Full after fruit?
1)That’s an atypical satiation response
2) The is probably accurate bc of what the peach 🍑 would replace
3) most modern fruit isn’t “natural.” 10,000 gen of selection for sweetness …
4) Ppl would also lose weight eating more hard boiled eggs 🥚

Cont’…
5) of all fruit, I think peach isn’t a “bad” choice, and I’m not anti fruit. But the notion that fruits are healthy by virtue of being fruits is problematic. Most people think dried fruit is healthy, including dried 🍍 at the extreme. May as well be eating sour patch kids…
6) again, I’m not anti-fruit but let’s try to discuss in what context the fruit is being consumed and how “processed” the fruit is re artificial selection or other processing. Let’s also discuss the actual nutrient content and other options…
Like, Is a banana the best source of potassium? No, avocado is better source and more filling. What about oranges and vitamin C? Strawberries are lower GI with more vitamin C and cauliflower is higher than both…
To sum, If I had to choose between more fruit or less fruit for Americans I’d choose more, but that simple dichotomy is an inefficient and problematic line of recommendation. An avocado isn’t a strawberry isn’t a peach isn’t a banana isn’t dried pineapple
.@allicovington not trying to “gotcha” on this one, just wanted to elaborate my thoughts. Also, I saw you use a princess bride GIF. Thus, I respect you 😅

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More from @nicknorwitz

19 Sep
1/ Another in my biology series of How it Works. This time... How Does You Body Get Rid of Excess Nitrogen? #Protein

The short answer is that it transforms the nitogenous group (amino group) into urea, and it gets peed out. But let's dig in a bit...
2/ The first step is to get the Nitrogen-containing amino group off of the donor amino acid. This is done by a "transamination reaction" in which transaminase enzymes effectively shuffle the amino group, transfering it from one donor amino acid to an acceptor alpha keto acid...
3/ Again, just a simple shuffling. In the example shown Alanine is the donor amino acid, and it's amino group is transfered to alpha-ketoglutarate to make their respective alpha keto acid and amino acid pairs: Pyruvate & Glutamate...
Read 6 tweets
24 Jul
1/ Why does LDLc go up more if you're leaner and have higher energy demands, one explaination by @DaveKeto (and hopefully I recount it corrently):

In a low-carb state, dependence on fat metabolism is increased. Thus, ur fat cells r shrinking& growing in a more dynamic fashion...
2/ In order to expand, the fat cell (and other cells) needs material that can be provided by circulating lipoproteins.

Now let's pause and remeber that leanness & metabolic health are characterized by small fat cells (even if there are more). This is healthy but...
3/ If you fat cell is small its going to have a higher surface area to volume ratio than large fat cells. Thus, to grow and the same amount in terms of volume (as the TG pool is turned over more quickly) small fat cells will require more membrane components provided by LDL...
Read 4 tweets
24 Jul
1/ What does Lipid Trafficking and VLDL have to do with type II #diabetes?

Check out my new video on the "Twin Cycle Hypothesis"

In 9 min, you'll be smarter than you were before!
🤓🤓🤓👇👇👇
#LEM #Lipids #Insulin
2/ After you watch the video, can you answer the following "quiz" questions?

(i) How does the contribution of de novo lipogenesis to Triglyceries in VLDL change as liver fat accumulates?
...
3/ T/F and why?
(ii) Palmitic acid is transported by VLDL1 to the pancreas, harming beta cells in the pancreas. Palmitic acid is a major saturated fat (16:0) found in animal foods. So, you should eat less red meat and dairy and substitue in healthy whole grains & fruit, like 🍌?
Read 4 tweets
14 Jul
1/ New Human study supports twin-cycle hypothesis of #diabetes … thread incoming!
#metabolism #insulinresistance

sciencedirect.com/science/articl…
2/ The twin cycle hypothesis postulates that accumulation of liver fat can drive diabetes in the following way: more liver fat promotes hepatic insulin resistance which increases gluconeogenesis and thus increases insulin to promote more de novo lipogenesis. Basically…
3/ Basically, more liver fat more insulin resistance more liver fat and so on. New human data provide support for the model. One of the key findings of the paper is that more liver fat = more de novo lipogenesis, creating specifically the saturated fat palmitic acid (PA)…
Read 14 tweets
12 Jul
Circulating levels of Lipoprotein Lipase inhibiting factor ANGPTL8 are associated with increased all-cause mortality and CVD risk .@DaveKeto Thoughts?
#metabolism #cvd #LEM
P.S. (ANGPTL8 aka "betatrophin" in the literature)
nature.com/articles/s4159…
cell.com/trends/endocri…
2/ Also, it's all very mechanistic, with ANGPTL4 vs. 3/8 being oppositely regualted by feeding and fasting in a tissue specific manner such that fasting decreases fat storage in adopicytes and feeding promotes it.

And, perhaps, unsuprislingly, the lipid metabolism is...
3/ w.r.t ANGPTLs (and specifically 4, which controls local LPL activity) is linked with glucose homeostasis...
Read 5 tweets
6 Jul
The #ketone body, acetoacetate (AcAc) regulates lipid metabolism through receptor GPR43
pnas.org/content/116/47…

Cool study .@DaveKeto and I were discussing...

AcAc binds to the GPR43/FFAR2 receptor to promote Lipoprotein Lipase activity and help burn fat.

Some more details...
2/ Short-chain fatty acids (SCFAs) in the gut r known to modulate energy homeostatis. Butyrate, acetate, proprionate all have recptors. The acetate receptor is GPR43.

The ketone BhB is all well studied as a signaling molecule, and binds HCAR2 etc., but AcAc is less well studied.
3/ This paper provides good evidence that, during fasting and ketogenic conditions, its AcAc that helps promote fat burning (lypolysis) throughout the body (except in the gut, more on that in a bit). Again, AcAc binds GPR43 and promotes Lipoprotein lipase (LPL activity)...
Read 10 tweets

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