Acne

Many people wonder about the connection between diet and acne.

This brief video presents very recent research on this.

NOTE: there is one statement in this video that is not substantiated and seems to be based on dated assumptions. The research showed that a specific fatty acid called “palmitic acid” is involved in the inflammation in acne. Palmitic acid is one of the fatty acids we call a saturated fatty acid. It is present in the diet. Importantly, we also make this molecule ourselves in our livers.

When we eat more carbs than we can use at the time, the liver needs to protect us from having the glucose level in the blood stream go up. Your body can only store a small amount of glucose at a time. Remember that all starch in every form is actually chains of glucose molecules. Starch gets digested to single glucose molecules before being absorbed from the digestive tract and shunted straight to the liver. All carbs in your diet are turned to sugars before they are absorbed.

Part of your liver’s strategy for dealing with this inflow of sugars is to turn it into fat. Palmitic acid is the main fatty acid that your liver produces from carbs in your diet.

It is out-dated and false to suggest that blood levels of saturated fats (or tissue levels of palmitic acid) can be interpreted as being directly caused by saturated fat intake in the diet.

PLoS One. 2014 Nov 21;9(11):e113605. doi: 10.1371/journal.pone.0113605.
Effects of step-wise increases in dietary carbohydrate on circulating saturated Fatty acids and palmitoleic Acid in adults with metabolic syndrome.
Volk BM1, Kunces LJ1, Freidenreich DJ1, Kupchak BR1, Saenz C1, Artistizabal JC2, Fernandez ML3, Bruno RS4, Maresh CM1, Kraemer WJ1, Phinney SD5, Volek JS6.

From the abstract:

“The results show that dietary and plasma saturated fat are not related”

Full text of this article, from November 2014, is here.

“A consequence of consuming dietary sugars and starches above levels that can be directly oxidized is that a greater proportion is converted to fat (i.e., de novo lipogenesis). De novo lipogenesis (DNL) increases several-fold when carbohydrate is fed above energy needs [3], but isocaloric high-carbohydrate diets [4] and high-carbohydrate meals [5], [6] also promote DNL and hypertriglyceridemia in individuals with insulin resistance. The major product of DNL is palmitate (16∶0), a saturated fatty acid (SFA), but monounsaturated fatty acids (MUFA) are also formed as a result of desaturation, most notably palmitoleic acid (cis-16:1n-7). Healthy men overfed carbohydrate showed increased very low-density lipoprotein-triglyceride (VLDL-TG) palmitic (28.3 to 37.9%) and palmitoleic (3.8 to 10.0%) acids [3]. Thus, high-carbohydrate intake in individuals with an impaired ability to oxidize glucose stimulates DNL and secretion of SFA- and MUFA-enriched VLDL particles; a serum profile associated with insulin resistance [7].”

With that in mind, now on to the recent research findings: