I thought y’all might find this interesting. It is from the Essentials of Strength Training and Conditioning, 4th Ed. This is from the Bioenergetics and Energy chapter in my textbook for my strength and conditioning coaching certification.
According to the text, one molecule of palmitic acid creates over 300 ATP versus one glucose molecule making a net of 38 through the Kreb’s cycle.
I’d say a roughly 9x increase in energy production from a fatty acid versus a carbohydrate.
I love this stuff! It’s amazing to me all the millions of chemical reactions that happen in our bodies!
But also Steric acid (saturated fat) or its equivalent Palimitic acid is going to be produced endogenously from carbohydrates; so eating these types of fat directly has nothing to do with cited biological pathway being utilized exclusively.
Either your body is making it from carbohydrates or your eating it?
Being Ketogenically fat adapted (6 months or 27 weeks) or a sugar burner; does it even matter?
You could just as well drink Apple Cider Vinegar, MCT oil or eat exogenous ketones for one of many energy derived biological pathways?
References:
[1] “…Palmitic acid can also be synthesized endogenously by elongation of C14:0, although this pathway is thought to be less active in the context of Western, high-fat diets (Hellerstein, 1999) and it is by far the largest component of circulating SFAs (Khaw et al., 2012; Wu et al., 2011). …” From: Handbook of Lipids in Human Function, 2016
[2] ”…Palmitic acid (97.3%) is more readily absorbed than stearic acid (94.1%), while other fatty acids (lauric, myristic, oleic, elaidic, and linoleic acids) are nearly completely absorbed (>99.0%) (Baer et al., 2003). …” From: Soybeans, 2008
The difference is whether or not, and how often, the body will be triggered to use the saturated fat/palimitic acid.
Yes, you can produce a lot of it from carbohydrates that the body converts into fat/body fat after the glycogen stores are filled (may not need to be completely filled first, but at least some will go to that). However, one of the problems with insulin is that it prevents the usage or release of body fat into the bloodstream. So, even if you have the fat to use, you may not use it very much if you frequently have a significant amount of insulin around. Since carbohydrate consumption/processing causes significantly more insulin production than fat consumption/processing, you’re less likely to tap into the fat stores, and thus less likely to get that extra ATP burn from the krebs cycle. Probably you’ll still tap into it sometimes, and if you are fasting often you’ll tap into it and get similar benefits, but that’s often considered to be going into ketosis as well (this is why for a long time many treated ketosis and starvation as the same thing).
I was also under the impression that most of bodyfat was monounsaturated fat, rather than just saturated fat. Granted, the fat you eat isn’t likely to be just saturated fat unless you are consuming certain unnaturally concentrated fats, but that does change what is going on when tapping into bodyfat periodically vs tapping into what has been eaten.
Saturated fats are more readily oxidized by the body of the dietary sort (per Dr. Phinney) than polyunsaturated fats which are more prone to be stored. Immediate oxidation of saturated fatty acids (similar to medium chain triglycerides) just ingested rather than stored (fatty acid turn over pool) then oxidized.
Quid Pro Quo (Adipose Storage of Fats: Carbohydrates vs. Dietary Fat): DNL (De Novo Lipogenesis):
Same with carbohydrates they are not going to be stored (immediately oxidized); as fat in adipose cell tissue if kept under a certain threshold when ketogenically fat adapted, so if you carb up a little, it is more than likely going to be burned (oxidized) for energy (TEE) rather than stored or less likely to be stored (immediately oxidized) in adipose tissue as it would be on a SAD diet. And according to the science on DNL, it is not possible unless your eating an enormous amount of carbohydrates over a long period of time? In other words trying to defeat being in ketosis is not as easy as you would think, once fat adapted (27 weeks/6 months)? There is much more to this than simply depleting glycogen stores and making ketones?
What I’m trying say here is you don’t magically pop out of being fat adapted if you occasionally eat big sugary carbohydrate filled meal! Just stay away from high fructose corn syrup or HFCS?
References:
[1] De novo lipogenesis in humans: metabolic and regulatory aspects: “…The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO (carbohydrates) does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO (carbohydrates). Eucaloric replacement of dietary fat by CHO (carbohydrates) does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO (carbohydrates) to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO (carbohydrates) energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO (carbohydrates) replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO (carbohydrates) oxidation to increase and match CHO (carbohydrates) intake. Only when CHO (carbohydrates) energy intake exceeds TEE does DNL in liver or adipose tissue contribute significantly to the whole-body energy economy. It is concluded that DNL is not the pathway of first resort for added dietary CHO (carbohydrates), in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO (carbohydrates) and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO (carbohydrates) and fat in humans are discussed, but require further investigation. …”
[2] De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose: “…Hepatic de novo lipogenesis (DNL) is the biochemical process of synthesising fatty acids from acetyl‐CoA subunits that are produced from a number of different pathways within the cell, most commonly carbohydrate catabolism. In addition to glucose which most commonly supplies carbon units for DNL, fructose is also a profoundly lipogenic substrate that can drive DNL, important when considering the increasing use of fructose in corn syrup as a sweetener. In the context of disease, DNL is thought to contribute to the pathogenesis of non‐alcoholic fatty liver disease, a common condition often associated with the metabolic syndrome and consequent insulin resistance. Whether DNL plays a significant role in the pathogenesis of insulin resistance is yet to be fully elucidated, but it may be that the prevalent products of this synthetic process induce some aspect of hepatic insulin resistance. …”
