In a major breakthrough, scientists from the Physicians Committee for Responsible Medicine (PCRM), a nonprofit health organization based in Washington, D.C., found that 16 weeks of a plant-based diet can enhance gut microbiota, induce weight loss and ameliorate markers of insulin resistance in overweight adults without diabetes.
Their findings, published in the journal Nutrients, provide empirical evidence that plant protein, as part of a plant-based diet, is associated with significant improvements in weight and insulin resistance, two of the major risk factors for diabetes.
Lead researcher Hana Kahleova presented their findings at the European Association for the Study of Diabetes (EASD) 55th Annual Meeting in Barcelona, Spain.
Plant-based diet promotes weight loss, slashes diabetes risk
Existing studies on diabetes maintain that diet is a modifiable risk factor for the disease. This means cutting back on some foods and eating more of others can reduce the risk of diabetes and improve its markers, such as overall weight, blood glucose and abdominal fat.
But little is known about the exact mechanisms behind the beneficial effects of plant-based diets on markers of diabetes. In addition, high blood sugar resulting in insulin resistance can also occur in overweight people with no prior diagnosis of diabetes, according to Kahleova.
If left untreated, an overweight, non-diabetic person could lose 50 percent of their beta cells before he or she can be given a proper diagnosis. Beta cells are the cells that produce insulin, the hormone responsible for controlling blood glucose.
To test the effects of a plant-based diet on the beta cells of overweight, non-diabetic adults, Kahleova and her colleagues conducted a randomized trial on 75 overweight adults who had no prior diagnosis of diabetes. Half of the participants followed a low-fat vegan diet consisting of vegetables, grains, legumes, and fruits for 16 weeks. The researchers instructed them to avoid animal products and added oils.
Meanwhile, the other half made no changes to their diet throughout the trial period. Neither group restricted their calorie intake. In addition, none of the participants had been smoking, drinking, lactating or adopting a plant-based diet at the time of the trial, which can all influence diabetes risk.
Prior to and after the trial, the researchers measured the participants' weight, fat mass, visceral fat, insulin resistance and gut microbiota composition. Using this data and the participants' food records, the researchers found that participants in the plant-based diet group experienced significant reductions in their weight, fat mass and visceral fat.
Total protein and animal protein intake also decreased in the plant-based diet group, but their plant protein intake increased. The researchers found that this increase corresponded to the proliferation of certain beneficial bacteria in their guts.
These included Faecalibacterium prausnitzii and Bacteoides fragilis. Both bacteria are part of the normal microbiota of the human colon and are among the most abundant bacteria in the gut. These bacteria also help in degrading complex sugars and starches that could raise blood glucose.
The researchers speculated that the fiber from the plant-based foods fed the bacteria in the gut and promoted their proliferation.
Furthermore, participants in the plant-based diet group had a marked increase in their insulin secretion compared to those in the control group. This indicates better blood sugar management. The researchers attributed these benefits to the antioxidant properties of plant-based foods.
The group also noted that, in most cases, those with prediabetes at the start of the trial were able to put the condition in remission after adopting a plant-based diet. (Related: Understanding the diet-diabetes connection: What you need to know about preventing and managing your risk.)
Based on these findings, the researchers concluded that a 16-week low-fat plant-based diet can induce changes in gut microbiota that correspond to improvements in weight, fat and insulin resistance in overweight, non-diabetic adults.
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