Overfeeding Studies

There are quite a few interesting overfeeding studies. The typical format of these studies is to take subjects and first determine the caloric intake to keep them in energy balance (weight stable). The study will then increase one of the three macronutrients (fat, carbohydrate or protein) and then look at the effects. Often studied are fat accumulation, body composition changes or blood lipids. The change is then attributed to the changed macronutrient.

Both fat and carbs are shown to increase weight and make body composition worse. Protein has been shown to not increase weight and increased protein improves body composition.

The problem I have with the study methodology is that the changes can’t all be attributed to the increased macronutrient alone since the increased macronutrients interacts with the other baseline macronutrients. 

Take as an example a baseline diet which provides 25% of calories from protein, 50% from carbohydrates and 25% from fat. For a 2000 calorie a day person that’s 500 calories from protein (125g), 1000 calories from carbohydrates (250g) and 500 calories from fat (55.6g).

Adding 500 calories a day of fat, for instance would change the fat from 500 calories to 1000 calories (111g) while leaving the carbohydrates and protein at the same amounts. So if there’s an increase in body fat how much of a change in body fat can be attributed to the fat alone? How much of the increase in weight is due to the interaction between fat and, say, carbohydrates? Perhaps there’s a carbohydrate/fat limit where if you exceed the amount of carbs/fat it causes much more fat storage due to the combination of the two?

Low Carb Diet Reduces the Variables

The Low Carb Diet essentially reduces the three [macronutrient] variables to two. The calories from carbohydrates are typically 5% on a very low carb diet. So the only two macronutrients left are protein and fat. Yet, even this is no guarantee for weight loss. There are people (think Jimmy Moore) who eat on the very low protein and high fat end. There are others (think Ted Naiman) who eat on the higher protein and lower fat end.

Jimmy and Ted

Clearly, what Jimmy is doing isn’t working well for Jimmy and what Ted is doing is working quite well for Ted. Jimmy is an n=1 for overeating fat. Ted is an n=1 for eating more protein. However, Ted controls for total calories and Jimmy seems to have no clue how many calories he eats in a particular day.

The difference may be exercise. It may be diet. I have a hard time finding a picture of a higher protein advocate who looks like Jimmy but I can find plenty of keto personalities who eat a lot of fat and look more like Jimmy (the Two Keto Dudes comes to mind).

A Fear of Protein?

Jimmy and others have been afraid of protein with the fear that eating protein causes the protein to turn to chocolate cake (Jimmy is infamous for making the comparison to chocolate cake at one point). I’ve looked at this subject in many posts in this BLOG (Protein does not turn into chocolate cake). 

Ted says he spends most of his day trying to convince diabetics that they should eat more protein. It is true that protein does raise blood sugar by a small amount in a diabetic but the benefits outweigh that small rise and if a person is not a diabetic protein will lower blood sugar (Glucose Response to Protein).

Problem with Protein Studies

Protein studies are used to determine protein requirements. These studies look at nitrogen balance which is either negative (the person isn’t getting enough nitrogen from their diet) or positive (the person is getting enough nitrogen from their diet). 

The problem is that protein studies are based on so-called “balanced” diets where carbohydrates are available to make the amount of glucose required by the body (Low Carbs and Gluconeogenesis). These studies don’t include the effects of gluconeogenesis (GNG). If you are eating low carb then protein provides the substrate materials (from your diet) for (GNG). For diabetics their body is already really good at making glucose via GNG (Gluconeogenesis – Later Thoughts). 

If you barely eat enough protein to meet the minimum (nitrogen replacement) requirements then your body will get it’s GNG needs from fat. Suppose that the body requires 120g of carbohydrates per day for the brain and other essential organs. If you eat 20g of carbohydrates a day that’s 100 short. If half the protein gets converted to glucose and your body requires 200g of protein to provide that glucose. (Note these are very rough numbers but the idea applies).

So, if you are on a low carbohydrate diet you need more protein than just your replacement needs. You also need protein to meet your GNG needs.

Many Ways to Lose Weight

There are quite a few ways to lose weight. Most of them involve eating less calories than you burn. You can lose weight with Low Fat or Low Carb diets. You can even lose weight with a Low Protein diet. All of these work if you are at a caloric deficit. High fat and high carbs at the same time don’t work at the same time unless your goal is weight gain.

Also, there’s an interaction with the macronutrient type. Some macronutrients encourage fat gain. Truthfully, fat is always stored easily as fat – but only accumulates in a caloric surplus. You burn off what you eat if you are in fat balance. If you eat less fat you lose body fat. If you eat more fat you will gain body fat.

Even people who eat a carnivore diet are eating a large portion of their calories as fat. As an example: Ribeye Steak from Walmart has 22g of protein and 20g of fat in an 4 oz serving. That’s 88 calories from protein and 180 calories from fat. Or 33% of calories from protein and 67% of calories from fat.

Consuming large amounts of fat is unavoidable in the weight maintenance portion of Low Carb diets. There’s a top limit on the amount of protein that you can/should eat. As an example, if you are eating 1 g of protein per lb of body weight and you weigh 200 lbs that’s 200 gram of protein or 800 calories. The rest of your daily caloric needs will then come from fat.  If you are eating 2000 calories a day that’s 1200 calories from fat.

The problem is that many people, like Jimmy Moore, eat at a maintenance or higher level of calories and macros when they need to be in a weight loss phase. Jimmy eats low protein and carbs so it’s not protein or carbs that are making Jimmy fat. The extra fat that Jimmy eats accumulates as fat when he eats more calories from fat regardless of whether he avoids carbohydrates or not. Fat doesn’t magically vanish when you eat it and it doesn’t require much energy to store -it is about 95% efficient to store fat (Eat Too Much Fat – Get Fat).

Maximizing Weight Loss

The only way for someone like Jimmy to lose weight is to get enough protein and limit dietary fat. If Jimmy has a goal weight of 200 lbs he should eat 200 grams of protein spread over four meals a day of 50 grams per meal  (Protein Gurus – Part 2). That maximizes Muscle Protein Synthesis and provides enough substrate to maintain his blood glucose. Jimmy should then eat enough fat to cover the amount he won’t be eating from his body. Jimmy has at least 100 lbs of fat mass and could easily have a 3000 calories a day deficit. It wouldn’t be at all pleasant but he could do it.

If you want to find out what you can do on a maximum fat loss diet, check out our Keto calculator.

Improved Overfeeding Studies

So how would you improve an overfeeding study? I would isolate the macronutrients and absolutely minimize the other macronutrients. Do a lean protein study (essentially a PSMF study) with variable protein levels. I’d do a carbohydrate variation study with minimal protein and fat. I’d do a fat level study with minimal carbs and protein. All of them in isolation. Wouldn’t be a very balanced diet at 90%, 5%, 5%. Couldn’t be too long a term. May not pass ethics boards. But it could tease out the interactions between the macronutrients. 

Not All [Sugar] Is Bad

It turn out that not all sugar is bad. Put another way, not everything in sugar is bad for diabetics. Sugar (sucrose) consists of one glucose and one fructose molecule, or 50% glucose and 50% fructose. The body does different things with glucose vs fructose.

There are several studies which tease out the differences between glucose and fructose. Here’s one of the studies (Kimber L. Stanhope, et.al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of Clinical Investigation, 2009;5:119, pp 1322-1334). The study:

To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks.

Switching out between the two sugars sounds like a fairly easy test and should have resulted in identical results. And the results were the same for weight gain so both parts of sugar can make you fatter.

There was a very important difference, though, where the fat was located. In the group eating fructose the visceral adipose volume was significantly increased only in subjects consuming fructose. 

Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption.

In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle–triglyceride and –cholesterol significantly increased during fructose but not glucose consumption.

In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose.

These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Interesting results. For a newer paper which summarized other studies on the subject see this (Stanhope KL, Schwarz J-M, Havel PJ. Adverse metabolic effects of dietary fructose: Results from recent epidemiological, clinical, and mechanistic studies. Current Opinion in Lipidology. 2013;24(3):198-206.)

Saturated Fat and Liver Fat

There’s a study which indicates that PUFAs protect against accumulation of liver fat but SFA (saturated fatty acids) contribute to the accumulation of liver fat (Fredrik Rosqvist, David Iggman, Joel Kullberg, Jonathan Cedernaes, Hans-Erik Johansson, Anders Larsson, Lars Johansson, Håkan Ahlström, Peter Arner, Ingrid Dahlman, Ulf Risérus. Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans. Diabetes Jul 2014, 63 (7) 2356-2368). The study overfed young subject muffins for seven weeks made with PUFA or SFA. The SFA participants gained fat in their liver and the PUFA group did not gain liver fat.

However, there’s one interesting point in the study:

In the current study, a fructose–SFA interaction on liver fat is possible since the muffins contained significant amounts of fructose. Early animal data showed that carbohydrate-induced lipogenesis was inhibited by adding linoleic acid, whereas palmitate had no effect, and SFAs have enhanced steatosis and increased hepatic lipogenesis compared with PUFAs.

That makes a lot of sense. 

The PUFA was Sunflower Oil. The SFA was Palm Oil. It would have been interesting if the SFA was plant based.

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.

Blood Sugar and Fasting

A while back, I noticed that my Blood Sugar peaks around the second day of extended fasting. George Cahill did the seminal work measuring blood markers during starvation (Cahill, George. Fuel Metabolism in Starvation.). Here’s an interesting chart from that study that explains the sources of glucose during starvation.

This demonstrates the increase in blood sugar around day 2-3. Diabetics are particularly adept at GNG. Eventually though, even that reduces as the body becomes physiologically Insulin Resistant.

The chart can provide some idea of what happens in a ketogenic diet. Although someone on a ketogenic diet is eating enough food, their exogenous glucose is greatly reduced due to the low carbohydrate content of the diet. Glycogen stores lower next. When the glycogen stores get low the body then upregulates Glyconeogenesis (GNG).

This could also explain why when I see an increase in blood sugars on one morning I often see a drop in weight the following morning. The body is signalling that it is switching fuel to up-regulated GNG due to dropped Glycogen stores. Although these two sources are of the same magnitude in Cahill’s chart above they could well be less equally matched in a diabetic. It is possible that GNG in a diabetic outpaces the ability to pull from Glycogen stores.


Fasting and Gluconeogenesis

In my previous post (Low Carbs and Gluconeogenesis) I took a look at the low carb diet and Gluconeogenesis (GNG). The study found that GNG was increased by 14% in low carb diets. For folks who view GNG as the enemy that is challenging. After all, why go on a diet which makes your GNG even worse?

But, did you know that fasting increases GNG even more? This study looked at fasting and GNG (Landau BR, Wahren J, Chandramouli V, Schumann WC, Ekberg K, Kalhan. SC. 1996 Contributions of gluconeogenesis to glucose production in the fasted state. J Clin Invest. 98:378–385.):

The contribution of gluconeogenesis to glucose production was 47+/-64% after 14 h, 67+/-64% after 22 h, and 93+/-62% after 42 h of fasting.

It would be wrong to think this means we should get up in the middle of the night to eat in order to prevent GNG. We should not fear GNG since it is necessary. Our bodies produce the amount of Glucose that our bodies need for those parts of the body which require Glucose. When we are on Low Carb diets we produce Glucose in response to demand.

A more interesting question is why GNG is overdriven in Type 2 Diabetics. This is the paper for that subject (Song S, Andrikopoulos S, Filippis C, Thorburn AW, Khan D, Proietto J. Mechanism of fat-induced hepatic gluconeogenesis: effect of metformin. Am J Physiol Endocrinol Metab. 2001 Aug;281(2):E275-82.).

The high-fat diet increased endogenous glucose production (21.9 +/- 4.4 vs. 32.2 +/- 4.8 micromol x kg(-1) x min(-1), P < 0.05) and alanine gluconeogenesis (4.5 +/- 0.9 vs. 9.6 +/- 1.9 micromol x kg(-1) x min(-1), P < 0.05).

Excess supply of dietary fat stimulates alanine gluconeogenesis via an increase in fructose-1,6-bisphosphatase protein levels

Looks like substrate availability can increase GNG – when the substrate is fat.



Fat as Glucose (Fuel)

This article cites a number of studies which show the ways that fat gets converted to glucose on a Low Carb diet (We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!).

The common objection to this is that insulin levels are low when eating fat.

Thus, when insulin levels fall and ketone levels rise, as occurs when our carbohydrate intake is low, our cells increase their supply of CYP2E1 and thereby activate the conversion of fatty acids to glucose.

And more details:

methylglyoxal inhibits the breakdown of glucose … when this pathway is activated, we not only convert fatty acids to glucose, but methylglyoxal concentrations rise and inhibit the breakdown of glucose.

Thus, when glucose runs low and we begin subsisting primarily on fatty acids for fuel, we have a coordinated effort to both spare glucose and to make more of it.

Here’s a study of the subject (

Christoph Kaleta, Luís F. de Figueiredo, Sarah Werner, Reinhard Guthke, Michael Ristow, and Stefan Schuster. In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans. PLoS Comput Biol. 2011 Jul; 7(7): e1002116.). If we could not make glucose from fatty acids then we would not be able to survive long fasts because there are parts of our bodies which absolutely require glucose.

Analyzing evidence concerning the detected pathways lends support to their importance during times of starvation, fasting, carbohydrate reduced and ketogenic diets and other situations in which the nutrition is low on carbohydrates. Moreover, the energetic investment required for this pathway can help to explain the particular efficiency of carbohydrate reduced and ketogenic diets such as the Atkins diet.


Although the brain can use ketone bodies in these situations, it still needs a certain amount of glucose, which has critical implications upon starvation and similar conditions.

Another Line of Evidence

An interesting writeup (Glucose from fatty acids: RQ of 0.454) on the generation of glucose from fatty acids(originally from Heinbecker. Studies on the Metabolism of Eskimos., 1928). The Eskimo woman has a very low RQ value on day 3.5 of her fast.

An RQ below 0.69 suggests the generation of oxygen rich molecules from fatty acids. An RQ of 0.454 suggests a huge amount of (probable) gluconeogenesis from fat is going on.


Low Carb Diet and Type 1 Diabetics – Part 2

Part 1 took a look at a Systematic Review of this subject.

A new study (May 2018) on the subject of Low Carb and Type 1 Diabetes (Leow ZZX1, Guelfi KJ1, Davis EA2,3,4, Jones TW2,3,4, Fournier PA1. The glycaemic benefits of a very-low-carbohydrate ketogenic diet in adults with Type 1 diabetes mellitus may be opposed by increased hypoglycaemia risk and dyslipidaemia. Diabet Med. 2018 May 8. doi: 10.1111/dme.13663.).



To investigate whether very-low-carbohydrate high-fat diets, typical of ketogenic diets, can improve glycaemic control without causing any ill health effects in adults with Type 1 diabetes.


In this observational study, 11 adults with Type 1 diabetes (seven men, four women, mean ± sd age 36.1± 6.8 years, mean ± sd duration of diabetes 12.8 ± 10.3 years), who followed a ketogenic diet (< 55 g carbohydrate per day) for a mean ± sd of 2.6 ± 3.3 years (β-hydroxybutyrate 1.6 ± 1.3 mmol/l), underwent sampling and analysis of fasting blood, and were fitted with a blinded continuous glucose monitor for 7 days to measure glycaemic variability.


The mean ± sd HbA1c levels were 35±4 mmol/mol (5.3±0.4%), and participants spent 74±20 and 3±8% of their time in the euglycaemic (4-8 mmol/l) and hyperglycaemic (>10 mmol/l) ranges, respectively, with little daily glycaemic variability (sd 1.5±0.7 mmol/l; coefficient of variation 26±8%). Blood glucose levels were <3.0 mmol/l for 3.6% of the time, and participants experienced a median (range) of 0.9 (0.0-2.0) daily episodes of hypoglycaemia.

Total cholesterol, LDL cholesterol, total cholesterol/HDL cholesterol ratio, and triglycerides were above the recommended range in 82%, 82%, 64% and 27% of participants, respectively; however, HDL cholesterol levels were within the recommended range for all participants. Participants displayed no or little evidence of hepatic or renal dysfunction.


This study provides the first evidence that, ketogenic diets in adults with Type 1 diabetes are associated with excellent HbA1clevels and little glycaemic variability, but may also be associated with dyslipidaemia and a high number of hypoglycaemic episodes.

A failure of this abstract is that it was an observational study which didn’t have a control group. Hence, the objection about hypoglycemia lacks a comparison.

Yes, there is a chance of going too low but the very fact that the participants had “little glycaemic variability” reduces the chance of hypoglycemia rather than increases the chance. How were these participants trained? When the details of the study are released we may find out more.

Also, as I have noted on many occasions it is not unusual to have low blood sugar levels while on the ketogenic diet with no ill effects. The presence of ketone bodies as fuel reduces the dependence on blood glucose.

The other complication was the cholesterol numbers. The total cholesterol and total cholesterol to HDL ratio is a function of the LDL cholesterol so this is really one issue not two particularly since this was the value most affected. This BLOG has numerous articles about LDL cholesterol on the ketogenic diet. This is a well understood subject.

Overall, this is an encouraging study for Type 1 Diabetics who want to control their HbA1c values more closely.


Low Carb Diet and Type 1 Diabetics

Part 2 takes a look at newer studies.

Here’s a 2018 systematic review  which looked at Type 1 Diabetics and the Low Carb Diet (Jessica L. Turton, Ron Raab, Kieron B. Rooney. Low-carbohydrate diets for type 1 diabetes mellitus: A systematic review. PLoS ONE 13(3): e0194987). They looked through a lot of studies and narrowed down to:

A total of nine studies were eligible and included for this review.

The nine studies were:

two randomised controlled trials , four pre-post intervention studies two retrospective case-series, and one case-report.

There was considerable differences between the nine studies:

Results for our primary outcome (HbA1c) were available from eight of nine studies reviewed. Results for secondary outcomes of interest were inconsistently reported. Two studies reported the effect of a low-carbohydrate diet on frequency of severe hypoglycaemia, five studies reported total daily insulin, three studies reported BMI, and one study reported mean daily blood glucose.

Here’s the detailed data (click to see large image).

The results were disappointing for HbA1C.

Four studies reported non-significant changes in HbA1c with a low-carbohydrate diet and three studies reported statistically significant reductions (P < 0.05).


Of the five studies that reported daily insulin usage, two TLCD studies  demonstrated statistically significant reductions in total daily insulin within carbohydrate restriction groups (P < 0.05) with one study also reporting a statistically significant difference between the low-carbohydrate group and high-carbohydrate comparator (P < 0.05). Levels of significance could not be calculated or obtained in three studies due to inadequate sample size and lack of raw participant data.

The reduction in Insulin use is important since that could forestall Insulin Resistance in the Type 1 diabetic. It’s a serious problem when the Type 1 Diabetic becomes resistant to the very medication that they need to live. As the paper put it:

The excessive use of insulin that is often required to achieve glycaemic control in type 1 diabetes increases susceptibility to severe hypoglycaemia and may lead to some measure of hyperinsulinemia. Hyperinsulinemia is associated with; excessive weight gain, development of the metabolic syndrome, inflammation and atherosclerosis, Alzheimer’s Disease and cancer. Findings of the present review suggest that low-carbohydrate intakes may assist in reducing or preventing hyperinsulinemia in type 1 diabetes by decreasing the absolute amount of insulin required for tight glycaemic control.

The conclusion of the study was:

This systematic review presents all available evidence for low-carbohydrate diets in the management of type 1 diabetes mellitus. The existing body of evidence is limited and more primary studies evaluating the short and long-term effects of low-carbohydrate diets on type 1 diabetes management outcomes are necessary to support its use in practice.



Long Term Adherence to Low Carb for Diabetics?

I don’t personally find long term adherence to a low carb diet to be difficult. It will be two years next month for me on Low Carb. The rewards outweigh any desire to change away from the low carb diet. In fact, the only pressure has been to maintain my weight on Low Carb since I keep losing. I never thought I would weight 165 lbs and I’ve been in this range for months.

But, there is evidence that many people who are in trials are less motivated to keep the benefits of the low carb diet past a year. Here’s a study which makes that point (Ole Snorgaard, et.al. Systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes. BMJ Open Diabetes Res Care. 2017; 5(1): e000354.).

We identified 10 randomized trials comprising 1376 participants in total. In the first year of intervention, LCD was followed by a 0.34% lower HbA1c (3.7 mmol/mol) compared with HCD (95% CI 0.06 (0.7 mmol/mol), 0.63 (6.9 mmol/mol)).

The greater the carbohydrate restriction, the greater the glucose-lowering effect (R=−0.85, p<0.01).

At 1 year or later, however, HbA1c was similar in the 2 diet groups.

The effect of the 2 types of diet on BMI/body weight, LDL cholesterol, QoL, and attrition rate was similar throughout interventions.

Does Low Carb Itself Only Work for a Year?

There’s nothing about the Low Carb diet itself which means that if you follow the Low Carb diet for a year the benefits end. My own HbA1C before Low Carb ranged from around 7-9 and now it is 5.2 at 18 months after I started Low Carb. Low Carb didn’t stop for me at a year.

My 90 day average blood sugar is 92 per my meter.

“Diet is Temporary”

Rather, it is lack of long term adherence to the diet which is the problem. If a diabetic thinks that they can do Low Carb and all their problems will go away without any potential for re-occurrence they are missing the point of how they got messed up to start with. Re-introduce a high carb load and the diabetic symptoms will quickly return.

Transition to Maintenance

People take the advice that they should increase their carbohydrates once the intervention ends and they just can’t do that. The Low Carb diet has to be followed for as long as a person wants to be non-diabetic. The transition strategy to higher carbs needs to be “just say no” rather than “try and find your carb tolerance”.

Motivated by a Study

On some level this is a problem with the nature of a study since the participants have a different set of motivations than someone who undertakes a Low Carb diet by their own choice. People who do a study are motivated by the study. A diabetic who finds low carb and reverses their diabetes has an entirely different motivation.

Study Participants

Many times these studies are very selective in the population they are studying.  Inclusion criteria is often to be newly diagnosed and un-medicated. That’s a less motivated crowd. They often have no serious symptoms (at least that they can see) and are less motivated to stay non-diabetic.

Study participants are rewarded for participating in studies not long term adherence. Once the study is over their motivation ends.

Too Easy to Pop a Pill

At the start of diabetes it is really simple to just pop a pill. And the HbA1c will react quite nicely to the pill. At least for a while.

What they don’t tell you is that you will eventually be on Insulin. I used to be in a small Bible study group with older men. There were around 6-8 of us and all of us except once guy were Type 2 diabetics. We all shared the same trajectory. We all started with Metformin which worked for a couple of years. Then our blood sugar numbers got worse. And we were prescribed additional oral medications. Eventually, we were all put on Insulin. Once of the guys commented one day that they never tell you when they put you on Metformin that it would eventually result in you getting put on Metform.

One Significant Takeaway

It seems obvious to me but the study found that the greater the carbohydrate restriction the greater the reduction in HbA1c value. This is worth noting all by itself. Here’s the figure from the study:


The cross over point is somewhere around 40% of energy. Assuming a 2000 calorie diet that’s 800 calories or 200 grams of carbohydrates. Above that point things get worse.

Equally the maximum benefit of around 0.8% reduction in HbA1c was found at 15% of energy from carbs. Again assuming a 2000 calorie diet that’s 300 calories or 75 grams of carbohydrates. That’s still high by my own standards.