse model in which they inducibly knocked out the lamin A/C gene in adipocytes, which is mutated in patients with FPLD2…The team observed in both animal models and in patient donor tissue that dramatic gene expression changes lead to the fat cells being unable to carry out their normal lipid handling and storage functions. In addition, the fat cells themselves and the immune cells within adipose tissue became pro-inflammatory. Finally, mitochondria inside the fat cells became dysfunctional. Said Maung, “All of these effects come together to create this perfect environment for the tissue to be really unhealthy and eventually disappear.” In the absence of healthy adipose tissue, the normal maintenance of lipids and release of metabolic hormones goes awry, leading to metabolic diseases like diabetes and fatty liver disease. “This is really underscoring the importance of healthy fats in keeping metabolism intact and functional,” said Oral. People think of Type 2 diabetes as a disease of beta cells, but it’s actually a disease of fat cells, too.” The team hopes that these insights will help identify future therapeutic targets, enable targeting of adipose tissue to prevent it from disappearing, and correct metabolic dysfunction in this disease.”
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@haidut thoughts on this?
Vitamin K2 cannot substitute Coenzyme Q10 as electron carrier in the mitochondrial respiratory chain of mammalian cells
https://pubmed.ncbi.nlm.nih.gov/31024065/The authors conclude that, although vitamin K2 can act as an electron carrier in certain bacteria and has been proposed to do so in Drosophila, this role is not generalizable to mammalian mitochondria
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@user73636
Vit. K3 and C can bypass Q10 to cyt.c
Vit .K3 is intermediate to K2
https://pmc.ncbi.nlm.nih.gov/articles/PMC5953218/