If you eat 3 oz of plain pork rinds, you get 52g of protein and 26g of fat. Of that protein, 19% is glycine, 10g. Of that fat, 11% is linoleic acid, 2.9g, which is 16% of average American daily intake. Of course, you might be unusually adversely sensitive to linoleic acid, which would be a reason to get glycine some other way.
Chicken is a much less efficient glycine delivery vehicle. If you eat a pound of roasted skin-on chicken (roughly half a Costco rotisserie chicken) you get 125g of protein and 62g of fat. Of that protein, 6.5% is glycine, 8g. Of that fat, 19% is linoleic acid, 12g, which is 2⁄3 of the average American daily intake.
Chicken skin alone is even worse per unit of linoleic acid. If you eat 1⁄3 kg of roasted chicken skin (wow, that’s a lot), you get 67g of protein and 137g of fat. Of that protein, approximately 13% is glycine, 9g. Of that fat, 20% is linoleic acid, 27g, which is 1.5x the average American daily intake.
I didn’t know that until I looked up the numbers just now. It probably varies a lot based on what the animals are fed. Typical Chinese chickens are probably meaningfully better than the American ones on this metric, as the Chinese tend to prefer chickens that taste like chicken over ones bred to maximize meat yields above all else, though this is changing.
If you want to avoid linoleic acid, and want to get glycine from whole foods, best to do things like eat tendons and skimmed bone broth.
On linoleic acid as a “dietary villain,” I’m familiar with two plausible stories:
1 PUFAs generally as oxidative liability (via Masterjohn), which seems mechanistically tight but doesn’t seem to generate a clear observational signal so the effect size is probably small, though I can think of ways to save the hypothesis (snapshots of PUFA consumption may not reflect AUC or PUFA levels). This should only be a problem if you’re storing rather than burning PUFAs, so I’d expect a lot of heterogeneity in response depending on many other factors. It’s also not specific to LA except insofar as LA is a common PUFA in Western diets.
2 Brad Marshall’s torpor story. I looked into this a bit, and while there aren’t experimental results on humans, there are both positive and negative results in animals; the main negative one I found was Gerson et al. (2008). I’m skeptical of external validity as applied to a species that doesn’t have what seem to be the relevant physiological torpor mechanisms.
Poultry and pork rinds will get you a bunch of linoleic fatty acid, which is a whole separate dietary villain.
If you eat 3 oz of plain pork rinds, you get 52g of protein and 26g of fat. Of that protein, 19% is glycine, 10g. Of that fat, 11% is linoleic acid, 2.9g, which is 16% of average American daily intake. Of course, you might be unusually adversely sensitive to linoleic acid, which would be a reason to get glycine some other way.
Chicken is a much less efficient glycine delivery vehicle. If you eat a pound of roasted skin-on chicken (roughly half a Costco rotisserie chicken) you get 125g of protein and 62g of fat. Of that protein, 6.5% is glycine, 8g. Of that fat, 19% is linoleic acid, 12g, which is 2⁄3 of the average American daily intake.
Chicken skin alone is even worse per unit of linoleic acid. If you eat 1⁄3 kg of roasted chicken skin (wow, that’s a lot), you get 67g of protein and 137g of fat. Of that protein, approximately 13% is glycine, 9g. Of that fat, 20% is linoleic acid, 27g, which is 1.5x the average American daily intake.
I didn’t know that until I looked up the numbers just now. It probably varies a lot based on what the animals are fed. Typical Chinese chickens are probably meaningfully better than the American ones on this metric, as the Chinese tend to prefer chickens that taste like chicken over ones bred to maximize meat yields above all else, though this is changing.
If you want to avoid linoleic acid, and want to get glycine from whole foods, best to do things like eat tendons and skimmed bone broth.
On linoleic acid as a “dietary villain,” I’m familiar with two plausible stories:
1 PUFAs generally as oxidative liability (via Masterjohn), which seems mechanistically tight but doesn’t seem to generate a clear observational signal so the effect size is probably small, though I can think of ways to save the hypothesis (snapshots of PUFA consumption may not reflect AUC or PUFA levels). This should only be a problem if you’re storing rather than burning PUFAs, so I’d expect a lot of heterogeneity in response depending on many other factors. It’s also not specific to LA except insofar as LA is a common PUFA in Western diets.
2 Brad Marshall’s torpor story. I looked into this a bit, and while there aren’t experimental results on humans, there are both positive and negative results in animals; the main negative one I found was Gerson et al. (2008). I’m skeptical of external validity as applied to a species that doesn’t have what seem to be the relevant physiological torpor mechanisms.
Am I missing something big here?