Too Much Protein?

Here’s an interesting study on protein overfeeding (Jose Antonio, Corey A Peacock, Anya Ellerbroek, Brandon Fromhoff and Tobin Silver. The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. Journal of the International Society of Sports Nutrition 2014:11:19.).

The HP group consumed significantly more protein and calories pre vs post (p < 0.05). Furthermore, the HP group consumed significantly more protein and calories than the CON (p < 0.05). The HP group consumed on average 307 ± 69 grams of protein compared to 138 ± 42 in the CON. When expressed per unit body weight, the HP group consumed 4.4 ± 0.8 g/kg/d of protein versus 1.8 ± 0.4 g/kg/d in the CON. There were no changes in training volume for either group. Moreover, there were no significant changes over time or between groups for body weight, fat mass, fat free mass, or percent body fat.

Consuming 5.5 times the recommended daily allowance of protein has no effect on body composition in resistance-trained individuals who otherwise maintain the same training regimen. This is the first interventional study to demonstrate that consuming a hypercaloric high protein diet does not result in an increase in body fat.

Here’s the table for the data (BW= Body Weight, FFM = Fat Free Mass, FM = Fat Mass, BF = Body Fat percentage).

Body composition









BW (kg)

76.4 ± 9.9

77.2 ± 9.9

0.8 ± 1.6

71.8 ± 12.2

73.5 ± 12.5

1.7 ± 1.9

FFM (kg)

65.2 ± 11.7

66.5 ± 11.7

1.3 ± 2.0

59.5 ± 10.9

61.4 ± 11.6

1.9 ± 2.4

FM (kg)

11.2 ± 4.7

11.4 ± 5.0

0.3 ± 4.7

12.3 ± 7.0

12.0 ± 6.2

−0.2 ± 2.2

% BF

15.1 ± 6.9

14.2 ± 6.9

−0.9 ± 1.7

16.9 ± 8.3

16.3 ± 7.5

−0.6 ± 2.6

The High Protein group actually lose body fat and gained fat free mass in spite of overeating Protein and calories.

From the paper:

The results of the current investigation do not support the notion that consuming protein in excess of purported needs results in a gain in fat mass. Certainly, this dispels the notion that ‘a calorie is just a calorie.’ That is, protein calories in ‘excess’ of requirements are not metabolized by the body in a manner similar to carbohydrate.


Low Carb Maintenance Plans

It seems like there are [at least] three basic ideas of how to implement maintenance on Low Carb. I picked representatives of each of three and look at their methodology for maintenance. Each of these three has their merits and downsides.

Dr Atkins – Titrate Carbs

Sometimes the first idea is the right idea and Dr Atkins sure did suffer a lot of slings and arrows in his day. He was tormented even in death by his opponents. I did his diet back in the 1990s and did well for over a year on it. I tapped out due to heart rhythm issues which seem to be recurring now (PVCs in particular). I think they are likely electrolyte imbalances. (Later note: See this post for my current strategy which seems to be working].

The Atkins diet starts with a 2 week induction period at 20g of carbs a day and then increases. At maintenance, the person is supposed to work up to their personal carb limit and remain at that level with an occasional adjustment if they go too far off the rails.

This approach might work well for some. It worked OK for me and at least taught me to avoid really stupid amounts of carbs but I never went below about 228 lbs before I transitioned over to maintenance carbs.

Later on, my Insulin pump data showed my average was 200 grams of carbs a day before I got off Insulin which is less than SAD and proof that I did learn something about carbs back when I was on Atkins. But, clearly 200 g of carbs was above my personal threshold. And there’s good evidence that 100 g is probably too much, too.

Carbs have a way of sneaking back in and this method is a way to get back on the blood sugar roller coaster for some. Above some point the benefits of the keto diet get lost because carb cravings get stoked. Plus it is difficult to add carbs and keep them clean carbs. It’s really easy to add back in junk carbs.

Dr Berstein – Titrate Protein

Dr Bernstein is a Diabetic Type 1 medical doctor who is also a pioneer. Bernstein recognizes the problems with titrating down carbs in his patients. Here is Bernstein’s own words (from 2015):

Bernstein – “When we want to halt weight loss we increase protein“.

I think Bernstein nicely addresses the problems with bringing back in carbs but I don’t think his method works for me. I’ve essentially done it when I did carnivore and I kept losing weight in spite of eating a lot more protein. It might work for others. My normal diet gives me enough substrate for GNG (which is demand driven) plus substrate for Muscle Protein Synthesis. Beyond some point Protein just gets eliminated via urea.

The reason this is ineffective may be that increasing protein over my normal diet significantly has a very marginal effect on FQ. Holding carbs constant (22.8g) and fat constant (191g) and taking my Protein from 179 to 300 only takes my FQ from 0.740 to 0.749 at the expense of a whole lot more protein.

Dr Ted Naiman – Balance Energy (P:NPE)

Dr Ted takes a unique approach which seeks to take into account the strengths of both of the previous methods. His method is to balance the energy from protein with the non-protein energy (in terms of grams of each not in terms of calories). His formula is essentially 30% of calories from Protein and 70% from fat and carbs. His method keeps ketogenic levels of carbs (20 or 30 or less a day) from good sources and avoids carb cravings that come with higher carb levels (no blood sugar roller coaster).

I Picked Dr. Ted

I am currently trying Dr Ted’s method. His method sets the Protein grams to body weight in lbs. I am currently 169 lbs, so if I want to stay in the 165-175 lbs range (nominal 170 lbs) I need to eat 170g of protein a day. That would be matched with 20 grams of carbs and 150g of fat a day. That is a FQ of 0.744-0.745. That is slightly more than my current 0.740 from last week.

P:NPE Balanced
FQ g cals portion cals Numer. Denom.
Carbs 20 80 0.032 0.0071 0.0071
Fat 145-155 1305-1395 0.52-.56 0.0817 0.1161
Protein 165-175 660-700 0.26-.28 0.0562 0.0708
Total 2045-2175 0.1450 0.1940
FQ 0.744-0.745

I am interested to see how this works out since that’s a lower total calorie count than I have been eating (and I was still losing weight). I was at an average of 2526 calories a day last week and my starting/ending weights were the same.

Dr. Ted’s method doesn’t adjust up or down for physical activity. I will do this for a month and see how it works out. If I drop below 165 lbs for any extended period I will evaluate whether I need to increase calories or not.


Protein and Metabolic Syndrome

Another study (Obes Facts. 2017 Jul; 10(3): 238–251. Effect of a High-Protein Diet versus Standard-Protein Diet on Weight Loss and Biomarkers of Metabolic Syndrome: A Randomized Clinical Trial. Ismael Campos-Nonato, Lucia Hernandez, and Simon Barquera) on protein and the Metabolic Syndrome. The study was a:

Randomized controlled trial in 118 adults aged 47.4 ± 11.5 years and meeting the established criteria for MeS were randomized to prescribed hypocaloric diets (500 kcal less than resting metabolic rate) providing either 0.8 g/kg body weight (standard protein diet (SPD)) or 1.34 g/kg body weight (higher protein diet (HPD)) for 6 months.

Was there a downside to higher protein diet?

There were 105 subjects (51 for SPD and 54 for HPD) who completed the trial. Overall weight loss was 5.1 ± 3.6 kg in the SPD group compared to 7.0 ± 3.7 kg in the in HPD group. Both groups lost a significant percent of centimeters of waist circumference (SPD −6.5 ± 2.6 cm and HPD −8.8 ± 2.6 cm). There was no statistical difference Except for the varying weight losses the two groups did not show any further differences overall. However in the subgroup judged to be adherent more than 75% of the time with the prescribed diets, there was a significant difference in mean weight loss (SPD −5.8% vs. HPD −9.5%) after adjusting for baseline BMI.

Both groups demonstrated significant decreases in waist circumference, glucose, insulin, triglycerides, and VLDL cholesterol, but there were no differences between the groups. There were no changes in blood tests for liver or renal function.

Good result for higher protein.

Insulin Resistance – Everything You Want to Know and Probably a Lot More

A great write-up on Insulin Resistance (Clin Biochem Rev. 2005 May; 26(2): 19–39. Insulin and Insulin Resistance. Gisela Wilcox).  It is not an understatement that the paper says:

…More than a century after scientists began to elucidate the role of the pancreas in diabetes, the study of insulin and insulin resistance remain in the forefront of medical research, relevant at all levels from bench to bedside and to public health policy

First some definitions:

Insulin resistance is defined where a normal or elevated insulin level produces an attenuated biological response; classically this refers to impaired sensitivity to insulin mediated glucose disposal.

Compensatory hyperinsulinaemia occurs when pancreatic β cell secretion increases to maintain normal blood glucose levels in the setting of peripheral insulin resistance in muscle and adipose tissue.

Insulin resistance syndrome refers to the cluster of abnormalities and related physical outcomes that occur more commonly in insulin resistant individuals. Given tissue differences in insulin dependence and sensitivity, manifestations of the insulin resistance syndrome are likely to reflect the composite effects of excess insulin and variable resistance to its actions.

Metabolic syndrome represents the clinical diagnostic entity identifying those individuals at high risk with respect to the (cardiovascular) morbidity associated with insulin resistance.

Interesting graphic (major pathways and influences on insulin secretion):

Here’s why Low Carb works so well:

Glucose is the principal stimulus for insulin secretion

Pancreatic β cells secrete 0.25–1.5 units of insulin per hour during the fasting (or basal) state, sufficient to enable glucose insulin-dependent entry into cells. This level prevents uncontrolled hydrolysis of triglycerides and limits gluconeogenesis, thereby maintaining normal fasting blood glucose levels. Basal insulin secretion accounts for over 50% of total 24 hour insulin secretion. … In healthy lean individuals circulating venous (or arterial) fasting insulin concentrations are about 3–15 mIU/L or 18–90 pmol/L

At rest we don’t need glucose for our muscles.

Muscle cells do not rely on glucose (or glycogen) for energy during the basal state, when insulin levels are low. Insulin suppresses protein catabolism while insulin deficiency promotes it, releasing amino acids for gluconeogenesis.

Perhaps of importance to low carb eaters a low level of glucose may produce a lower level of protein synthesis due to its similarity with starvation:

In starvation, protein synthesis is reduced by 50%. hilst data regarding a direct anabolic effect of insulin are inconsistent, it is clearly permissive, modulating the phosphorylation status of intermediates in the protein synthetic pathway.

In insulin resistance, muscle glycogen synthesis is impaired

We get fatter via:

Intracellular glucose transport into adipocytes in the postprandial state is insulin-dependent via GLUT 4; it is estimated that adipose tissue accounts for about 10% of insulin stimulated whole body glucose uptake.

As relates to low carb diets:

Insulin stimulates glucose uptake, promotes lipogenesis while suppressing lipolysis, and hence free fatty acid flux into the bloodstream.

As adipocytes are not dependent on glucose in the basal state, intracellular energy may be supplied by fatty acid oxidation in insulin-deficient states, whilst liberating free fatty acids into the circulation for direct utilization by other organs e.g. the heart, or in the liver where they are converted to ketone bodies.

Ketone bodies provide an alternative energy substrate for the brain during prolonged starvation.


…glucose uptake into the liver is not insulin-dependent

Another interesting section:

Whilst in insulin deficiency, e.g. starvation, these processes are more uniformly affected, this is not necessarily the case with insulin resistance. Compensatory hyperinsulinaemia, differential insulin resistance and differential tissue requirements may dissociate these processes. Resistance to insulin’s metabolic effects results in increased glucose output via increased gluconeogenesis (as in starvation), however, unlike starvation, compensatory hyperinsulinaemia depresses SHBG production and promotes insulin’s mitogenic effects. Alterations in lipoprotein metabolism represent a major hepatic manifestation of insulin resistance. Increased free fatty acid delivery, and reduced VLDL catabolism by insulin resistant adipocytes, results in increased hepatic triglyceride content and VLDL secretion. Hepatic synthesis of C-reactive protein, fibrinogen and PAI-1 is induced in response to adipocyte-derived pro-inflammatory cytokines such as TNFα and IL-6. Insulin may also increase factor VII gene expression.

Other factoids:

The insulin resistance syndrome describes the cluster of abnormalities which occur more frequently in insulin resistant individuals. These include glucose intolerance, dyslipidaemia, endothelial dysfunction and elevated procoagulant factors, haemodynamic changes, elevated inflammatory markers, abnormal uric acid metabolism, increased ovarian testosterone secretion and sleep-disordered breathing. Clinical syndromes associated with insulin resistance include type 2 diabetes, cardiovascular disease, essential hypertension, polycystic ovary syndrome, non-alcoholic fatty liver disease, certain forms of cancer and sleep apnoea.

Good write-up on Diabetes:

Compensatory hyperinsulinaemia develops initially, but the first phase of insulin secretion is lost early in the disorder. Additional environmental and physiological stresses such as pregnancy, weight gain, physical inactivity and medications may worsen the insulin resistance. As the β cells fail to compensate for the prevailing insulin resistance, impaired glucose tolerance and diabetes develops. As glucose levels rise, β cell function deteriorates further, with diminishing sensitivity to glucose and worsening hyperglycaemia. The pancreatic islet cell mass is reported to be reduced in size in diabetic patients; humoral and endocrine factors may be important in maintaining islet cell mass



Flexible Dieting and IIFYM

There’s a concept out there that is termed Flexible Dieting or IIFYM (If it fits your macros). It promises no limits to the types of food you can eat.

Nuts and Bolts of Flexible Dieting

The system is basically this.

  • Calculate TDEE
  • Determine macro ratios (typically from Zone 30/30/40 ratios)
  • Eat to your macros every day (no more, no less)

“Positives” of IIFYM

IIFYM has some obvious benefits. With it you can  “eat whatever you want”. If you want pizza, as long as it fits your macros you can eat it. Same goes for ice cream, etc. Anything you want just not in quantities which will push you past your macros.

Although there is no calorie counting but you weigh/count the surrogates of protein/fat/carb macros. IIFYM macros are typically higher protein than the Standard American Diet (SAD) so they tend to produce good results.

They also tend to be lower than the SAD in carbohydrates which has a positive benefit. And they limit the carbohydrates in quantity which may be the first time someone who tries the diet has ever limited their carbs. This is a way to learn portion control perhaps without feeling like you are not getting something you really want (like cake, ice cream or pasta).

IIFYM requires measurement and recording of food and tracking macros daily. It emphasizes day-to-day consistency in eating which may (or may not) be beneficial. You can use tools like MyFitnessPal or Cronometer to track your macros.

IIFYM Macro Selections

My primary concern about IIFYM is that while the initial selection of macros is great compared to the Standard American Diet (SAD) it’s only so good for someone with Metabolic Syndrome/Insulin Resistance. Setting the protein macro to 30% of calories is going to be a good thing in nearly every case (except in rare cases like kidney failure).

Dropping carb consumption is going to be good for otherwise healthy people. For the 40% of the population with Metabolic Syndrome, eating 30% of their calories from carbohydrates may lead to worsening blood sugar control and hasten the complications from diabetes.

In my case, before LCHF I was eating 200 grams a day of carbs which is about 800 calories a day. That was around 33% of my approximately 2400 calories I ate a day. Increasing my carbohydrate intake to 40% would have been 140 additional calories from carbohydrates or an addition 40 grams of carbohydrates (from 200 to 240g) that my already overloaded system would have pushed into my bloodstream.  That would have meant I would have had to take an additional 10 units of Insulin (at a minimum) and maybe more to cover the carbohydrates. Not the recipe for reducing Insulin Resistance.

Another concern is the idea that the 30/30/40 ratio is somehow a “balanced” ratio. I haven’t seen any evidence in the literature establishing this ratio as ideal in any sense of the word. In particular, the studies on diabetics I have seen show this balance is a bad balance compared to ketogenic ratios.

Fitness World and IIFYM

This approach seems to have gained traction in the fitness community where glycogen stores are important for high intensity work (CrossFit and Nutrition – Part 3). And someone who works out intensely every day can probably tolerate a higher level of carbohydrates than someone who works out much less frequently.

Micro-nutrients and IIFYM

There seems to be a de-emphasis on micronutrients/vitamins/minerals in IIFYML. For instance this article claims that there’s no such thing as clean eating (What is Flexible Dieting? Here’s How to Get Started). A gram of carbs from a twinkie and a gram of carbs from broccoli work just the same in your body. And that’s just simply false. Some carbs are slowly digested and raise blood sugar by a small amount and others send blood sugar up sky high.

Equally there are some IIFYM/Flexible Dieting sources out there who are concerned about micronutrients and vitamins. For instance, this YouTube guy who expresses the idea that micronutrients matter (Flexible Dieting 101: The Simple Facts).

This may be made more difficult to track with MyFitnessPal (MFP). I don’t use MFP but reading the process to see your micronutrients with MFP seems clumsy (Where can I find my micronutrients?).

With Cronometer I see the micronutrients every single day and know exactly where I am at for each micronutrient/vitamin/mineral.

Here are my micro nutrients (averaged for this past week although it’s the same data day-by-day).

And here are my vitamins and minerals for the week (same for the day).

Higher Carb Diets Have Lower Compliance

One thing I have observed is that higher carb level diets don’t produce good compliance beyond a very short term. That is because they really don’t blunt carb cravings like a low carb diet does. This means they still have the potential roller coaster of blood sugar spikes.

Eating Carb Macros

Trying a theoretical case with someone who weighs 200 lbs and wants to maintain their weight. That is:

  • Protein = 2000 * 30% = 600 calories or 150 g
  • Fat = 2000 * 30% = 600 calories or 67g
  • Carbs = 2000 * 40% = 800 calories or 200g

Reduced to familiar food, 150g of protein is 26 ozs of boneless, skinless chicken breast. I picked that because it is low fat and there’s no much fat on IIFYM macros. That very low fat option takes up 16 of the 67 g of fat leaving around 51g of fat for the rest of the day.

So we have 200g of protein and only 51g of fat left. If we pick a “healthy” carbohydrate like a potato.

To get to 200g of “healthy” carb choices we would need to eat almost 8 potatoes. If we put a bit of butter or olive oil on the potatoes:

We only get less than 4 tablespoons worth of olive oil and we are out of fat, carbs and protein. This might be where fruit comes in handy since fruit has a lot of carbs and little fat/protein.

Using Healthier Vegetable Choices

Let’s try replacing the potato with a low carb vegetable like broccoli:

At 6g a cup to get 200g of broccoli we’d need to eat 33 cups of broccoli. This demonstrates the difficulty of getting a lot of carbs and doing it with low carb vegetables.

Unhealthier Choices

But none of this matches the promise of IIFYM which is that you can eat whatever you want as long as it fits your macros. And today let’s say I want to eat ice cream, tacos and pizza.

My pizza Choice will be a moderate 2 slices of Little Caesar’s pizza. MFP has lower macros than Cronometer so let’s go with MFP:

What do I have left?

  • Protein = 150 – 28g = 122g
  • Fat = 67 – 22g = 45g
  • Carbs = 200 – 64g = 136g

Now I get my Ben and Jerry’s:

  • Protein = 122 – 8g = 114g
  • Fat = 45 – 25g = 20g
  • Carbs = 136 – 49g = 87g

Still a fair amount left but I haven’t had my four tacos yet.

This is where MFP numbers don’t match the company website. The Taco Bell site has:

  • Protein = 114 – (8*4) 32g = 82g
  • Fat = 20 – (9*4) 36g = -16g <<< OOPS, I’ve already gone over for fat
  • Carbs = 87 – (13*4) 52 g = 35g

This is where the rubber meets the road. I’ve not gone crazy this day. Nothing that I don’t feel like I deserve to eat. But they don’t fit my macros. So I need to only have 2 tacos. It’s lunch time and I feel pretty deprived.

  • Protein = 114 – (8*2) 16g = 98g
  • Fat = 20 – (9*2) 18g = 2g
  • Carbs = 87 – (13*2) 16 g = 16g

So I can have some carbs but I’ve got not much fat so no chips, etc. And I’ve got a whole lot of protein I still need to get in. Sounds like I will be eating two protein shakes that day. So how did I do?

  • Protein = 2000 * 30% = 600 calories or 150 g (I went over by 3g)
  • Fat = 2000 * 30% = 600 calories or 67g (I went over by 15g)
  • Carbs = 2000 * 40% = 800 calories or 200g (I ended up 75g under)

Time for a handful of jelly beans or gummy bears. Trouble is I only have 80 calories and I need to get in 75*4 = 300 calories to hit my carb number. Still not horrible for my first day.

No, don’t worry. I’m not going to do it. Just wanted to demonstrate what I see with people who eat this way. Perhaps they get better at planning and meal prep. Some of them do. And they probably have better compliance.


Objections to the Keto Diet – Part 7 – Keto is Low Protein

I would say that there is also some truth to this charge from Dietitians (Dietitians Weigh in on the Low Carb/Ketogenic Diet) . There are prominent proponents of the keto diet who do recommend what I consider to be very low levels of protein (Jason Fung, etc).

Remember that Jason Fung is a kidney doctor and his kidney dialysis patients need to be on limited protein to spare their kidney function. This is not a normal issue for most diabetics.

Studies show that the US RDA for protein are too low (Are the Protein RDA Values Enough?).  I’ve written at length on the value of protein for diabetics (High Protein Diets are Good for Type 2 Diabetics).

Keto is not inherently low protein. And a Dietitian could and should recommend higher levels of protein.


The keto community should have a protein summit and let all of the proponents debate this subject. I am convinced that if the facts get out that protein will remain king.

In the meanwhile, Dietitians can recommend ketogenic diets with the caveat that higher levels of protein are generally beneficial for diabetics.  It’s probably even more important that dietitians teach people how to know how many grams of protein that they are getting.


Protein vs Carbs

Chocolate cake is chocolate cake (carbs and fat). We know that Protein doesn’t turn into chocolate cake. But we also know that Protein does turn, at least in part, into glucose.

At what rate does Protein turn into glucose?

Turns out this question was studied a very long time ago. Nowadays, Type 1 diabetics are given guidance that when they pump Insulin they need to pump for the number of grams of carbohydrates and half the number of grams of protein. That’s a rough approximation of the results of this study (J Clin Invest. 1936 Nov; 15(6): 665–671. THE GLYCEMIC RESPONSE TO ISOGLUCOGENIC QUANTITIES OF PROTEIN AND CARBOHYDRATE. Jerome W. Conn and L. H. Newburgh.)

The study is a PDF of the original 1936 study but it demonstrates that the glucose response to protein is much less than to an equivalent amount of carbohydrates. More importantly, the response is very slow in comparison.

(1) is the blood sugar in a diabetic subject after consuming 53 grams of glucose.

(4) is the blood sugar in the same subject after consuming 485 grams of lean beef.

The paper concludes:

There’s another interesting observation in the paper:

In other words, diabetics have a larger increase in blood sugar than non-diabetics in response to protein. (Glycosuria happens when you pass blood sugar (blood glucose) into your urine.).


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.


Overfeeding Protein – Carnivore Diet

I’ve been doing the carnivore diet for the past 9 days. My weight dropped a couple of pounds and has stayed low in spite of eating a large excess of calories.

I am eating almost twice my protein macro and my blood sugars have been doing fine.

High Protein Stimulates Metabolism and Fat Doesn’t

That raises the question of whether eating too much protein results in a weight gain. Somebody actually studied the effect of overeating protein on 24-hour Energy Expenditure (24EE). (Bray GA, Redman LM, de Jonge L, Covington J, Rood J, Brock C, Mancuso S1, Martin CK, Smith SR. Effect of protein overfeeding on energy expenditure measured in a metabolic chamber. Am J Clin Nutr. 2015 Mar;101(3):496-505.). The objective was to quantify the effects of excess energy from fat or protein on energy expenditure of men and women living in a metabolic chamber.

The study reached the conclusion:

Excess energy, as fat, does not acutely increase 24EE, which rises slowly as body weight increases. Excess energy as protein acutely stimulates 24EE and SleepEE. The strongest relation with change in 24EE was the change in energy expenditure in tissue other than muscle or fat-free mass.


2018-05-31: Interesting article on overfeeding in general. Lot of good studies listed at the end. Not a Low Carb study but it points out that Protein overeating is not all that well studied.

More Protein Please

A great study shows an inverse association between Protein intake and body composition (Clin Med Insights Endocrinol Diabetes. 2010; 3: 25–35. Higher Dietary Protein Intake is Associated with Lower Body Fat in the Newfoundland Population. Kristian K. Green, Jennifer L. Shea, Sudesh Vasdev, Edward Randell, Wayne Gulliver, and Guang Sun).

Significant inverse relationships were observed between dietary protein intake (g/kg body weight/day) and weight, waist circumference, waist-to-hip ratio, BMI, %BF, and %TF (P < 0.001). Significant positive relationships were observed with %LM and %TLM (P < 0.001). Additionally, significant differences in weight (12.7 kg in men, 11.4 kg in women), BMI (4.1 BMI units in men, 4.2 units in women), and %BF (7.6% in men, 6.0% in women) were observed between low and high dietary protein consuming groups (P < 0.001). Dietary protein explained 11% of the total variation in %BF in the NL population.

This study provides strong evidence that higher protein intake, even in the absence of energy restriction, is associated with a more favorable body composition in the general population.

Eat more protein, get leaner.