Do you obsessively count carbs? The good news is you probably don’t need to—if you eat the right foods. Recent research suggests that the answer to obesity and metabolic disease lies not in how much carbohydrate we eat, but rather what types of carbohydrate we eat. Read on to see what we can learn from ancestral diets, how the Paleo diet shapes up in controlled studies, and what carbohydrates should make up the bulk of your diet.
The media and scientific community are constantly changing their minds as to what macronutrient (protein, carbs, or fat) is making us fat. “If it fits your macros” is a common mantra among individuals in the weightlifting and bodybuilding community. Meanwhile, weight loss “experts” point to the total “calories in, calories out” as the answer to health. On the carbohydrate spectrum, you have people who eat plenty of carbs (but avoid fat at all costs), those who reduce carb intake so much that they enter ketosis, and just about everything in between. I’ve weighed in on this topic myself, with several blog posts about the risks and benefits of low-carb diets and how to optimize your carbohydrate intake.
As I pointed out in those posts, the bulk of the evidence suggests that the quality of food matters a lot more than the quantity of macronutrients—at least for most people. A recent hypothesis suggests that the dense, acellular carbohydrates (bear with me; I’ll define that shortly) found in processed foods may be contributing to our epidemic of modern chronic disease. The researchers propose that foods with a high carbohydrate density promote an inflammatory microbiota, leading to leptin resistance, metabolic syndrome, and obesity (1). In this article, we’ll break this down and see how we might use this information.
Leptin Resistance and Its Role in Obesity
Leptin is a mediator of long-term regulation of energy balance. It is secreted by adipose tissue and signals to the brain: “Hey, we’ve got enough energy stores!” This suppresses food intake and thereby induces weight loss. In fact, the most common mouse model of obesity is the mutant “ob/ob” mouse, which is unable to produce leptin at all. These mice eat excessively and quickly become two to three times the size of a normal mouse.
Similar to insulin resistance, chronic overexposure to the leptin hormone results in a decreased sensitivity of leptin receptors to the circulating leptin hormone. To compensate, the body produces more leptin, almost as if “shouting” at the brain and other parts of the body that are not responding to the leptin signal. Meanwhile, the person does not get the food intake suppression signal and continues to eat.
So what causes leptin resistance? Studies suggest that inflammation can damage the hypothalamus (2), the center of the brain that receives the primary signal from leptin and suppresses food intake. Inflammation can come from many sources, but diet and the gut microbiota tend to be prime sources in developed countries. In the next section, we’ll look at leptin levels among ancestral populations and how they compare to the typical consumer of a Western diet.
Carbohydrates: why quality—not quantity—matters most.
Comparison of Western Diets with Ancestral Diets
We can learn a lot from looking at the diets of populations that eat more ancestral health diets. Many of them have similar macronutrient compositions to a Western diet, yet they have a virtual absence of Western-type diseases.
For example, the Kitavan Islanders of Melanesia live as horticulturists, with little access to Western foods. Carbohydrates make up 60 to 70 percent of their energy intake, much of that coming from fruit or tubers with a fairly high glycemic index (3). Their saturated fat intake is also high. Yet despite obvious similarity between Kitavan and Western diets in both macronutrient composition and glycemic index, Kitavans boast levels of fasting insulin and blood glucose that are even lower than the levels deemed healthy in Western populations (4, 5). They also have lower levels of leptin and a virtual absence of diabetes, atherosclerosis, and excess weight (6, 7, 8).
These people aren’t just genetically superior: islanders who leave for the mainland and begin to eat a Western diet quickly become overweight (5). Similarly, when they maintain a traditional lifestyle, the Ache hunter–gatherers of Paraguay and the Shuar people of the Amazon are lean and have low leptin concentrations (9, 10). However, hunter–gatherer populations that transition to a Western diet develop Western metabolic diseases (11). Maintaining high levels of physical activity only provides a small degree of protection (12).
Other analyses of modern hunter–gatherer populations, including the Masai, Kavirondo, and Turkhana, suggest that high intake of unprocessed meat and saturated fat does not result in poor cardiovascular or metabolic health (13). I’ve written and talked extensively on the meat-heart disease myth though, so for this article, we’ll focus more on carbohydrates.
Paleolithic Diets Prevail in Randomized Controlled Trials
Many of us have adopted a modern “Paleolithic” diet in an attempt to restore our health. Does mimicking the diet of our ancestors have proven benefits?
Absolutely. While replacing refined grains with whole grains results in only modest health improvements (14), removing grains altogether and adopting a Paleolithic diet improves health across the board. Twelve weeks on a Paleolithic diet with unrestricted food intake reduced leptin levels by 31 percent and caloric intake by 20 to 30 percent (15). In another study, a Paleolithic diet resulted in greater reductions in weight and waist circumference compared to Mediterranean or diabetes diets and normalized type 2 diabetic glucose intolerance (16, 17).
Unfortunately, this is the extent of the RCTs assessing the effectiveness of a Paleo diet—after all, no pharmaceutical or food manufacturer serves to profit from a study that finds that real food prevents disease! Nevertheless, in these few studies, the effects of a Paleo diet in restoring health are robust.
The Role of Chronic Inflammation in Obesity and Metabolic Disease
Obesity is increasingly recognized as a condition characterized by low-grade, systemic inflammation that often begins in the gut. Early GI inflammation, changes in the gut microbiota, and increased GI permeability (leaky gut) precede and predict obesity in mouse models (18). A leaky gut allows bacteria and components of bacterial cell walls, like lipopolysaccharide (LPS), to cross the gut barrier. Termed “metabolic endotoxemia,” this influx of bacterial toxins into the bloodstream launches an inflammatory immune response that is thought to be a major mechanism in the pathology of obesity.
Furthermore, the microbiota of obese individuals show altered expression of bacterial genes involved in metabolism of carbohydrates, lipids, and amino acids (19). Microbial changes in the upper GI tract can result in leptin resistance in the vagus nerve, reducing satiety signaling (20). We’ll see in the next section how carbohydrate density might lead to these microbial changes and gut inflammation.
Cellular plant foods have a low carbohydrate density compared to Western foods. Root tubers, fruits, leaves, and stems store their carbohydrates as part of fiber-walled living cells. These cells are thought to remain largely intact during cooking (21). The fact that carbohydrates are stored within cells means that the maximum carbohydrate density they can have is around 23 percent.
In contrast, flour, sugar, and grains are among the most commonly consumed foods in the Western diet and are considered “acellular” carbohydrates, meaning they lack intact cells. Processed foods made from these ingredients can have a very high carbohydrate density—as high as 75 percent. This leads to a dramatic difference in the slurry of food and stomach acid that reaches the gut:
“The chyme produced after consumption of acellular flour and sugar-based foods is […] suggested to have a higher carbohydrate concentration than almost anything the microbiota of the upper GI tract from mouth to small bowel would have encountered during our coevolution.” (22)
We can easily imagine how this increased carbohydrate concentration could lead to small intestinal bacterial overgrowth (SIBO), gut dysbiosis, and ultimately leptin resistance and obesity. Inflammation caused by changes in the gut microbiota can cause damage to the hypothalamus and afferent vagus nerve endings, inducing leptin resistance. Without leptin to curb food intake, overeating and weight gain is highly likely.
Summary: Eat Real Food
Hopefully this research has helped convince you that food quality trumps quantity. Here are a few of the main takeaways:
- Macronutrient composition is important, but the quality of those macronutrients and the context they are found in are likely far more important. Our ancestors ranged from an intake of as little as 8 percent of calories from carbohydrate to as high as 70 percent calories from carbohydrate with few health problems. Only when they introduce refined Western foods do they develop metabolic disease.
- Low-carb diets are somewhat effective at achieving weight loss because they tend to reduce acellular carbohydrates, but if an individual is still eating enough to produce an inflammatory microbiota, he or she may stall in weight loss.
- Even small amounts of sugar or refined grains could lead to an inflammatory microbiota and leptin resistance. Ancestral peoples’ health tends to be very sensitive to even small influences of Western foods (23, 24). This means that the popularized 80-20 rule may not work for many people if that 20 percent is carbohydrate-dense enough to cause dysbiosis.
- Eat real food. Focus on fresh, whole foods that are minimally processed and have their carbohydrates encased in cellular compartments. These foods will not only have a lower carbohydrate density but will also likely be accompanied by a wide variety of micronutrients.
Now I’d like to hear from you. How does your diet shape up to that of your ancestors? How carbohydrate-dense is your typical meal? Do you follow the 80-20 rule? Let us know in the comments!