Baked potatoes are a healthy component of a low-fat, whole food, plant-based diet.

For years, I’ve been citing studies that provide evidence for the contribution of dietary fat in the development of insulin resistance and type 2 diabetes. Here’s another, and it’s one great study. It shows that consumption of a high-fat diet makes you spectacularly sensitive to any amount of carbohydrate you eat. This could be why people say that eating carbs makes you fat … the carbs are being eaten against a backdrop of a high-fat diet. Strip away the fat and the carbs you eat won’t make you fat. They also won’t increase your cholesterol, blood glucose, blood insulin, or make you insulin resistant. So says this study:

A Small Amount of Dietary Carbohydrate Can Promote the HFD-Induced Insulin Resistance To A Maximal Level, PloS One, 23 July 2014

Mice were fed one of 5 diets:

• Control diet: 65.1% carb, 23.1% protein, 11.8% fat
• Various High-Fat Diets (HFDs) with increasing amount of carbs: 0.1%, 5%, 10%, 25.5% carb, 58% fat, (protein was varied to keep calories constant)

After 5 weeks:

• “Mice on all high-fat diet (HFD) groups took less food and fewer calories than the mice on chow diet.”

Yet the high-fat-fed mice gained more weight, more body fat, and had higher levels of blood lipids:

• Animals on HFD gained more weight when the level of dietary carbs was increased.
• Mice on HFD with 5% carbs caused absolutely more body weight gain and the HFD with 10% carbs caused equal amount of body weight gain as the HFD with 25.5% carbs.
• White fat proportion was increased in mice on HFD with little (0.1%) dietary carbs, but the increase was further enhanced by dietary carbs in a dose-dependent manner.
• Serum levels of cholesterol, triglyceride (TG), and free fatty acids (FFA) were increased in all groups of HFD
• Together, these results show that dietary carbs are not essential for the HFD-induced body fat gain but can enhance the HFD-induced body fat gain in a dose-dependent manner, and a very small amount of carbs (10%) in the HFD can cause the maximal level of body weight gain.

The high-fat-fed mice had higher levels of blood glucose, blood insulin, and development of insulin resistance:

• Fasting blood glucose level was increased in mice of all HFD groups including the HFD with little (0.1%) carbs starting from week 1, and the increase was promoted by dietary carbs in a dose-dependent manner.
• Fasting plasma insulin level was also increased in mice of all HFD groups, and the increase reached a maximal level when the carbs in the HFD reached 10%.
• Insulin tolerance was significantly decreased in mice on HFD with little (0.1%) dietary carbs, and addition of carbs to HFD worsened insulin tolerance in a dose-dependent manner.
• Animals on chow diet that is a typical high carb (65.1%) and low fat diet (11.8%) did not have insulin resistance.
• Together, these results show that dietary carbs are not essential for the HFD-induced insulin resistance but can promote the HFD-induced insulin resistance dramatically¹, and 10% calories from dietary carbs can promote insulin resistance to a maximal level in mice on HFD.

The high-fat-fed mice also had more fat accumulation in and around the liver. The high-fat diet also induced oxidative stress, not seen in control mice.

Did you see that? The control mice ate more, both in weight of food and calories. But all their lab values were better … and they weighed less!  This has been demonstrated in human studies, both clinical trials (e.g. Barnard’s 2006 study), and population studies, and recently in the experience of Benji Kurtz, who lost over 100 pounds in a year eating his fill of a low-fat, whole food, plant-based diet.

One reason the control mice didn’t gain weight was, as the authors noted, more thermogenesis or heat generation. Eating a low-fat, high-carb diet leads to more thermogenesis, while eating a high-fat diet leads to less body heat (and so more fat accumulation).

¹ “Results from this study show that mice on HFD containing little carb (0.1%) developed severe insulin resistance (Fig. 2). How did that happen? … Glucose from gluconeogenesis is sufficient to stimulate sufficient secretion of insulin, which is necessary for the fat- or glucose-induced insulin resistance.”