What if the History of Diabetes Went Wrong?

In an interesting paper the question is asked what if the history of the development of our understanding of diabetes has it wrong? The paper (J. Denis McGarry. What If Minkowski Had Been Ageusic? An Alternative Angle on Diabetes. Science, Vol. 258, No. 5083 (Oct. 30, 1992), pp. 766-770).

Despite decades of intensive investigation, the basic pathophysiological mechanisms responsible for the metabolic derangements associated with diabetes mellitus have remained elusive. Explored here is the possibility that traditional concepts in this area might have carried the wrong emphasis. It is suggested that the phenomena of insulin resistance
and hyperglycemia might be more readily understood if viewed in the context of underlying abnormalities of lipid metabolism.
Some powerful food for thought in the paper. Another paper (Arius, Energy Metabolism) summarizes the argument as:
The author considers the possibility that the hyperinsulinemia of early non-insulin—dependent diabetes is coincident with hyperamylinemia, since insulin and amylin are cosecreted. Amylin would cause an increase in plasma lactate (Cori cycle); and lactate, a better precursor than glucose for fatty acid synthesis, would indirectly promote the production of very-low-density lipoproteins (VLDL). There would follow an increased flux of triglycerides from liver to muscle (and adipose tissue) and, as proposed and elaborated on, an increase in insulin resistance and production of many of the metabolic disturbances occurring in diabetes.
 The author of the paper draws heavily on the Randle Cycle.
The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle and adipose tissue. The cycle controls fuel selection and adapts the substrate supply and demand in normal tissues. This cycle adds a nutrient-mediated fine tuning on top of the more coarse hormonal control on fuel metabolism. This adaptation to nutrient availability applies to the interaction between adipose tissue and muscle. Hormones that control adipose tissue lipolysis affect circulating concentrations of fatty acids, these in turn control the fuel selection in muscle. Mechanisms involved in the Randle Cycle include allosteric control, reversible phosphorylation and the expression of key enzymes.[5] The energy balance from meals composed of differing macronutrient composition is identical, but the glucose and fat balances that contribute to the overall energy balance change reciprocally with meal composition.
Interesting thoughts.
Fatty acids may act directly upon the pancreatic β-cell to regulate glucose-stimulated insulin secretion. This effect is biphasic. Initially fatty acids potentiate the effects of glucose. After prolonged exposure to high fatty acid concentrations this changes to an inhibition.[13] Randle suggested that the term fatty acid syndrome would be appropriate to apply to the biochemical syndrome resulting from the high concentration of fatty acids and the relationship to abnormalities of carbohydrate metabolism, including starvation, diabetes and Cushing’s syndrome.
My own weight had been in the 280 range for a long time. In the months before I was diagnosed as Type 2 Diabetic my weight dropped 50 lbs without any lifestyle changes. After I went on Metformin my weight was relatively lower for a while. When I eventually went on Insulin my weight went up 40+ lbs fairly quickly. It is well known that Insulin adds weight.
My own thought is that the Insulin is both the lock and the key. Increased levels of Insulin pushes glucose or fat into cells and decreased levels of Insulin allows fat to come out of cells. That’s why Intermittent Fasting is such a great bullet for Type 2 diabetics. It allows our fasting Insulin levels to drop. Add to that Low Carbohydrate diets and the perfect recipe for controlling Diabetes comes into play.
The problem never really was Insufficient Insulin. The problem was too much Insulin. And clearly it is a fat related problem.

Blood Sugar Responses Compared

I asked a friend to be part of an experiment which involved him poking himself with a needle most of the morning. And he agreed. We are both fat adapted (me for 15 months and him for more than 6 months).

We both started fasted from the previous night (no breakfast for myself or my friend). We both ingested 50 g of Whey Protein (IsoPure Zero Carb Protein Powder) at the same time and measured our blood sugar responses over the course of the same morning.

I am a Type 2 Diabetic who has their Blood Sugar “under control” via diet and am no longer on meds. I am 57-years old and do some exercise (CrossFit) five times a week for the past two months.

My fried is a Tri-athlete in his mid-30’s. He’s not a Diabetic and runs frequently.

Here’s the two responses to the same amount of Whey Protein:

 

The results were very interesting.

  1. His fasted (starting) Blood Sugar number was higher than mine. We’ve compared numbers before and noted this same thing. We did not use the same meter since we were looking for relative differences not absolute values.
  2. After ingesting Protein, the Tri-athlete’s blood sugar went down. My blood sugar (the Type 2 Diabetic) went up.
  3. His Blood Sugar returned to normal much more quickly than mine (less than 2 hours. Mine took over three hours to return to normal.

I am not sure if his Blood Sugar went down due to him not having Insulin Resistance. If his Insulin went up in response to the Protein it could have driven his Blood Sugar down. Since I still have some degree of Insulin Resistance my Blood Sugar doesn’t go down nearly as well.

Support for this idea comes from (“Liver Metabolism“):

Overall, gluconeogenesis is stimulated by glucagon and
epinephrine and inhibited by insulin, as observed most
dramatically in insulin-dependent diabetes mellitus, in
which uninhibited gluconeogenesis contributes significantly
to the hyperglycemia.

Insulin favors oxidative decarboxylation of pyruvate and, therefore, also indirectly tends to diminish gluconeogenesis.

Interesting!

 

High Protein Diets are Good for Type 2 Diabetics

High Protein Diets are good at reducing NAFLD (Non-Alcoholic Fatty Liver Disease). From the study (February 2017, Volume 152, Issue 3, Pages 571–585.e8. Isocaloric Diets High in Animal or Plant Protein Reduce Liver Fat and Inflammation in Individuals With Type 2 Diabetes. Mariya Markova, Etc.):

In a prospective study of patients with type 2 diabetes, we found diets high in protein (either animal or plant) significantly reduced liver fat independently of body weight, and reduced markers of insulin resistance and hepatic necroinflammation. The diets appear to mediate these changes via lipolytic and lipogenic pathways in adipose tissue. Negative effects of BCAA or methionine were not detectable. FGF21 level appears to be a marker of metabolic improvement.

And from the conclusions section:

Postprandial levels of BCAAs and methionine were significantly higher in subjects on the AP vs the PP diet. The AP and PP diets each reduced liver fat by 36%−48% within 6 weeks (for AP diet P = .0002; for PP diet P = .001). These reductions were unrelated to change in body weight, but correlated with down-regulation of lipolysis and lipogenic indices. Serum level of FGF21 decreased by 50% in each group (for AP diet P < .0002; for PP diet P < .0002); decrease in FGF21 correlated with loss of hepatic fat. In gene expression analyses of adipose tissue, expression of the FGF21 receptor cofactor β-klotho was associated with reduced expression of genes encoding lipolytic and lipogenic proteins. In patients on each diet, levels of hepatic enzymes and markers of inflammation decreased, insulin sensitivity increased, and serum level of keratin 18 decreased.

 

Protein Turns into Cupcakes?

Dr Fung makes the following statement on this webpage (Why Low Carb Is High in Fat – Not Protein):

Once again, these amino acids are absorbed into the portal circulation and directed towards the liver where excess amino acids get turned into glucose.

Turns out the process is much more complicated. To be fair Dr Fung may be simplifying the process for his readers, but the process is more like this (which is probably still an oversimplification). From (Amino Acid Metabolism and Synthesis Explained):

Amino acids that are in excess of the body’s needs are converted by liver enzymes into keto acids and urea. Keto acids may be used as sources of energy, converted into glucose, or stored as fat. Urea is excreted from everyone’s body in sweat and urine.

So it is not quite as simple as Dr Fung lays it out. And keto acids are exactly the goal of any Low Carb diet, ie, the production of ketone bodies. We know that the production of glucose from ketones is necessary to feed brain cells (and some other cells) since they don’t get glucose from carbohydrates when we are on a ketogenic diet. In the absence of any dietary carbohydrates we may actually need more Protein to fuel this very path.

Are the Low Protein LCHF folks then making a serious mistake with very low levels of Protein? Are they relying on studies for necessary Protein levels where subject were not in Ketosis? I will bet a donut they are.

What is the basis for “in excess of the body’s needs”? On what timeframe? Is that per day, meal, hour?

Another Protein Experiment

I did a previous Protein Experiment where I compared the response of my Blood Sugar to 50 grams of Whey Protein vs 50 grams of Casein Protein. Since both of those were “pure” Protein with very little fat, I was curious how those results would compare to animal protein which had fat.

For this experiment I chose Chicken Drumsticks. I weighed them amount of mean (total minus bones left at the end) and the nutritional information shows them to have been close to 50g of Protein:

Here is the Blood Glucose numbers (smoothed) over several hours added to the data from the original Whey/Casein test.  The chicken drumsticks are in yellow.

Accounting for Differences

  1. The drumsticks (in yellow) are lower overall because I have been on the PSMF longer and my blood sugar levels have dropped. This is evidence, at least to me, that the PSMF is doing good things for my metabolic health.
  2. There was a dip at the start of the chicken wing experiment which was due to exercise. In this case it was a particularly grueling Saturday morning routine with a lot of lifting and burpees, etc.  That explains the drop from 72 down to 64 at the start.
  3. The highest number was very comparable to the Whey and Casein numbers in terms of rise from the minimum. The max rise in Blood Sugar in all of these cases was no more than 20 units.
  4. The slope down with the animal Protein is longer and slower. That may explain less feelings of hunger as the consumption of the Protein ends.
  5. The curve is longer than either of the “pure” Proteins. The fat may extend that longer than the pure proteins. I’d like to repeat the experiment with low fat chicken breasts and see if it’s the fat or if it is the animal Protein vs Milk Protein of the Whey/Casein choices that makes a difference.

Conclusions

50 grams of Protein is a decent serving size. It is more than enough to stimulate Protein Muscle Synthesis.

All in all, I see nothing to worry about with eating Protein even for Type 2 Diabetics like myself. With all of the “Protein turns into candy bars” fear mongering out there, some sanity needs to be applied to the subject.

Disclaimer

Of course, I would encourage any diabetic to test to see where they are with this same test. At least this way they know what effect Protein would have on their body. If they are a Type 1 Diabetic this information could be helpful to determine what amount of Insulin they should add for Protein.

 

Explanations for Blood Sugar Rise with Protein Consumption

 

Here’s my questions/comments for the KetoGains thread on this subject.

I’ve been trying for a while to wrap my head around this subject. Here’s what I think at the moment. Would welcome any feedback on where I am missing it.

1 – My blood sugar meter shows that my blood sugar goes up 25 points with Protein (50g of whey) for a couple of hours. Not a bad increase since it’s only from 85 to 110 (US units). I have documented this at: http://land-boards.com/T2D/2017/09/26/blood-sugar-response-to-proteins/ .

2 – My blood sugar drops fairly rapidly at the end of the two hours (makes me hungry) which decreases when the blood sugar levels out. As long as I keep that in mind and keep food out of reach in that time frame I am OK. Otherwise, it seems like my body is telling me that it wants is ready to eat more Protein (or just food).
3 – Blood sugar production proceeds at a constant rate which isn’t all that much affected by Protein consumption. I’ve seen enough studies to believe that is probably the case such as //diabetes.diabetesjournals.org/content/62/5/1435. Also, the demand vs supply GNG argument seems strong. This rules out the idea of GNG being increased by the Protein.
4 – In a non-diabetic blood sugar doesn’t rise as much with ingested Protein as it does in a T2 Diabetic. It may not raise at all. I plan on an experiment with a “healthy” friend to confirm this for myself although the studies say it is “minimal”. But is that difference due to broken Insulin Resistance in the T2 Diabetic? As the Insulin goes up to deal with the Protein does that increase the Insulin Resistance of the cells at the same time and block the glucose from being consumed?
5 – The failure for a T2 Diabetic seems to be able to reduce the production of glucose in response to consumption of Protein (or one of the downstream aspects of the consumption). The Glucose (argued above) is getting “backed up” in the process and not being disposed by Insulin since the Insulin is “busy” dealing with the Amino Acids (all in all a very good use of Insulin).

So although arguably Protein doesn’t turn into glucose directly since Protein does lead to a rise in Blood Sugar (in T2 Diabetics) then what difference does it make if it is increased levels of GNG or an inability to reduce the rate of GNG or due to Insulin Resistance? Either way, the result is the same, Blood Sugar goes up (for T2 Diabetics) with protein consumption.

So then the question for me is whether or not Blood Sugar going up by a relatively small amount in a keto dieter who is eating lots of Protein actually a problem? Normally, us diabetics are trained to do things to minimize their blood sugars. This notion is leading a lot of people to eat a lot of fat and less Protein than they probably should.

Put another way, does the advantage of eating more Protein (maintain or growing Lean Body Mass among others) outweigh the disadvantage (marginally higher blood sugars for short periods of time)?

Survey of the Scientific Literature

From an 20 year old article (Diabetes Educ. 1997 Nov-Dec;23(6):643-6, 648, 650-1. Protein: metabolism and effect on blood glucose levels. Franz MJ):

Insulin is required for carbohydrate, fat, and protein to be metabolized. … Protein has a minimal effect on blood glucose levels with adequate insulin. However, with insulin deficiency, gluconeogenesis proceeds rapidly and contributes to an elevated blood glucose level. With adequate insulin, the blood glucose response in persons with diabetes would be expected to be similar to the blood glucose response in persons without diabetes. The reason why protein does not increase blood glucose levels (sic: in a non-diabetic) is unclear. Several possibilities might explain the response: a slow conversion of protein to glucose, less protein being converted to glucose and released than previously thought, glucose from protein being incorporated into hepatic glycogen stores but not increasing the rate of hepatic glucose release, or because the process of gluconeogenesis from protein occurs over a period of hours and glucose can be disposed of if presented for utilization slowly and evenly over a long time period.

Questions raised by this article:

  1. They don’t define “minimum effect” so is a 20 point rise considered to be a “minimum effect”?
  2. Another study indicates that GNG is much more efficient in a Diabetic. Is that because of an Insulin deficiency (the way it is worded above)? Or is that due more to Insulin Resistance?

Here’s a curve from one paper which shows the body’s Insulin response to Protein vs Carbohydrates which shows that the body has a similar response to Protein as it does to Carbohydrates when it comes to Insulin Levels:

This seems to be a reasonable study (Claire Fromentin1,2, Daniel Tomé1,2, Françoise Nau3, Laurent Flet4, Catherine Luengo1,2, Dalila Azzout-Marniche1,2, Pascal Sanders5, Gilles Fromentin1,2 and Claire Gaudichon1,2. Dietary Proteins Contribute Little to Glucose Production, Even Under Optimal Gluconeogenic Conditions in Healthy Humans. Diabetes 2013 May; 62(5): 1435-1442.) which concludes:

We showed that after a normal intake of protein (20–25 g), the contribution of dietary protein to glucose production was small and did not exceed 10% of the total flux during the 8-h postprandial period, contributing the production of 4 g glucose to 50 g of total glucose production.

While that is true in healthy humans (the subject of this study), is it also true of Diabetic persons?

From one of the comments in this thread

Higher protein intake, which needs insulin response to get it where it needs to be, will increase physiological insulin resistance (adaptive glucose sparing) in order to get the protein into where it needs to go without pushing more glucose into the cells. this will result in seeing a higher fasting blood glucose, and lower circulating ketones, as they replace glucose as a fuel for the tissues that previously used more of it.

Here’s the pieces of the puzzle.

  • Body produces a relatively constant level of blood sugar
  • Non diabetics have little to no rise in Blood Sugar when they eat Protein
  • In a diabetic the down regulation of blood sugar in the presence of Insulin is faulty
    1. Eat Protein
    2. Body begins digesting Protein
    3. Pancreas increases Insulin production to push protein into muscle cells
    4. As Insulin goes up so does Insulin Resistance of the muscle cells to Glucose (difference between a diabetic and a non-diabetic)
    5. Because Glucose is not being disposed by the muscle cells as well, the level of Blood Sugar rises temporarily
    6. After the Protein is processed by the body the Blood Glucose drops

So the theory here is that while the blood sugar rises over the short term it is not being pushed into the cells.

 

Electrolytes, Water Retention, Low Carb Diets

Low Carb Diets reduce the Insulin load on the body. They are also known for requiring more electrolytes. Here’s a study that shows that salt levels are directly impacted by Insulin levels (J Clin Invest. 1975 Apr; 55(4): 845–855. The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. R A DeFronzo, C R Cooke, R Andres, G R Faloona, and P J Davis).

Another related subject (Metabolism. 2011 Jul;60(7):965-8. doi: 10.1016/j.metabol.2010.09.005. Epub 2010 Oct 30. Low-salt diet increases insulin resistance in healthy subjects. Garg R1, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK.)

Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR.

Is Type 2 Diabetes a disorder of Insulin, Glucose or Glucagon ?

The popular notion is that Diabetes is too much glucose in the blood. Hence, treatment is given to reduce the production of blood sugar. Hence a low carbohydrate diet is given as the solution since it removes the substrate for glucose.

Dr Fung and others present the insight that the problem is that there is too much Insulin present. Type 2 Diabetics usually produce a normal level of Insulin but their blood sugars are so high that they can’t produce enough Insulin. (Type 1 is someone who just can’t produce Insulin). Low Carb works with this since it reduces the demand for Insulin to combat higher glucose levels.

There’s another player that may be more important than either Glucose or Insulin. That’s Glucagon. Hyperlipid BLOG has an article on the subject. The key insight is:

Eating 75g of casein protein more or less triples your blood insulin level but doesn’t budge blood glucose down any more than cream does, which leaves insulin pretty well alone.

The author links (Unger RH1, Cherrington AD.; Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover; J Clin Invest. 2012 Jan;122(1):4-12. doi: 10.1172/JCI60016. Epub 2012 Jan 3).

Here we propose that glucagon excess, rather than insulin deficiency, is the sine qua non of diabetes. We base this on the following evidence: (a) glucagon increases hepatic glucose and ketone production, catabolic features present in insulin deficiency; (b) hyperglucagonemia is present in every form of poorly controlled diabetes; (c) the glucagon suppressors leptin and somatostatin suppress all catabolic manifestations of diabetes during total insulin deficiency; (d) total β cell destruction in glucagon receptor-null mice does not cause diabetes; and (e) perfusion of normal pancreas with anti-insulin serum causes marked hyperglucagonemia. From this and other evidence, we conclude that glucose-responsive β cells normally regulate juxtaposed α cells and that without intraislet insulin, unregulated α cells hypersecrete glucagon, which directly causes the symptoms of diabetes. This indicates that glucagon suppression or inactivation may provide therapeutic advantages over insulin monotherapy.

Here’s another paper with the same premise (Lee YH, Wang MY, Yu XX, Unger RH.; Glucagon is the key factor in the development of diabetes; Diabetologia. 2016 Jul;59(7):1372-5. doi: 10.1007/s00125-016-3965-9. Epub 2016 Apr 26.).

 

Creatine for Muscles and Diabetes

An early study (C. P. EARNEST; The effect of creatine monohydrate ingestion on anaerobic power indices, muscular strength and body composition; Acta Physiol Scand 1995, 153, 207-209) shows creatine increases workout performance.

 

Here’s a study on creatine loading (E. Hultman, K. Soderlund, J. A. Timmons, G. Cederblad, P. L. Greenhaff; Muscle creatine loading in men; ). My conclusion is to just do 5 g/day and don’t bother with loading.

 

Creatine may not be all that effective for some people (Terjung RL; American College of Sports Medicine roundtable. The physiological and health effects of oral creatine supplementation; Medicine and Science in Sports and Exercise [01 Mar 2000, 32(3):706-717]):
Cr supplementation does not increase maximal isometric strength, the rate of maximal force production, nor aerobic exercise performance. Most of the evidence has been obtained from healthy young adult male subjects with mixed athletic ability and training status. Less research information is available related to the alterations due to age and gender. Cr supplementation leads to weight gain within the first few days, likely due to water retention related to Cr uptake in the muscle.

 

Another study (Engelhardt M; Creatine supplementation in endurance sports; Medicine and Science in Sports and Exercise [01 Jul 1998, 30(7):1123-1129]):
RESULTS: Creatine supplementation was found to have no influence on the cardiovascular system, oxygen uptake, and blood lactate concentration. The fall in blood glucose during the exercise test was significantly reduced after consumption of creatine. Although interval power performance was significantly increased by 18%, endurance performance was not influenced. CONCLUSIONS: We conclude that creatine supplementation at doses of 6 g daily has positive effects on short-term exercise included into aerobic endurance exercise.

Good news for the kidneys (Gualano B; Creatine supplementation does not impair kidney function in type 2 diabetic patients: a randomized, double-blind, placebo-controlled, clinical trial; Eur J Appl Physiol. 2011 May;111(5):749-56. doi: 10.1007/s00421-010-1676-3)

Creatinine clearance, serum and urinary urea, electrolytes, proteinuria, and albuminuria were unchanged. CR supplementation does not affect kidney function in type 2 diabetic patients, opening a window of opportunities to explore its promising therapeutic role in this population.

Perhaps most important given the mission of this BLOG – Creatine lowers HbA1C in Diabetics (Gualano B; Creatine in type 2 diabetes: a randomized, double-blind, placebo-controlled trial; Med Sci Sports Exerc. 2011 May;43(5):770-8. doi: 10.1249/MSS.0b013e3181fcee7d.):

RESULTS:
Twenty-five subjects were analyzed (CR: n=13; PL: n=12). HbA1c was significantly reduced in the creatine group when compared with the placebo group (CR: PRE=7.4 ± 0.7, POST=6.4 ± 0.4; PL: PRE=7.5 ± 0.6, POST=7.6 ± 0.7; P=0.004; difference=-1.1%, 95% confidence interval=-1.9% to -0.4%).

 

Interesting. Two things are striking about these results:
  1. Creatine dropped the HbA1C number by one full point. That’s on the order of what Metformin does.
  2. The exercise only number did not drop the HbA1C number at all. In fact, their HbA1C wen up a small amount.

n=1 – Update 2017-11-08

I took a look at my blood test from back in July and it showed:

Test Low Normal High Reference Range Units
creatinine, serum 0.77 0.76-1.27 mg/dL

So my Creatinine (produced from creatine by the muscles) number was within normal range but at the bottom of the range. This would be consistent with a Low Protein diet (I was eating less Protein at the time) and with the data above (diabetics need more dietary Creatine).

My Creatinine number from 2015 was 1.00 so there was definitely a drop in the number over the two years (from mid 2016 to the time of the test in 2017 I was definitely limiting my protein input due to my LCHF diet).

I will be curious to see if taking Creatine as a supplement along with increasing Protein and adding exercise to build more muscle mass will help in my next Creatinine test result.

Chart of Normal Blood Test Result Ranges

 

Diabetics on Low Carb Diet

Here’s a really nice study on the effect of Low Carb diet on Diabetics (Guenther Boden; Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes; Ann Intern Med. 2005; 142(6):403-411. DOI: 10.7326/ 0003-4819-142-6-200503150-00006). This study was funded by grants from the National Institutes of Health and the American Diabetes Association.

All of the results were positive for the Low Carb diet for treating diabetics. The objective of the study was:

To determine effects of a strict low-carbohydrate diet on body weight, body water, energy intake and expenditure, glycemic control, insulin sensitivity, and lipid levels in obese patients with type 2 diabetes.

One thing in the conclusions was particularly noteworthy:

On the low-carbohydrate diet, mean energy intake decreased from 3111 kcal/d to 2164 kcal/d. The mean energy deficit of 1027 kcal/d (median, 737 kcal/d) completely accounted for the weight loss of 1.65 kg in 14 days (median, 1.34 kg in 14 days).

This does contradict some of the magical thinking in the Low Carb community. Calories do count in this sense. You lose weight on a Low Carb diet because you are eating less calories. The Second Law of Thermodynamics is rescued.

However, this point goes against the other side in that the people on this study ate as much as they wanted, they were just limited to Low Carb foods. And when eating Low Carb foods, their calorie consumption dropped to their actual healthy caloric needs levels. As the conclusions noted:

In a small group of obese patients with type 2 diabetes, a low-carbohydrate diet followed for 2 weeks resulted in spontaneous reduction in energy intake to a level appropriate to their height

And of course all of their Blood Glucose numbers improved greatly.

The question that is begging to be asked in the article is why a Low Carb diet dropped these people to a “level of energy intake appropriate to their height”. The article stated:

Thus, our data did not support the concept that the weight loss induced by the low-carbohydrate diet was due to different metabolic utilization of macronutrients

True, the calories in and calories out did balance but the reason that the calories in was reduced was because of the macronutrients. In particular, the lowering of Insulin levels results in less weight. In fact, for many of the participants their insulin injections were reduced. The reduction in Serum Insulin provides the most compelling explanation for why this diet worked.

Mean 24-hour serum insulin and leptin levels profiles were statistically significantly lower at the end of the low-carbohydrate diet than before this diet, while ghrelin profiles increased marginally.

Explaining Stalls

This brings up a novel idea for stalls. Perhaps the reason that people stall is that they are now eating the calories to maintain their appropriate body weight. Even under Low Carb the same laws apply. Calories out and calories in match. And yes, when the calories come from carbs our bodies treat them different than our bodies treat calories of protein or fat which is the key insight of the Low Carb community.

Breaking Stalls

So the only way to break stalls is to actually reduce calories.

And this is where Protein Sparing Modified Fasting comes into play. Eat low carbs to keep Insulin Levels low. Eat enough Protein to preserve Lean Body Mass but not too much which stimulates Insulin. Eat enough fat from the body to meet daily calories out. And for what your body can’t provide from fat stores eat it as fat in your diet.

High Fat or High Protein

The participants in this study were allowed to eat fat and protein in whatever proportions they preferred. And in the end most ate fat and protein pretty much at the rates that they ate them before the diet.

That’s not what the Low Carb High Fat folks are telling us we need to do. Some are telling us with this same magical thinking that if we are stalled we need to eat more fat. And this isn’t working for a lot of people. In fact, I don’t know of anyone that it has worked for. Maybe it has some effect to shake things up momentarily but not to reach goal weights.

Conclusion

And everyone lived happily ever after – as long as they stayed Low Carb.