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.
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.
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.
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).
We conducted a one-year, multicenter, randomized, controlled trial to evaluate the effect of the low-carbohydrate, high-protein, high-fat Atkins diet on weight loss and risk factors for coronary heart disease in obese persons. The subjects were randomly assigned to follow either a low-carbohydrate, high-protein, high-fat Atkins diet or a high-carbohydrate, low-fat, energy-deficit conventional diet.
The Low Calorie group was pretty restrictive:
1200 to 1500 kcal per day for women and 1500 to 1800 kcal per day for men, with approximately 60 percent of calories from carbohydrate, 25 percent from fat, and 15 percent from protein
You’d think that with the Low Carb group able to eat what they want that the calorie restricted group would beat them hands down. The results were:
Subjects on the low-carbohydrate diet had lost more weight than subjects on the conventional diet at 3 months (mean [±SD], –6.8±5.0 vs. –2.7±3.7 percent of body weight; P=0.001) and 6 months (–7.0±6.5 vs. –3.2±5.6 percent of body weight, P=0.02), but the difference at 12 months was not significant (–4.4±6.7 vs. –2.5±6.3 percent of body weight, P=0.26). After three months, no significant differences were found between the groups in total or low-density lipoprotein cholesterol concentrations. The increase in high-density lipoprotein cholesterol concentrations and the decrease in triglyceride concentrations were greater among subjects on the low-carbohydrate diet than among those on the conventional diet throughout most of the study. Both diets significantly decreased diastolic blood pressure and the insulin response to an oral glucose load.
…average daily energy expenditure of traditional Hadza foragers was no different than that of Westerners after controlling for body size.
The metabolic cost of walking (kcal kg−1 m−1) and resting (kcal kg−1 s−1) were also similar among Hadza and Western groups. The similarity in metabolic rates across a broad range of cultures challenges current models of obesity suggesting that Western lifestyles lead to decreased energy expenditure. We hypothesize that human daily energy expenditure may be an evolved physiological trait largely independent of cultural differences.
Isoenergetic 1000 kJ (240 kcal) servings of 38 foods separated into six food categories (fruits, bakery products, snack foods, carbohydrate-rich foods, protein-rich foods, breakfast cereals) were fed to groups of 11-13 subjects. Satiety ratings were obtained every 15 min over 120 min after which subjects were free to eat ad libitum from a standard range of foods and drinks.
A satiety index (SI) score was calculated by dividing the area under the satiety response curve (AUC) for the test food by the group mean satiety AUC for white bread and multiplying by 100.
Thus, white bread had an SI score of 100% and the SI scores of the other foods were expressed as a percentage of white bread.
The results were:
There were significant differences in satiety both within and between the six food categories. The highest SI score was produced by boiled potatoes (323 +/- 51%) which was seven-fold higher than the lowest SI score of the croissant (47 +/- 17%).
Most foods (76%) had an SI score greater than or equal to white bread.
The amount of energy eaten immediately after 120 min correlated negatively with the mean satiety AUC responses (r = -0.37, P < 0.05, n = 43) thereby supporting the subjective satiety ratings. SI scores correlated positively with the serving weight of the foods (r = 0.66, P < 0.001, n = 38) and negatively with palatability ratings (r = -0.64, P < 0.001, n = 38).
Protein, fibre, and water contents of the test foods correlated positively with SI scores (r = 0.37, P < 0.05, n = 38; r = 0.46, P < 0.01; and r = 0.64, P < 0.001; respectively) whereas fat content was negatively associated (r = -0.43, P < 0.01).
This goes a long way to explain the Kitavan diet which is largely sweet potatoes. Can you imagine eating sweet potatoes every day as a main staple? Even though they are high carbohydrates it would be tough to over eat them.