One of the reasons for pursuing my Ketotard Chronicles campaign is to promote a greater sense of critical distinction when talking about ketogenic diets or other situations where ketones are elevated.
I think there exists a great deal of confusion, conflation, and in some cases, outright obfuscation and larceny (which I’ve touched on). Basically, “Keto” has become synonymous with The Epileptic Diet, a serious, clinical-level, supervised intervention to help diminish seizures in some people. However, such diets are by no means without serious complications in some subjects (see also: Stewart, et al., 2001, Kang, et al., 2004, Kang, et al., 2005, Bank, et al., 2008, Suo, et al., 2013, and Ketogenic Diet Literature Review – PDF).
People don’t even talk about “Atkins Induction” anymore, a two-week carbohydrate restricted diet that should have most people entering ketosis prior to going on some form of Atkins Maintenance, a more flexible LC approach that could have some people consuming upwards of 100 – 120g of carbohydrate daily. Those were the days. But were they the “Ketogenic Days?”
Well, as we shall see, it depends. It depends both upon dietary factors and also, what people generally regard as ketogenic.
I’ll source from this paper: Measuring breath acetone for monitoring fat loss: Review (Obesity; Joseph C. Anderson, 2015). The abstract:
Endogenous acetone production is a by‐product of the fat metabolism process. Because of its small size, acetone appears in exhaled breath. Historically, endogenous acetone has been measured in exhaled breath to monitor ketosis in healthy and diabetic subjects. Recently, breath acetone concentration (BrAce) has been shown to correlate with the rate of fat loss in healthy individuals. In this review, the measurement of breath acetone in healthy subjects is evaluated for its utility in predicting fat loss and its sensitivity to changes in physiologic parameters.
BrAce can range from 1 ppm in healthy non‐dieting subjects to 1,250 ppm in diabetic ketoacidosis. A strong correlation exists between increased BrAce and the rate of fat loss. Multiple metabolic and respiratory factors affect the measurement of BrAce. BrAce is most affected by changes in the following factors (in descending order): dietary macronutrient composition, caloric restriction, exercise, pulmonary factors, and other assorted factors that increase fat metabolism or inhibit acetone metabolism. Pulmonary factors affecting acetone exchange in the lung should be controlled to optimize the breath sample for measurement.
When biologic factors are controlled, BrAce measurement provides a non‐invasive tool for monitoring the rate of fat loss in healthy subjects.
Here’s the first thing to jump out at me: “BrAce is most affected by changes in the following factors (in descending order): dietary macronutrient composition, caloric restriction, exercise, pulmonary factors, and other assorted factors that increase fat metabolism or inhibit acetone metabolism.”
Now put your thinking caps on, here, and note the distinction. This is part of the Ketotard problem. They see “ketones” and think, instinctively, ‘oh, fat oxidation (true), so, per se body fat loss (not necessarily).’ Of course, elevated ketones mean that some kinda fat is being burned somewhere. It does not follow, necessarily, that it’s body fat being recruited and burned over and above what’s being stored after meals, i.e., resultant net body fat loss.
So, what this means in terms of the quoted sentence, above, is that while BrAce is “most affected” by dietary macronutrient composition and less so by calorie restriction that’s not the case of actual body fat loss. This is the crux of the confusion and conflation going on because, actual body fat loss is “most affected” by calorie restriction, and NOT dietary macronutrient composition. To put it another way, macro composition can exert causal tendencies in terms of how much breath acetone you measure—which correlates with actual body fat loss (provided calories are also reduced)—but it’s not the ketones causing that, it’s the caloric deficit causing it and the ketones being produced by that are an effect of the cause of eating below energy balance significantly and consistently.
Here, I’ll show you and it’s right in the paper if you read carefully enough. First is that we must get over the notion that ketone elevation is an exclusive function of very low carbohydrate intake (and high-fat combined lowish protein in current Ketotarded iterations). “Ketosis” exists on a spectrum.
They only include the most extreme form of calorie restriction which is outright fasting, but that too exists on its own spectrum depending upon how much restriction and also, what the macro composition is within the context of that energy intake deprivation. Here’s one of the papers Anderson reviewed showing clearly that one can be fully in ketosis on a high-carbohydrate diet, provided calories are sufficiently restricted.
Following these studies, Kundu et al. performed a confirmative study (full text). BrAce was measured in humans (n = 58) on a 30 day calorie restriction diet 8. Initial body weights were 10‐30% over the ideal weight (a body mass index, BMI, range of 27.5‐32.5 with ideal BMI = 25 kg m−2). The composition of the diet was high carbohydrate, moderate protein, and low fat. Breath samples, collected upon awakening, sampled the first 380ml of exhaled breath after a 5 s breath hold. On average, BrAce increased over the first 8 days and reached a relative stable plateau after day 7. Fat loss (g day−1) increased with the average BrAce after day 7. Fat loss and BrAce were greater for experimental subjects than controls. Maintaining a BrAce= 85 nM (∼2.1 ppm) corresponded to a fat loss of 227 g week−1 (0.5 lbs week−1). [emphasis added]
Here’s another study where, though I could find no figures on macro composition or calories consumed…since it’s a post-surgery liquid diet provided by the hospital, you can bet it’s not HFLC (Googling around suggests that these liquid diets provide a minimum of 200g/d carbohydrate and “should not be sugar-free.”)
Ross 25 described a patient who after oral surgery had his mouth “wired shut.” The patient consumed a liquid diet during the weeks following surgery. At 3 weeks post‐surgery, BrAce was almost four‐fold greater than the baseline value (∼0.5 ppm). During this time, the patient lost 18 lbs of body weight most likely due to caloric restriction from the imposed liquid diet. The proportion of this weight loss resulting from fat loss was not measured.
Here’s a glaring detail from the paper.
There’s your Fauxtosis right there. These are ketones from dietary fat, not body fat. This is “Ketosis” for the purpose of fooling one’s self and for promoting the prestige and income of various Ketoshyster Usual Suspects.
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Here’s a bit for the numbskulls out there who seem to think it’s only eating HFLC that can make you into one of those very elusive so-called fat burners. Everyone’s a damn fat burner. All day. Every day. Exercise boosts it. You can hit the paper to check the references.
Just as a reduced calorie diet can increase BrAce, exercise can increase BrAce levels. In multiple studies, BrAce was twofold greater at the end than the beginning of exercise 44, 45, 46. BrAce is expected to increase during exercise. In some subjects, BrAce fell at the onset of exercise and then increased with continued exercise 45. During graded exercise tests, BrAce increased (∼twofold) with exercise intensity 44, 46, 47, maximum BrAce corresponded to the onset of the lactate threshold 48, and the fat oxidation rate was shown to be logarithmically related to BrAce 44. Additionally, the fat oxidation rate and BrAce were shown to have parallel increases over 2 h of steady treadmill exercise 44.
Exercise can affect day‐to‐day measurements of BrAce. Subjects submitting to caloric restriction and daily exercise had greater daily BrAce than caloric restriction alone 24, 27. In one study, exercise alone (no caloric restriction) increased day‐to‐day BrAce 29. […]
Studies showed the initial state of ketosis affected BOHB changes during exercise 52. In subjects on a standard moderate‐ to high‐carbohydrate diet, exercise caused increased BOHB throughout exercise 49. […]
…Ingesting carbohydrate in the minutes after the start of exercise reduced fat oxidation for low‐ to moderate‐intensity exercise but did not appear to impact fat oxidation for high‐intensity exercise 50.
Now, here’s the money quote for all the Ketotards out there.
Like carbon dioxide, acetone is a by‐product of metabolism. By itself, the presence of acetone in exhaled breath does not indicate underlying disease. Low concentrations (1 to 2 ppm) of breath acetone represent a basal level of ketosis. High levels of breath acetone (75 to 1,250 ppm), associated with diabetic ketoacidosis, represent the other end of the breath acetone spectrum. Between these extremes lie healthy individuals participating in high‐fat, low‐carbohydrate (HFLC) diets, calorie restriction diets, and fasting. Their BrAce can span two orders of magnitude (Figure 1).
Within that intermediate group are individuals on HFLC diets in which the macronutrient composition (i.e., fat, carbohydrate, and protein) is altered relative to the standard mixed diet. In non‐diabetic subjects, the dietary composition appears to have the greatest impact on BrAce relative to the other factors reviewed. This factor has the greatest impact because acetone is produced when fat is metabolized; increased fat metabolism causes increased acetone production. Eating a standard mixed diet will result in a basal ketosis and BrAce of 1 to 2 ppm. Changing to a HFLC diet (carbohydrate intake <50 g day−1) causes the body to shift from using carbohydrates to using fats as its primary energy source. Relying on fats as the primary energy source increases ketosis levels to what has been termed “nutritional ketosis.” Adults in nutritional ketosis have BOHB ranging from 0.5‐3.0 mM 13, 14, 20, which corresponds to a breath acetone range of 4 to 30 ppm (Figure 2). As important, nutritional ketosis resulting from a HFLC diet increases fat oxidation rates as compared to a standard mixed diet because the primary energy substrate is fat 50. [emphasis added]
See? Want more?
Less extreme than fasting is moderate caloric restriction which allows some food intake and appears to cause modest changes in breath acetone. Breath acetone levels rise as stored fat is metabolized to make up the difference between basal energy requirements and caloric intake. Using caloric restriction, multiple studies have shown a correlation between fat loss and increases in breath acetone 8, 24, 25, 27, 29. Specifically, individuals that maintain a breath acetone of 2 ppm should realize a fat loss rate of at least 114‐227 g week−1, based on the scientific literature 8, 27, 29. On the high end, BrAce could reach 8 ppm which could correspond to a fat loss of 1,200 g week−1 8.
Now let’s quote the paper’s conclusion.
Endogenous breath acetone is correlated with and can be used to understand the rate of fat loss in healthy subjects. Maintaining a 2 ppm BrAce while on a calorie restriction diet should cause a fat loss rate of ∼227 g week−1. Acetone is correlated with fat loss because it and two other ketone bodies are the by‐products of fat metabolism. Breath acetone is strongly correlated with the blood ketone body BOHB. Breath acetone can range in concentration from 1 ppm in healthy non‐dieting subjects to 1,250 ppm in diabetic ketoacidosis. In healthy individuals, breath acetone is affected by multiple factors. Dietary macronutrient composition has the greatest impact followed, in rank order, by caloric restriction, exercise, pulmonary factors, and other factors. Because of its relationship to fat metabolism, a high‐fat, low‐carbohydrate diet will generate more breath acetone than a standard mixed diet. A reduction in consumed calories relative to that needed for weight maintenance can increase breath acetone and fat loss. [emphasis added]
Putting all this together, here’s the takeaway:
- Breath acetone (and other ketones) are markers of fat oxidation
- Fat oxidation can be dietary fat, body fat, or both
- A very high-fat dietary intake will produce higher levels of elevated ketones because the primary energy intake is fat
- The only way to ensure that your measured ketones are primary the by-product of body fat and not dietary fat oxidation is to sustain a significant average energy intake deficit
- The variation in ketone elevation between subjects once a calorie deficit is in place is not only representative of body fat loss—which should be similar for similar subjects on similar caloric restriction—but is also representative of differences in macro composition.
In other words, on point 5, given roughly the same amount of fat loss between two calorie-restricted dieters, one low-fat-high-carb and the other, low-carb-high-fat, we would expect a higher level of measured ketones in the latter dieter since his higher levels of dietary fat will produce more “fauxtones” when they’re oxidized. At the extreme, you have many Ketotards out there actually eating to energy excess (See the section Do You Consume Less Food When Eating a High Fat Diet? here) seeing all these fauxtones and they think they’re in body-fat-loss ketosis when they’re only in fauxtosis.
So, in conclusion, I can find only one benefit to an LC diet in terms of sustained body fat loss and that is adherence in free living situations. And that makes perfect sense since the most delicious foods (meat, fish, and fowl) are found there and they are the best sources of protein. Swapping out carbohydrate (or, for that matter, fat) for higher levels of protein is really the perfect dietary strategy and the better approach is the one you find yourself better sticking to for the long haul.
So the next time someone says they’re in ketosis or doing a ketogenic diet, ask them which kind and thereby, expose their ignorance for them.