How Much Protein on Low Carb Diets?

The DRI (Dietary Reference Intake) is 0.8 grams of protein per kilogram of body weight, or 0.36 grams per pound.  This amounts to:

* 56 grams per day for the average sedentary man.
* 46 grams per day for the average sedentary woman.

As I noted in a prior post (Overfeeding Studies) minimum protein requirements are determined by nitrogen studies which typically give standard diets with adjusted protein contents until excess nitrogen is produced in the urine. This indicates that the person is in a positive protein intake since the excess protein is being expelled as urea (nitrogen).

The problem is the standard diet is used for the baseline which includes carbohydrates. In the standard diet glucose needs are completely met from carbohydrates. In a Low Carb diet glucose needs come from fat and protein in the diet (via GNG).

It is important to determine if the Dietary Recommended Intake (DRI) for protein is adequate for people on a Low Carb Diet (Protein Intake – How Much Protein Should You Eat Per Day?).

So how should we determine if those are adequate levels for a person on a low carb diet? Protein Sparing Modified Fasts (PSMF) are low carb diets which also are low fat. They are typically higher levels of protein with the intent of preserving Lean Body Mass (LBM) in the face of a high caloric deficit. There is a study which determined the Protein needs via nitrogen balance on the PSMF diet (Bruce R Bistrian, George L Blackburn, Jean-Pierre Flatt, Jack Sizer, Nevin S Scrimshaw, Mindy Sherman. Nitrogen Metabolism and Insulin Requirements in Obese Diabetic Adults on a Protein-Sparing Modified Fast. Diabetes Jun 1976, 25 (6) 494-504).

 In the three patients who had extensive nitrogen-balance studies, balance could be maintained chronically by 1.3 gm. protein per kilogram IBW, despite the gross caloric inadequacy of the diet. 

This seems like a reasonable approximation for the minimal protein needs on a Low Carbohydrate Diet. The number 1.3g/kg of body weight is significantly more than 0.8g/kg of body weight. A 200 lb (100kg) person would need to eat a minimum of 130g of protein a day.

Here is a similar view from Dr Donald Layman (Donald K. Layman; The Role of Leucine in Weight Loss Diets and Glucose Homeostasis, The Journal of Nutrition, Volume 133, Issue 1, 1 January 2003, Pages 261S–267S).

More recently, the overall contribution of dietary amino acids to glucose homeostasis received further support on the basis of quantitative evaluations of hepatic glucose production. Jungas et al. provided an elegant argument that amino acids serve as a primary fuel for the liver and the primary carbon source for hepatic GNG. Other investigators extended this thinking with the findings that endogenous glucose production in the liver is a critical factor in maintenance of blood glucose. After an overnight fast, GNG provides 70% of hepatic glucose release, with amino acids serving as the principal carbon source. These studies provide further evidence for a linkage between dietary protein and glucose homeostasis.

Continuing…

…a diet with low carbohydrates and increased protein would reduce the role of insulin in managing acute changes in blood glucose and maximize the liver’s role in regulating blood glucose through hepatic GNG.

We need additional protein in a low carb diet to provide the substrate for GNG.

A Tale of Two Breakfasts

Some people have Bulletproof coffee for breakfast. For myself, I eat four eggs and four pieces of bacon for breakfast. What’s the nutritional difference between the two meals?

Here is the nutritional facts for Bulletproof coffee compared to 4 Eggs and 4 slices of bacon.

The calories are nearly identical. The energy cost of eating protein (about 35%) more than offsets the small number of calories more in the bacon and eggs. There’s almost no energy cost to eating fat (around 95% gets stored).

The Bulletproof Coffee recipe is almost all fat. The bacon and eggs breakfast provides a nearly matched number of fat and protein grams.

Protein Components in the Bacon/Eggs

The protein components of the bacon and eggs are:

I specifically selected the ingredients to meet the Leucine Threshold for Muscle Protein Synthesis. It is valuable to hit this threshold after the overnight fast.

What About Vitamins?

Once again, bacon and eggs for the win. The complaint could then be made that vitamins are fat soluble. The beauty of the bacon and eggs breakfast is that there’s still plenty of fat.

Carbs, Not Saturated Fats, Increase Fat in Blood

Interesting study that gradually increased carbs and decreased fats shows that fats don’t increase fat in the blood, but carbs do (Volk BM, Kunces LJ, Freidenreich DJ, Kupchak BR, Saenz C, et al. (2014) Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLOS ONE 9(11): e113605.).

Sixteen adults with metabolic syndrome (age 44.9±9.9 yr, BMI 37.9±6.3 kg/m2) were fed six 3-wk diets that progressively increased carbohydrate (from 47 to 346 g/day) with concomitant decreases in total and saturated fat. Despite a distinct increase in saturated fat intake from baseline to the low-carbohydrate diet (46 to 84 g/day), and then a gradual decrease in saturated fat to 32 g/day at the highest carbohydrate phase, there were no significant changes in the proportion of total SFA in any plasma lipid fractions. Whereas plasma saturated fat remained relatively stable, the proportion of palmitoleic acid in plasma triglyceride and cholesteryl ester was significantly and uniformly reduced as carbohydrate intake decreased, and then gradually increased as dietary carbohydrate was re-introduced.

The Carbohydrate-Insulin Model of Obesity

Here’s a very fresh study published in JAMA (David S. Ludwig, MD, PhD; Cara B. Ebbeling, PhD. The Carbohydrate-Insulin Model of Obesity: Beyond “Calories In, Calories Out”JAMA Intern Med. Published online July 2, 2018.). From the abstract:

According to the carbohydrate-insulin model (CIM) of obesity, recent increases in the consumption of processed, high–glycemic-load carbohydrates produce hormonal changes that promote calorie deposition in adipose tissue, exacerbate hunger, and lower energy expenditure.

Basic and genetic research provides mechanistic evidence in support of the CIM. In animals, dietary composition has been clearly demonstrated to affect metabolism and body composition, independently of calorie intake, consistent with CIM predictions.

Meta-analyses of behavioral trials report greater weight loss with reduced-glycemic load vs low-fat diets, though these studies characteristically suffer from poor long-term compliance.

Feeding studies have lacked the rigor and duration to test the CIM, but the longest such studies tend to show metabolic advantages for low-glycemic load vs low fat diets.

Beyond the type and amount of carbohydrate consumed, the CIM provides a conceptual framework for understanding how many dietary and nondietary exposures might alter hormones, metabolism, and adipocyte biology in ways that could predispose to obesity.

Pending definitive studies, the principles of a low-glycemic load diet offer a practical alternative to the conventional focus on dietary fat and calorie restriction.

Here’s a good graphic from the paper:

Worth a read.

 

One of the Good Guys – Dr. Benjamin Bikman

I’ve spent too much time covering the keto hucksters (OK, mostly just Jimmy Moore but he’s a big enough target) so I thought I’d switch it up and look at one of the good guys – Dr. Benjamin Bikman (our YouTube playlist of Dr Bikman). I mentioned Ben in (Great BLOGs). He is a PhD who teaches at BYU and he’s got a lot to say about Protein over at his InsulinIQ site.

Here’s a video (High Intensity Health Episode 200) where he is interviewed.

Ben is one of the folks who came to nutrition from the exercise side. Ben really gets it about Insulin and obesity.

A video on Insulin and Glucagon.

 

The Big Fat Hack – Day 4

Jimmy Moore is doing a big fat hack. He’s on day 4. And Jimmy is producing more drama than ketones at this point.

Jimmy’s claim to have developed glucagon resistance is a curious one. Jimmy may have actually dropped his glycogen stores down to where there’s not enough glycogen to convert to glucagon when needed. Since Jimmy eats low protein he lacks protein as a substrate for GNG.

We know that Jimmy does everything possible to keep GNG from refilling his glycogen stores (other than stop eating fat). Does Low Carb PLUS Low Protein create a problem in refilling glycogen? This article has the clues (Glycogen Stores in Low Carb).

If that’s the case it really could be true that Jimmy’s low blood sugar isn’t met by glucagon. Equally, I don’t know how someone could differentiate between glucagon resistance and a lack of production of glucagon.

Jimmy’s ketones and blood sugar were:

Here’s Jimmy’s recovery strategy. Note the strategic placement of the F-Bomb products (one of the products Jimmy Moore promotes).

Looks like the big fat hack may have stopped his big fat hack.

Low Fat Vs Low Carb

Interesting one year long study to compare low fat and “low-carb” diets points out the effect of individual variability on dietary results (Gardner CD, Trepanowski JF, Del Gobbo LC, Hauser ME, Rigdon J, Ioannidis JPA, Desai M King AC. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion: The DIETFITS Randomized Clinical Trial. JAMA. 2018 Feb 20;319(7):667-679.). The study was a

…randomized clinical trial included 609 adults aged 18 to 50 years without diabetes with a body mass index between 28 and 40

The study looked at the two diets with respect to three categories:

weight change

genotype pattern

insulin secretion

The results were surprising (from my perspective).

…weight change over 12 months was not significantly different for participants in the HLF diet group (−5.3 kg) vs the HLC diet group (−6.0 kg),

there was no significant diet-genotype interaction

[there was no significant ] diet-insulin interaction

Genetic Distribution in this Study Population

This may be the most interesting result from this large population group. The distribution of low-fat and low-carb genotypes were 40% vs 30%.

  • 244 [40%] had a low-fat genotype;
  • 180 [30%] had a low-carbohydrate genotype

The genetic tests were for  (Dieting With A New Twist — A Double Helix):

3 genes (PPARG, ADRB2, and FABP2)  that are involved with fat and carbohydrate metabolism

Here is a critique of the genes that the study selected by the Genetic testing company (Arivale responds to DIETFITS study in Journal of American Medical Association (JAMA)).

The DIETFITS study considered three genetic variants in their analysis: FABP2 (rs1799883), PPARG (rs1801282), and ADRB2 (rs1042714). It is unclear why the investigators chose these specific genetic variants given that other variants also had evidence of gene/diet interaction at the time the study was designed.

Further, it appears that the investigators weighted each variant equally in their genetic model, regardless of the strength of the evidence or other factors. This may have affected the study outcomes, as which genetic variants are included in a genetic risk profile and how they are individually weighted is likely to play a role in what findings emerge.

Dietary Macronutrient Contents

This was not a ketogenic diet study by any stretch of the imagination.

In the HLF vs HLC diets, respectively, the mean 12-month macronutrient distributions were 48% vs 30% for carbohydrates, 29% vs 45% for fat, and 21% vs 23% for protein.

A well formulated ketogenic diet would have had 5% of calories from carbohydrates 20-30% from protein and the remainder 65-75% from fat.

[2018-06-20: Interesting commentary here – Registered Dietitian Health Educators: how fat do you want to get?].

Insulin Sensitivity

Insulin sensitivity was done with an Oral Glucose Tolerance Test (Dieting With A New Twist — A Double Helix).

…the study participants were administered an oral glucose tolerance test*, and their patterns and amounts of insulin secreted in response to a 75-gram glucose challenge were determined — the 30-minute response was used as an indicator of carbohydrate sensitivity

Not a surprise that there was no correlation of insulin sensitivity levels and weight loss. This was due to the high level of the low-carbohydrate diet. Assuming 2,000 calories and 30% of calories from carbs would have been 600 calories from carbs or 150 grams from carbohydrates. This is too high of a level to be all that effective in dropping Insulin levels.

Insulin Sensitivity and Diet Type

Another study specifically looked at Insulin Sensitivity vs diet type (Cornier MA1, Donahoo WT, Pereira R, Gurevich I, Westergren R, Enerback S, Eckel PJ, Goalstone ML, Hill JO, Eckel RH, Draznin B. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women. Obes Res. 2005 Apr;13(4):703-9.).

Obese nondiabetic insulin-sensitive (Si) (fasting insulin < 10 microU/mL; n = 12) and obese nondiabetic insulin-resistant (fasting insulin > 15 microU/mL; n = 9) women (23 to 53 years old) were randomized to either a high carbohydrate (CHO) (HC)/low fat (LF) (60% CHO, 20% fat) or low CHO (LC)/high fat (HF) (40% CHO, 40% fat) hypocaloric diet. Primary outcome measures after a 16-week dietary intervention were: changes in body weight (BW), Si, resting metabolic rate, and fasting lipids.

The results were interesting:

Insulin-sensitive (Si) women on the HC/LF diet lost 13.5 +/- 1.2% (p < 0.001) of their initial BW, whereas those on the LC/HF diet lost 6.8 +/- 1.2% (p < 0.001; p < 0.002 between the groups). In contrast, among the insulin-resistant women, those on the LC/HF diet lost 13.4 +/- 1.3% (p < 0.001) of their initial BW as compared with 8.5 +/- 1.4% (p < 0.001) lost by those on the HC/LF diet (p < 0.04 between two groups).

The state of Si determines the effectiveness of macronutrient composition of hypocaloric diets in obese women. For maximal benefit, the macronutrient composition of a hypocaloric diet may need to be adjusted to correspond to the state of Si.

The Great Noakes-McDonald Debate

One of my new favorite podcasts is the Sigma Nutrition Radio Podcast.

Podcast 210 was a debate between Dr. Tim Noakes and Martin McDonald. It was conducted in a gentlemanly way. Given the personality of Tim Noakes it is hard to imagine it not being handled that way.

The subject was Insulin Resistance and the effectiveness of the Low Carb diet compared to other interventions. Both sides had good points but to my way of thinking Dr. Noakes clearly won the debate.

Both sides pointed to studies (linked on the page above).

How Type 2 Diabetics Gain Weight on Insulin

This study looks at how a Diabetic is affected strongly by taking Insulin (A. Franssila-Kallunki, L. Groop. Factors associated with basal metabolic rate in patients with Type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia; October 1992, Volume 35, Issue 10, pp 962–966.). The study looked at:

66 Type 2 (non-insulin-dependent) diabetic and 24 healthy age- and weight-matched control subjects…

The interesting part is that some of the diabetics were looked at both before and after insulin therapy.

Eight Type 2 diabetic patients were re-studied after a period of insulin therapy.

In the following analysis, take note that the group put on Insulin therapy was a subset of the original group of Diabetics so their numbers were different (more exaggerated) from the rest of the Diabetics group.

Weight Gain on Insulin

The group on the Insulin treatment saw their BMI increase from 28.2 to 29.6 kg/m^2.

Basal Metabolic Rate

The control and Diabetics groups were weight matched. Surprisingly, the BMR in the Diabetics was 13% higher than the control group:

Basal metabolic rate was higher in Type 2 diabetic patients than in control subjects (102.8 ± 1.9 J · kg LBM−1-min−1 vs 90.7 ± 2.8 J · kg LBM−1;min−1; p<0.01)

Insulin treatment reduced the BMR of the Diabetics (115.5 ± 5.6 to 103.1 ± 5.7). It is question begging whether the lowered BMR caused the BMI increase with Insulin.

Diabetics Produce More Glucose

Not surprisingly the Type 2 Diabetics were producing glucose from their livers at significantly higher rates than the control group.

 The basal rate of hepatic glucose production was higher in Type 2 diabetic patients than in control subjects (1044.0 ± 29.9 vs 789.3 ± 41.7 μmol/min; p <0.001)

Insulin therapy decreased glucose production (1133 ± 92 to 983 ± 80). In theory this is good. A possible explanation of the effect of Insulin is that it took more insulin to overcome the Insulin Resistance of the liver. Insulin therapy isn’t a great long term solution, though, since the liver will eventually become even more Insulin Resistant and require ever increasing levels of exogenous Insulin.

Insulin Therapy Reduced Fat Oxidation Rate

The fat oxidation of the Diabetics was reduced when Insulin therapy was added:

Lipid oxidation was increased in Type 2 diabetic patients compared with control subjects (1.68 ± 0.05 vs 1.37 ± 0.08 μmol · kg LBM−1 · min−1‘; p <0.01) and decreased significantly after insulin therapy (p<0.05).

The lipid oxidation rate fell from 2.1 ± 0.1 to 1.4 ± 0.1 with the addition of Insulin therapy. A key phrase in the discussion section is:

lipid oxidation accounted for the major part of the BMR

So, putting someone on Insulin reduces their fat oxidation rate. If Type 2 Diabetes is a problem of fat build-up then Insulin therapy isn’t helping. It’s making Diabetics fatter. Yes, it is driving down Serum Glucose levels in the short term.

Fasting Insulin

Of note is the difference in the Fasting Serum Insulin levels between the Diabetics (64 ± 5) and the control group (37 ± 4).

The subset of the Diabetics put on Insulin therapy had higher Fasting Insulin levels than the lumped group of all diabetics. With the addition of exogenous Insulin therapy the Fasting Serum Insulin levels in the Diabetic (subset) increased from 84 to 132.

That would, of course, indicate that the part of the Diabetics group that was not put on Insulin had a much lower fasting Insulin level. This is interesting given that the error bar was ±5 so the group put on Insulin therapy at 84 +± 11 was many standard deviations out of the entire group.

The paradox here is that even with higher fasting insulin levels the fat oxidation rate in the diabetics indicates that the additional fasting insulin levels didn’t seem to stop the diabetics from being able to burn fat. The paradox is that the fat oxidation rate decreased with Insulin Therapy which would indicate the opposite conclusion.

This fits the hypothesis that Insulin Resistance in the liver is a primary driver rather than insulin resistance in adipose cells.

Calories out is much more complicated than just a number on a paper.