Great news. Read the story here.
Low Carb diets often result in greater weight loss than low fat diets – this BLOG has linked to many of these studies.
One explanation hypothesized for the greater weight loss on Low Carb diets is the Low Carb diet is said to have an inherent metabolic advantage. This metabolic advantage should manifest itself in a greater resting energy expenditure. The paper looked at two possible mechanisms – triglyceride cycling and glyceroneogenesis.
The critics of the Low Carb diet say that the advantage is that the comparisons aren’t done by holding protein constant. Overfeeding protein is not the same as overfeeding carbs or fat since protein stimulates 24 hour energy expenditure and fat doesn’t (Overfeeding Protein – Carnivore Diet).
Look to the Science
A short term (6 weeks) small (4 subjects) study was done on obese women to compare the Low Carb and Low Fat diets which held energy (total calories) and protein constant ( Segal-Isaacson CJ, Johnson S, Tomuta V, Cowell B, Stein DT. A randomized trial comparing low-fat and low-carbohydrate diets matched for energy and protein. Obes Res. 2004 Nov;12 Suppl 2:130S-40S). The study concluded that there is no significant differences when controlling for protein.
Our results showed no significant weight loss, lipid, serum insulin, or glucose differences between the two diets.
The study was a decently formulated study but there were weaknesses:
- Small study – only 4 subjects
- No control group
- Older obese females only
- Very short duration (6 weeks)
- Low fat didn’t get super-low (20% of calories from fat)
- The Low Carb diet results in more weight loss but the study was too small to have statistical power
The good parts of the study were:
- Controlled feeding
- Matched total calories and protein – varying carbs and protein
- Decent protein level (30% of calories)
- Low carb was 5% of calories – good level
- Randomized control trial
- Cross-over design so the subjects ate both foods in random order
- Starches and fruit were the carbohydrate choices (not jelly beans)
- Deficit was relatively small (200 calories below REE which is a fairly large amount below TDEE depending on activity level)
At the end of the study they gave the participants the choice to continue on for a year. They were given the choice of the two diets and three of the four participants chose the Low Carb diet. However, the Low Carb participants raised their carbohydrate amount from 5% to 23% over the rest of the study so their weight loss partially reversed. There were several distinct advantages for the Low Carb diet.
Lipids were dramatically reduced on both diets, with a trend for greater triglyceride reduction on the VLC diet. Glucose levels were also reduced on both diets, with a trend for insulin reduction on the VLC diet
This fits my own experiences with protein and Low Carb. I’ve seen people stall for a long time and then break the stall by increasing their protein (and dropping their fat). My conclusion is that the ketogenic diet advantage does come from the higher protein intake of the diet. The diet often causes people to increase their consumption of meat which a high quality food.
Just Eat More Protein?
Protein alone doesn’t produce the same advantage that protein and Low Carb have together. This is shown in studies which substitute carbohydrates for protein (Blatt AD, Roe LS, Rolls BJ. Increasing the protein content of meals and its effect on daily energy intake. Journal of the American Dietetic Association. 2011;111(2):290-294).
This study showed that varying the protein content of several entrées consumed ad libitum did not differentially influence energy intake or affect ratings of satiety over a day. When the appearance, taste, fat content, and energy density were controlled, simply adding meat to lunch and dinner entrées to increase the protein content within commonly consumed amounts was not an effective strategy to reduce daily energy intake.
Sigma Nutrition Radio
Here’s a good program on this subject (SNR #64: Are Low-Carb Diets More Effective For Fat Loss?). tl/dl – Low Carb probably has better adherence than Low Fat diets.
Does Calories-In and Calories-Out work on Keto? In the last 162 days I have averaged 2391 calories a day. My weight is the same at the end of these 162 days. My total energy expenditure (TDEE) is calculated at 2232 calories a day. This is only 159 calories a day from my TDEE or 7% off the calculated amount and that’s less than half the assumed measurement error in the food (typically assumed to be 15%).
So, yes, I conclude that Calories-In and Calories-Out do fairly closely match. At least in my particular case and macros.
So Why Keto?
Where Keto comes in is that I have maintained a 120 lb loss for the past 5+ months without hunger. My hormones are in balance. My insulin level is kept low. I don’t have the blood sugar roller coaster ride.
Here’s a good podcast covering this subject (Sigma Nutrition Radio #85: What Drives Fat Gain? – Thoughts on CICO, Insulin & Obesity).
Here’s an interesting study which provides evidence for the role of Insulin in Weight Gain (Velasquez-Mieyer P, Cowan P, Arheart K, et al. Suppression of insulin secretion is associated with weight loss and altered macronutrient intake and preference in a subset of obese adults. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. 2003;27(2):219-226).
For the entire cohort, significant insulin suppression was achieved with simultaneous improvements in insulin sensitivity, weight loss, and body mass index (BMI). Leptin, fat mass, total caloric intake, and carbohydrate craving significantly decreased.
When grouped by BMI response, high responders (HR; ΔBMI < −3 kg/m2) and low responders (LR; ΔBMI between −3 and −0.5) exhibited higher suppression of CIRgp and IAUC than nonresponders (NR; ΔBMI > −0.5). CISI improved and significant declines in leptin and fat mass occurred only in HR and LR.
Conversely, both leptin and fat mass increased in NR. Carbohydrate intake was markedly suppressed in HR only, while carbohydrate-craving scores decreased in HR and LR. For the entire cohort, ΔBMI correlated with ΔCISI, Δfat mass, and Δleptin. ΔFat mass also correlated with ΔIAUC and ΔCISI.
In a subcohort of obese adults, suppression of insulin secretion was associated with loss of body weight and fat mass and with concomitant modulation of caloric intake and macronutrient preference.
From the body of the study:
The role of increased carbohydrate craving and intake has been previously suggested to play a contributory role in the development of obesity. However, the connection between insulin and carbohydrate craving and intake is less clear. The frequent intake of highly refined carbohydrates may induce weight gain by initiating and sustaining a chronic state of hyperinsulinemia. Carbohydrate intake stimulates insulin secretion, raising circulating insulin levels, which in turn favors increased fatty acid uptake, lipid biosynthesis, and inhibition of lipolysis, leading to energy storage.
Conversely, it had been suggested that insulin stimulates hyperphagia and fosters carbohydrate cravings, producing increased levels of insulin that promote insulin resistance and exacerbation of the hyperinsulinemic condition. This suggests that a vicious cycle is set in motion that perpetuates hyperinsulinemia and weight gain, and that breaking this cycle can promote weight loss.
Our bodies burn carbs in preference to fats. That is because we only have a limited amount of storage for carbs and we have a very high capacity for fat storage.
We are typically burning some mixture of both fat and carbs (except at extremes). The amount of carbs we are burning is strongly influenced by the amount of carbs we have eaten. If you ate nothing but carbs and ate them at an amount matching your total energy expenditure you will pretty much just burn carbs.
Since most people don’t eat in their sleep there’s some point where the carbs go down and the body starts to draw from the carb stores, aka, glycogen. That can last as long as a day or so but as the glycogen stores draw down the body starts to shift to fat burning. This is known as glycogen sparing.
On a low carb diet our fuel mixture shifts to largely fat based. At very low levels of Insulin that come with a reduction in carbohydrates, our peripheral cells resist the small amount of glucose we produce and we spare the glucose for the parts of our body which rely on glucose for fuel. This is how the low carbohydrate diet is glucose/glycogen sparing.
A high carb diet is fat sparing since it spares our body fat from being burned and reduces the amount of time that glycogen stores are being drawn down.
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.
I’ve been meaning to write on bad associations for a long time but there are so many other good articles on it that I’ve saved my fingers until now. I really enjoy a lot of Marty Kendall’s Nutrient Optimising (British spelling) material but I’m getting a bit annoyed at some of the association data that is being put forward. I guess I should be as annoyed at the ketogenic community associations as well. None of them meet the Bradford Hill criteria.
So I am going to play the same game. My theory is that fresh broccoli causes obesity. Check out the blue graph below.
Here’s the chart for obesity.
Here’s a chart for the total calories in the food supply.
So it looks to me like obesity is caused by too much broccoli.
And when the rooster crows the sun comes up.
And fallacies go on and on.
A good small study comparing the blood sugar and insulin responses to breakfasts with different fat/carb/protein values at the same number of calories (Paula C. Chandler-Laney, et.al. Return of hunger following a relatively high carbohydrate breakfast is associated with earlier recorded glucose peak and nadir. Appetite. Volume 80, 1 September 2014, Pages 236-241).
Turns out that a Low Carb High Fat breakfast results in a lower Area Under the Curve (AUC) for Insulin and higher blood sugar levels hours after breakfast. The lower AUC makes sense since there’s less glycemic load from lower carbohydrates. However, the glucose response may be counter-intuitive. It happens because the problem with higher glucose in meals is a larger drop in glucose after the meal digests. Eating lower carbs results in less of a drop in blood sugar. And it also results in less hunger.
The study protocol was:
Overweight but otherwise healthy adults (n = 64) were maintained on one of two eucaloric diets: high carbohydrate/low fat (HC/LF; 55:27:18% kcals from carbohydrate:fat:protein) versuslow carbohydrate/high fat (LC/HF; 43:39:18% kcals from carbohydrate:fat:protein). After 4 weeks of acclimation to the diets, participants underwent a meal test during which circulating glucose and insulin and self-reported hunger and fullness, were measured before and after consumption of breakfast from their assigned diets.
The results of the study were:
The LC/HF meal resulted in a later time at the highest and lowest recorded glucose, higher glucose concentrations at 3 and 4 hours post meal, and lower insulin incremental area under the curve.
Participants consuming the LC/HF meal reported lower appetite 3 and 4 hours following the meal, a response that was associated with the timing of the highest and lowest recorded glucose.
Credit to Ted Naimam for pointing out this study.
The story of Ancel Keys is told in a way intended to correct the predominent keto narrative of Keyes as Anti-Christ (Denise Minger. THE TRUTH ABOUT ANCEL KEYS: WE’VE ALL GOT IT WRONG). Denise includes a table that looked at all cause mortality and not just the fat/cardio chart that Keyes is infamous for producing. Read Denise’s excellent BLOG post for the background of this table.
A positive number is an association. The larger the number, the larger the association. Of course we know that association is not causation. All cause mortality is associate the most strongly with carbohydrates (+0.396) and the least with calories from fat (-0.340).
This is also the subject of another paper (Pett, et.al. Ancel Keys and the Seven Countries Study: An Evidence-based Response to Revisionist Histories).
Here is another related BLOG post (From Ancel Keys and the diet-heart hypothesis to LCHF may not be a huge leap.).