Sunday, December 28, 2014

Macronutrient Myths from Alternatives

Excess Protein is converted to Glucose (Gluconeogenesis)
A widespread idea in the low carb community is that excess protein is converted to glucose by gluconeogenesis.  Therefore, many low carb advocates also recommend reducing/moderating protein intake to reduce blood glucose under the assumption that ↑ protein >> ↑ gluconeogenesis >> ↑ blood glucose.
However, only a very small amount of protein is converted to glucose (4g glucose from 23g of protein), and furthermore, dietary protein doesn’t increase total gluconeogenesis, nor does it increase glucose levels (even in diabetics) [1] [2].  So what happens to excess protein?  As you can see from the figure below (HT Carbsane), the gluconeogenic amino acids (green) can feed into the TCA cycle, so they are already in a good position to be oxidised.  They can of course also ultimately become glucose by first being converted to oxaloacetate, but gluconeogenesis is a very energy consuming process: “the cost of gluconeogenesis was 33% of the energy content of the produced glucose” [3], which is probably why gluconeogenesis from amino acids is so low.  Steak =/= cake
Protein Leaches Calcium from Bones
This is one the arguments in the acid-base theory of osteoporosis, which is often promoted by vegetarians and the early Paleo advocates, but is poorly supported by evidence [4] [5] [6] [7].  Protein does slightly increase urinary calcium (~1.2mg per 1g of protein) [8], but protein also increases calcium absorption [9] [10], resulting in a neutral calcium balance [9] [10].  High protein diets actually decrease the fraction of calcium from bone and reduce the rate of bone turnover [10].  This is consistent with a high protein intake resulting in a decrease in parathyroid hormone, suggesting the primary effect of protein is to increase calcium absorption and that increased calcium excretion is merely a consequence of increased absorption, rather than the calcium coming from bone to buffer the acidity of protein [9].  Overall, higher protein intakes tend to be associated with increased bone mineral density and lower fracture risk [7]
The US Reduced Fat Intake Following the Release of the Dietary Guidelines
People will cite a decline in the percentage of calories from fat following the 1970’s as evidence that we have reduced our overall fat consumption, we have gone on a low fat diet and/or that low fat is responsible for the obesity epidemic.  However, while the percentage of calories from fat has decreased, the absolute fat intake has stayed the same or increased (depending on the time period and source), which is due to a larger increase in energy from carbohydrates during that period (see the table below and More Thoughts on Macronutrient Trends).
404 (16.5%)
406 (15.1%)
261 (16.9%)
283 (15.1%)
904 (36.9%)
859 (32.8%)
557 (36.1%)
616 (32.8%)
1039 (42.4%)
1283 (49.0%)
700 (45.4%)
969 (51.6%)
It’s also incorrect to stay that low fat caused the obesity epidemic as ad libitum low fat diets can lead to weight loss [12].  And surely humans aren’t so precious that a minor change in macronutrient balance is sufficient to cause widespread obesity.
Excess Carbohydrate, Particularly Fructose, is Converted to Fat (De Novo Lipogenesis)
It’s often said that once glycogen stores are full, excess carbohydrate is converted to fat and stored.  However, de novo lipogenesis is very minor in humans contributing 0.5-10.0g depending on health (healthy, obese, diabetic) and diet (control, carb overfeeding) [13] [14] [15] [16] [17] [18], with the lower end of range (~0.5-3g) representing a standard diet and the upper end of the range (5-10g) representing pretty extreme carbohydrate overfeeding (50%).  This is consistent with the fatty acid composition of adipocytes being pretty much identical to the fatty acid composition of the diet.
Fructose is more lipogenic than glucose, but that’s not saying much.  Consuming 200g of fructose over 6 hours (far more fructose than most would have in a day) results in < 6g of palmitate from DNL in the liver and in total < 10% of the fructose was converted to fat.  By comparison, in the same study < 3% of glucose was converted to fat [18].  Another group found that following an oral fructose load the vast majority of fructose is either converted to glucose in the liver then exported to other tissues (50%), stored as liver glycogen (15%), metabolised to lactate (25%), with the remaining 10% being oxidised or undergoing de novo lipogenesis [19].  Fructose =/= fat
* It’s also ironic that the many of the people who are anti-carb or anti-fructose based on de novo lipogenesis are quite comfortable consuming ~10-50x more saturated fat from the diet than they would get on a (eucaloric) high carb diet from de novo lipogenesis (not that I’m anti-saturated fat)


  1. I think there's good experimental evidence that protein is highly gluconeogenic in diabetics without insulin. That is, uninhibited glucagon metabolism does on fact favour this myth, though in general (with some insulin) the picture is different.
    The rule of thumb for diabetics is that protein = 58% carbohydrate, fat = 10%.