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A batch of the best highlights from what Todd's read, .
Here’s the chain of events:
1. You think about eating a meal containing carbohydrates.
2. You begin secreting insulin.
3. The insulin signals the fat cells to shut down the release of fatty acids (by inhibiting HSL) and take up more fatty acids (via LPL) from the circulation.
4. You start to get hungry, or hungrier.
5. You begin eating.
6. You secrete more insulin.
7. The carbohydrates are digested and enter the circulation as glucose, causing blood sugar levels to rise.
8. You secrete still more insulin.
9. Fat from the diet is stored as triglycerides in the fat cells, as are some of the carbohydrates that are converted into fat in the liver.
10. The fat cells get fatter, and so do you.
11. The fat stays in the fat cells until the insulin level drops.
Why We Get Fat
Gary Taubes
Recent research also [points to a link](https://www.pharmacytimes.com/view/semaglutide-carries-potential-risk-of-worsening-diabetic-retinopathy) between the GLP-1 receptor agonist semaglutide and worsening diabetic retinopathy (DR). DR is a serious complication of diabetes that can ultimately lead to blindness. While it may seem surprising that treating diabetes would *worsen* one of the disease’s complications, this seemingly paradoxical relationship is well-established: any treatment that abruptly lowers blood glucose can [accelerate DR](https://bmcendocrdisord.biomedcentral.com/articles/10.1186/s12902-017-0213-3).
What Are GLP-1 Receptor Agonists, and How Do They Work?
The Levels Team
On a scale of 1 (least) to 10 (most), how would you rate your level of perseverance? Give some examples. How might you increase your number
The Map
Keith M. Eigel, PhD
...catch up on these, and many more highlights
Readwise