Ran across an older study (The American Journal of Clinical Nutrition, Volume 83, Issue 5, 1 May 2006, Pages 1055–1061. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Carol S Johnston Sherrie L Tjonn Pamela D Swan Andrea White Heather Hutchins Barry Sears) which indicates that LDL is directly tied to BHB levels:

LDL cholesterol was directly correlated with blood β-hydroxybutyrate (r = 0.297, P = 0.025)

The study was only six weeks so it was too short a term to provide much of value in the critique of ketogenic low-carbohydrate diets. The main criticism was that people had a lack of energy on low carb during what we now know is the adaptation phase.

More details:

Compared with baseline, the 6-wk LDL concentrations increased in 5 KLC dieters (0.08, 0.13, 0.41, 0.44, and 0.52 mmol/L, respectively) and decreased in the remaining 4 KLC dieters (0.57 ± 0.18 mmol/L)

Another interesting point:

 Weight-adjusted REE increased in both diet groups over the 6-wk trial, but blood β-hydroxybutyrate concentrations were not correlated with REE (r = −0.014, P = 0.921), which indicates that the protein content of the diet, rather than the severity of the carbohydrate restriction, likely contributed to the elevations in REE.  These data support the contention that calorie-reduced diets high in protein facilitate weight loss, in part, by preserving the metabolic rate (7818).


Low-ish Carb Diet and Diabetes

A five week long study was conducted to determine the effect of a non-ketogenic but still low-ish carb diet on blood sugar numbers in diabetes (Diabetes 2004 Sep; 53(9): 2375-2382. Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Mary C. Gannon and Frank Q. Nuttall).

The study compared diets with two different macros. The carbohydrate:protein:fat ratio of the Low Carb diet was 55:15:30. The test diet ratio was 20:30:50. Again, note this was not ketogenic levels of carbohydrates. The diet was “weight-maintaining”.  Assuming this is a 2000 calories a day diet that would be 2000 * 0.2 = 400 calories or 100 grams of carbohydrates a day.

The subjects were tested and their Plasma and urinary β-hydroxybutyrate were similar on both diets indicating that the lower carb group was not in nutritional ketosis.

The results were favorable for the Low Carb group.

The percentage of glycohemoglobin (HbA1c) was 9.8 ± 0.5 on the control diet and 7.6 ± 0.3 on the Low Carb diet. It was still decreasing at the end of the Low Carb diet. Thus, the final calculated glycohemoglobin was estimated to be ∼6.3–5.4%.

The reason they estimated the final HbA1c numbers would be lower was that:

The mean 24-h integrated serum glucose at the end of the control and LoBAG diets was 198 and 126 mg/dl, respectively.

Carbohydrate Control is the Key to Blood Sugar Control

As the study noted:

Data obtained in our laboratory (1–3) as well as from others (reviewed in 4) indicate that glucose that is absorbed after the digestion of glucose-containing foods (carbohyrates) is largely responsible for the rise in the circulating glucose concentration after ingestion of mixed meals. Dietary proteins, fats, and absorbed fructose and galactose resulting from the digestion of sucrose and lactose, respectively, have little effect on blood glucose concentration.

The study did increase protein by 2x but a previous study had isolated the protein affects on HbA1c:

We previously reported that a diet in which the protein content was increased from 15 to 30% of total food energy, with a corresponding decrease in carbohydrate content, resulted in a moderate but highly statistically significant mean decrease in glycohemoglobin (8.1–7.3%) after 5 weeks on the diet. This was the consequence of smaller postmeal glucose increases. The fasting glucose concentration was unchanged (12).

Thus, the increase in Protein did help the HbA1C due to the decrease in carbohydrates that came along with that increase.

The conclusion was unavoidable given the data:

Thus, the dietary modification that we refer to as the LoBAG diet has the potential for normalizing or nearly normalizing the blood glucose in people with mild to moderately severe type 2 diabetes.

Not as well as the ketogenic diet, but pretty good nevertheless. I did low carb some time back and get my HbA1C to 6.4 (with other meds). But I like my 5.2 number better now.


Protein does not turn into chocolate cake

From (The Journal of Clinical Endocrinology & Metabolism, Volume 86, Issue 3, 1 March 2001, Pages 1040–1047, Effect of Protein Ingestion on the Glucose Appearance Rate in People with Type 2 Diabetes. M. C. Gannon J. A. Nuttall G. Damberg V. Gupta F. Q. Nuttall.):

Amino acids derived from ingested protein are potential substrates for gluconeogenesis. However, several laboratories have reported that protein ingestion does not result in an increase in the circulating glucose concentration in people with or without type 2 diabetes. The reason for this has remained unclear. In people without diabetes it seems to be due to less glucose being produced and entering the circulation than the calculated theoretical amount. Therefore, we were interested in determining whether this also was the case in people with type 2 diabetes. Ten male subjects with untreated type 2 diabetes were given, in random sequence, 50 g protein in the form of very lean beef or only water at 0800 h and studied over the subsequent 8 h.

Protein ingestion resulted in an increase in circulating insulin, C-peptide, glucagon, α amino and urea nitrogen, and triglycerides; a decrease in nonesterified fatty acids; and a modest increase in respiratory quotient.

The total amount of protein deaminated and the amino groups incorporated into urea was calculated to be ∼20–23 g. The net amount of glucose estimated to be produced, based on the quantity of amino acids deaminated, was ∼11–13 g. However, the amount of glucose appearing in the circulation was only ∼2 g. The peripheral plasma glucose concentration decreased by ∼1 mM after ingestion of either protein or water, confirming that ingested protein does not result in a net increase in glucose concentration, and results in only a modest increase in the rate of glucose disappearance.


Is this Keto?

A very common question for those of us who eat a keto diet is “Is this [whatever] keto?”. Along with it comes comments like “you mean you can’t eat bread [or whatever]”.

It’s down to carbs

In the end, it’s as simple as the number of grams of carbohydrates. There are no hard and fast definitions of what constitutes Low Carb and what constitutes ketogenic. The technical answer is what amount of carbohydrates you can eat in a day/meal that keep you in ketosis.

But that begs the question of what constitutes being in ketosis. There’s also no accepted range of numbers or measurement methods. But the idea is that your body is using ketones for fuel. Even that is not an absolute since everyone uses some mixture of ketones and glucose. If you do an extended fast your body will generate glucose from your liver which converts fat to glucose in a process called Gluconeogenesis (GNG).

The easiest thing to measure and track are carbohydrates using a scale and an app like Cronometer which can show you the total number of carbs in your day.

Measuring Ketones

Ketones can be tested by three methods; blood, urine and breath. Each of these tests measure chemicals produced as a byproduct of ketosis. There’s some correlation between these three measurements but even that is not absolute.

Nutritional Ketosis Measures Blood Ketones

A widely accepted method is to use blood ketones and measure them against a standard. Except that there is no standard. Often cited is Stephen Phinney’s definition of “nutritional ketosis” illustrated below:

This says that blood ketones in the range of 0.5 to 3.0 mmol are optimal for brain and muscles.

Is this Food Keto?

Using this definition any food which you eat over a meal/day that drops your blood ketones below 0.5 mmol is not keto. But there’s no easy mapping of how many carbohydrates it takes to push someone to below that number. A commonly asserted amount is 20 grams of carbohydrates per day will take a person out of nutritional ketosis. For most people this number will be adequate. For others it may be too high and for others it may be too low.

The Only Way to Know is to Measure

The only way to know for sure is to measure the effect of a particular food or activity on your ketone levels. And testing isn’t cheap at around $5 a test strip. I’ve used the Precision Xtra meter for my measurements but I never actually mapped carb amounts to ketone levels. I mostly tracked the ketone levels vs days of fasting.

Cheaper Way to Measure

A cheaper way to measure is urine test strips. They are around $5 for 50 strips. You pee on a strip and compare the color of the strip to a scale. They work well for most people (at least at the beginning) but are affected by urine concentrations (which is a function of your level of hydration). They are also slow to react to diet changes. They can indicate what your level of ketosis was hours ago.

Another Expensive Way to Measure

I also bought a breath ketone measurement device, the ketonix. It is fairly expensive but can be reused.

The trouble is there’s a messy mapping from breath to blood ketones. Here’s the scatter diagram from breath to blood ketones with the best fit curce. Going up from 0.5 mMol to the line shows that that’s something like 2.0 PPM.

The ketonix has a USB interface and the data can be downloaded to your computer. Here’s a screen shot of one capture showing the level at 5.4 ppm which would be around 1 mMol.


In the end, the best way to be in ketosis is to eat a very limited amount of carbohydrates such as less than 20 grams a day.


Robb Wolf – Split from CrossFit

Eat meat and vegetables, nuts and seeds, some fruit, little starch, and no sugar

–Greg Glassman

I’ve been asked about the CrossFit split from Robb Wolf (Paleo Diet) and how/why CrossFit embraced the Zone Diet. After all they are vastly different approaches to eating. I have opined on the Zone Diet here.

Robb wrote about the split here.

Robb also was in a podcast where he talked about CrossFit:

Here’s another related video where Robb talks about Paleo and training.


Calories In Calories Out – Revisited Again

Here’s some thoughts I have on the Calories In/Calories Out (CICO) model.

The CICO perspective has value but I think where Fung’s contribution worked for me and others was the role of Insulin in weight gain and carbs being the driving force in Insulin Resistance. Combining Low Carb with Intermittent Fasting made for easy compliance. The reduction of Insulin levels over extended periods of time frees the body to release body fat. The release of body fat reduces the need for calories from the diet since part of the fuel that body needs comes from the body rather than meals.

I see Fung’s advice as focused on his patient population which as a kidney doctors is many older diabetic patients. He found that his patients were compliant with Intermittent Fasting and Low Carbohydrate diets. Probably much more so than the standard population because they were seeing a kidney doctor to begin with. Faced with the possibility of failing kidneys or eating OMAD/Low Carb the alternative seems pretty bad.

Also, there are differences in body composition between various diets. Some are more effective than others at shifting the lean mass/fat mass proportions. http://www.ergo-log.com/paleo-diet-makes-fat-cells-lazy.html

I think they do matter but not so much at the start of the diet. Eventually we have to pay attention to them when we stall with lazy keto. But I got from 285 to around 220 with being completely lazy keto. Never would have reached goal weight, though.

Put another way when we have 100 lbs of body fat that’s 3100 calories a day of fat we can easily pull from our fat stores. Easy to do a caloric “deficit” since we have plenty of surplus to draw from in our bodies.

I’ve been looking into the three compartment theory of diabetes and it seems to have legs to me. First our body’s fat cells fill up. Then our liver fills up with fat. Last our pancreas gets choked with fat which keeps us from making enough Insulin. When that happens our fat backs up into our blood in the form of very high triglycerides. When I was Dx with T2D my triglycerides were over 5000. In fact, they couldn’t get an assay on the number since it was too high. Putting someone on Insulin gets them over that by allowing the fat cells to get even fatter. I gained 50 lbs when the doctor put me on Insulin and my diet was not any different.

This has application in this situation since the fat cells stay locked closed due to high Insulin. There are studies which show CICO doesn’t exactly apply in these cases. Diabetics take more Insulin and eat less calories but still gain weight. There’s a strong relationship with Insulin and body fat.

Intermittent fasting and Low Carb break that relationship by lowering basal Insulin levels and allow the liver to begin dumping the fat. That only takes about a week. The pancreas gets less fatty within 2 weeks and the body’s fat cells drop thereafter.

To me the key is the role of Insulin and that’s Fung’s “contribution”. He’s not a researcher but applied what he learned in the clinical setting.

Bottom line is that if someone is Type 2 Diabetic they can get off meds very quickly by following Fung’s approach of Intermittent Fasting and Low Carb. They can learn to count calories/macros later on when they stall if they want to get lower in weight (and some of them may not care about their weight, they just want to be no longer diabetic).

The reason I think CICO matters later on is that our hormones, particularly Insulin, get in order and then the standard model applies.

There are studies which also show CICO is not matched by the data. For example: https://academic.oup.com/jcem/article/88/4/1617/2845298

The mechanism of the enhanced weight loss in the very low carbohydrate diet group relative to the low fat diet group is not clear. Based on dietary records, the reduction in daily caloric intake was similar in the two groups. For the greater weight loss in the very low carbohydrate group to be strictly a result of decreased caloric consumption, they would have had to consume approximately 300 fewer calories/d over the first 3 months relative to the low fat diet group.

I think Protein is the power multiplier between Low Carb and SAD. In part it has something to do with the Thermic Effect of Food with Protein using about 25% of the calories to process and fat and carbs being much less. So Calories in and Calories out need to take into account the source of the calories.

I’m eating about 2800 calories a day now on Carnivore diet with around 280g of Protein a day. Far in excess of my “Needs”. Some of that we just eliminate as Urea – again outside of the CICO model.

Or maybe the CICO model is just really, really complicated compared to what we see on the standard calculators?

My guess is that the standard calculations for BMR and TDEE are inherently based on the SAD macro ratios. They don’t correct for overconsumption of protein nor do they correct for underconsumption of carbohydrates. They don’t take into account hormonal factors either nor medications such as Insulin.

They are good first order approximations. Eat and track macros and by extension calories. Watch the scale. If you are gaining you need to cut back. If you are maintaining then things are set pretty close. If you want to lose you need to cut.

In my case my methodology is:
Less than 20 g of carbs
At least 1 gram of protein per lb of Lean Body Mass
Enough fat to fill the gap between the first 2 and what I want to lose.

Here’s the calculator I wrote to calculate macros.


Carbs After Workouts?

If you are exercising to improve your insulin sensitivity, then Carbs after workouts are bad. Here’s the science (Nutrients. 2018 Jan 25;10(2). pii: E123. PostExercise CarbohydrateEnergy Replacement Attenuates Insulin Sensitivity and Glucose Tolerance the Following Morning in Healthy Adults. Taylor HL, Wu CL, Chen YC, Wang PG, Gonzalez JT, Betts JA.)

In this study they put participants on a 90-minute treadmill at 70% of their VO2max. At the end they gave the participants either a placebo (no carbs) or maltodextrose that matched the caloric expenditure. Researchers then measured the glucose and insulin responses with an Oral Glucose Tolerance Test (OGTT) the following day and found that the participants who had the carbohydrates had reduced Insulin Sensitivity and increased blood glucose levels.

The practical conclusion of this is that to maximize Insulin Sensitivity it is best to both eat low carb and take no carbs after exercise. Decreased Insulin Sensitivity is one of the markers that lead to Diabetes and increasing Insulin Sensitivity is an important part of reversing Diabetes.

This study is the first to show that feeding carbohydrate to replace that utilized during exercise can reduce insulin sensitivity and glucose tolerance the next morning in healthy adults, when compared to a preservation of the exercise-induced carbohydrate deficit. Furthermore, carbohydrate replacement suppresses subsequent postprandial fat utilization. The mechanism through which exercise improves insulin sensitivity and glucose control is therefore (at least partly) dependent on carbohydrate
availability, and so the day-to-day metabolic health benefits of exercise might be best attained by maintaining a carbohydrate deficit overnight.

For those people who are not particularly concerned about their risk of getting Diabetes it’s worth noting that if they refill their Glycogen stores quickly with carbohydrates they are not burning fat. If they let the Glycogen stores be low then their body will burn fat.

Want to burn fat? Work out and don’t eat carbohydrates after working out.


STRRIDE-AT/RT – Exercise Study

I was considering dropping CrossFit in favor of a strength program when I came across an interesting study which compared Aerobic Training (AT) to Resistance Training (RT) for impact on Metabolic Syndrome (MS). (September 15, 2011, Volume 108, Issue 6, Pages 838–844. Comparison of Aerobic Versus Resistance Exercise Training Effects on Metabolic Syndrome (from the Studies of a Targeted Risk Reduction Intervention Through Defined Exercise – STRRIDE-AT/RT. Lori A. Bateman, Cris A. Slentz, PhD, Leslie H. Willis, MS, A. Tamlyn Shields, MS, Lucy W. Piner, MS, Connie W. Bales, PhD, RD, Joseph A. Houmard, PhD, William E. Kraus, MD.)

AT/RT induced a significant improvement in the MS z score (p = 0.004) and AT alone exhibited a trend toward improvement (p <0.07). However, RT alone failed to significantly alter the MS z score.

My conclusion is to stick with CrossFit and work in the resistance training as often as reasonable as an accessory to CrossFit.

Another view of the same data (J Appl Physiol (1985). 2015 Jun 15;118(12):1474-82. The effects of aerobic, resistance, and combination training on insulin sensitivity and secretion in overweight adults from STRRIDE AT/RT: a randomized trial. Abou Assi H, Slentz CA, Mikus CR, Tanner CJ, Bateman LA, Willis LH, Shields AT, Piner LW, Penry LE, Kraus EA, Huffman KM, Bales CW, Houmard JA, Kraus WE.). Conclusion:

AT/RT resulted in greater improvements in insulin sensitivity, β-cell function (disposition index), and glucose effectiveness than either AT or RT alone (all P < 0.05). Approximately 52% of the improvement in insulin sensitivity by AT/RT was retained 14 days after the last exercise training bout. Neither AT or RT led to acute or chronic improvement in sensitivity index. In summary, only AT/RT (which required twice as much time as either alone) led to significant acute and sustained benefits in insulin sensitivity.

Yet another look at the same data (Am J Physiol Endocrinol Metab. 2011 Nov;301(5):E1033-9. doi: 10.1152/ajpendo.00291.2011. Epub 2011 Aug 16.
Effects of aerobic vs. resistance training on visceral and liver fat stores, liver enzymes, and insulin resistance by HOMA in overweight adults from STRRIDE AT/RT. Slentz CA, Bateman LA, Willis LH, Shields AT, Tanner CJ, Piner LW, Hawk VH, Muehlbauer MJ, Samsa GP, Nelson RC, Huffman KM, Bales CW, Houmard JA, Kraus WE.) concluded:

AT was more effective than RT at improving visceral fat, liver-to-spleen ratio, and total abdominal fat (all P < 0.05) and trended toward a greater reduction in liver fat score (P < 0.10). The effects of AT/RT were statistically indistinguishable from the effects of AT. These data show that, for overweight and obese individuals who want to reduce measures of visceral fat and fatty liver infiltration and improve HOMA and alanine aminotransferase, a moderate amount of aerobic exercise is the most time-efficient and effective exercise mode.

Yet another view (Arch Intern Med. 2004 Jan 12;164(1):31-9. Effects of the amount of exercise on body weight, body composition, and measures of central obesity: STRRIDE–a randomized controlled study. Slentz CA1, Duscha BD, Johnson JL, Ketchum K, Aiken LB, Samsa GP, Houmard JA, Bales CW, Kraus WE.):

In nondieting, overweight subjects, the controls gained weight, both low-amount exercise groups lost weight and fat, and the high-amount group lost more of each in a dose-response manner. These findings strongly suggest that, absent changes in diet, a higher amount of activity is necessary for weight maintenance and that the positive caloric imbalance observed in the overweight controls is small and can be reversed by a modest amount of exercise. Most individuals can accomplish this by walking 30 minutes every day.

Note none of the results were comparable to the effect on the metabolic syndrome from the Low Carb High Fat diet.

Jason Phillips – Anti-keto Crusader

For some dumb reason I’ve started to listen to podcasts with Jason Phillips. He’s a macros diet guy. They maybe have even turned the generic word macros into a trademark or something.

My main objection to much of this sort of material is to take the dietary advise of someone who advises top athletes. At first blush it seems like you’d want to fuel your workout like the top athlete but you are doing nothing remotely similar to what they do for daily volume. So to say that nobody who is a top athlete in CrossFit does Paleo is not all that relevant to me as a local participant in CrossFit.

Phillips has a video against Paleo and keto diet on YouTube where he claims that the flight or fight response of intense exercise like Crossfit can only be handled by eating carbohydrates.

His claim is that you don’t get insulin from eating proteins and fats. It is true that the body does not produce much of an Insulin response to fats. But his claim is not true in the case of protein. In fact, your body has as much of a response to protein as it does to carbohydrates when it comes to using Insulin.

From (Effect of Protein Ingestion on the Glucose Appearance Rate in People with Type 2 Diabetes. M. C. Gannon J. A. Nuttall G. Damberg V. Gupta F. Q. Nuttall. The Journal of Clinical Endocrinology & Metabolism, Volume 86, Issue 3, 1 March 2001, Pages 1040–1047):

When beef was ingested there was a prompt rise in mean insulin concentration (∼3-fold). … at 2.5 h, the insulin concentration was still at a maximum at that time. The insulin concentration did not return to a fasting value until 7 h after the meal (Fig. 2).

In fact, your body creates Glucose out of protein. From the same page:

ALL OF THE amino acids commonly found in proteins can, at least in part, be converted into glucose, with the exception of leucine. Indeed, conversion of amino acids derived from either endogenous or exogenous proteins is the major source of new glucose formation