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It is common and well documented by Cahill in his landmark studies on starvation that at the start of carbohydrate restriction blood sugar often goes up in the first few days before it starts to drop.
I’ve seen this myself with long fasts (greater than 4 days). The first few days result in your body making a lot of glucose in spite of low carbs in your diet.
It takes several days for your ketone production to kick in. That’s why the body dumps glucose.
I’ve also noticed an association between weight loss and blood sugar. My blood sugar is often up on the day before I drop in weight. In reverse, my blood sugar is lower when my weight goes up.
A typical explanation for those of us who reversed our diabetes is that we did so because we lost weight. That can be found in a quite a few places like this (Nicola D. Guess. Dietary Interventions for the Prevention of Type 2 Diabetes in High-Risk Groups: Current State of Evidence and Future Research Needs. Nutrients 2018, 10(9), 1245).
Weight loss appears to be the primary driver of type 2 diabetes risk reduction, with individual dietary components playing a minor role.
I don’t buy it. I got off Insulin in two weeks. Can it be based on weight loss? I don’t believe so. The reason is that I was diabetic over a wide range of weights – from the 230’s into the 280’s. At the time I went on LCHF + IF I was at 285. I didn’t drop below 230 in two weeks. Here is my weight loss chart.
One of the common rebuttals to the Carbohydrates + Insulin => Obesity hypothesis is the case of the Kitavans (Lindeberg S, Nilsson-Ehle P, Terént A, Vessby B, Scherstén B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994 Sep;236(3):331-40). The Kitavans eat ancestral diets with huge amounts of carbohydrates, mainly sweet potatoes.
Low Caloric Density
Part of the answer may be found in the caloric density of Sweet Potatoes. Turns out not it takes a whole lot of potatoes to get in your daily calories.
One pound of Sweet Potatoes provides 340 calories. The typical Kitavan’s energy expenditure was measured at 2200 calories. To get in 2200 calories in a day that would be more than 6 lbs of Sweet Potatoes. That’s a lot of Sweet Potatoes.
Plus, if you could manage to eat 6 lbs of Sweet Potatoes a day it would only be ~40g of protein over the whole day.
Low Fat Choice
It is also a very low fat choice with 4.4g of fat in the 7 lbs of Sweet Potatoes. It is theoretically possible to be lean on very high carbohydrates but you have to be very low fat at the same time.
This diet isn’t the typical hyper-palatable diet of the west.
Serum Fasting Insulin Differences
As noted, the Kitavan diet is a common rebuttal to the Carbohydrate Insulin Obesity hypothesis. However, the insulin levels of the Kitavans show that they have much lower fasting insulin levels than Europeans (Lindeberg, Staffan et al. Low serum insulin in traditional pacific islanders—The Kitava study. Metabolism – Clinical and Experimental , Volume 48 , Issue 10 , 1216 – 1219).
Serum fasting insulin levels were lower in Kitava than in Sweden for all ages (P < .001). For example, the mean insulin concentration in 50- to 74-year-old Kitavans was only 50% of that in Swedish subjects. Furthermore, serum insulin decreased with age in Kitava, while it increased in Sweden in subjects over 50 years of age. Moreover, the age, BMI, and, in females, waist circumference predicted Kitavan insulin levels at age 50 to 74 years remarkably well when applied to multiple linear regression equations defined to predict the levels in Sweden. The low serum insulin that decreases with age in Kitavans adds to the evidence that a Western lifestyle is a primary cause of insulin resistance.
At best, then, it could be claimed that it is possible to have a low fasting insulin and a relatively high carbohydrate diet and the link of carbohydrates to fasting insulin levels is a central claim of the carbohydrate insulin obesity hypothesis.
Other Dietary Differences
Kitavans also eat a significant amount of fish. There are quite a few other interesting facts about the Kitavan diet (See: Interview with a Kitavan).
The Kitavans eat no grains. Their diet has a lot of tubers.
The Kitavans eat different starchy carbohydrate sources throughout the year. From the Interview above:
In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on.
Lot of Smokers
An interesting tidbit is that 75% of the Kitavans are smokers and yet they have little to no heart disease. Does that mean we should take up smoking?
More Speculation and Differences
Interesting paper on the subject (Ian Spreadbury. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012; 5: 175–189).
A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern “Paleolithic” diet on satiety and metabolism.
The standard Oral Glucose Tolerance Test (OGTT) does not measure first phase insulin response. To measure that it would be necessary to look at blood sugar at 30 minutes after the meal. There’s a study which makes this point (Hulman, et.al. Glucose patterns during an oral glucose tolerance test and associations with future diabetes, cardiovascular disease and all-cause mortality rate. Diabetologia. 2018 Jan;61(1):101-107.).
Elevated 30 min glucose is associated with increased risk of diabetes and all-cause mortality rate independent of fasting and 2 h glucose levels. Therefore, subgroups at high risk may not be revealed when considering only fasting and 2 h glucose levels during an OGTT.
This subject is covered in this review (Cheng K, et.al. First phase insulin secretion and type 2 diabetes. Curr Mol Med. 2013 Jan;13(1):126-39.).
Pancreatic β-cells secrete insulin in a biphasic manner, first and second phase insulin secretion, and loss of first phase insulin secretion is an independent predictor of T2D onset.
There’s a small set of people who have a genetic defect (GCK-MODY) which gives them high blood sugar levels but they have no diabetic side effects. This paper looks at this group (Ali J. Chakera, Anna M. Steele, Anna L. Gloyn, Maggie H. Shepherd, Beverley Shields, Sian Ellard, Andrew T. Hattersley. Recognition and Management of Individuals With Hyperglycemia Because of a Heterozygous Glucokinase Mutation. Diabetes Care Jul 2015, 38 (7) 1383-1392).
Even after 50 years of mild hyperglycemia, people with GCK-MODY do not develop significant microvascular complications, and the prevalence of macrovascular complications is probably similar to that in the general population.
They don’t treat these people since they don’t respond to medications.
Treatment is not recommended outside pregnancy because glucose-lowering therapy is ineffective in people with GCK-MODY and there is a lack of long-term complications.
These people don’t get extra high levels of blood sugar but they are in the range diagnosed for pre-diabetic up to diabetic.
People with GCK-MODY have an HbA1c between 5.8 and 7.6%.
It seems to me that this might be evidence of something other than the blood sugar being the cause of damage in diabetics. Could it be the higher Insulin levels (hyperinsulinemia)? The paper presents some possibilities.
This is likely to be due to a number of factors: the hyperglycemia is mild, stable, and under homeostatic regulation; the hyperglycemia is often lower than the threshold above which the risk of diabetes complications increases; and people with GCK-MODY do not have the additional burden of the metabolic syndrome, with weight, lipid profile, and blood pressure being comparable with the general population
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.
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.
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.)
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.
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.