White kidney bean extract is specifically known as alpha-amylase inhibitor isoform 1. It is extracted from any legume source although it is known as white kidney bean extract due to it's high prevalence in that specific bean.
Alpha-amylase inhibitor isoform 1 (henceforth Alpha-AI1) is one of the main starch inhibitors alongside Alpha-AI2 and Alpha-AIL. The starch inhibitors are bean lectins, alongside arcelins and phytohaemagglutinin (PHA), although they do not confer the same harms that PHA does since, despite a very similar structure, they have a differently structured 'binding loop' which does not allow carbohydrate binding. PHA, arcelins, and Alpha-AIL fail to inhibit amylase to a large degree due to steric hindrance from their looped structures, and only Alpha-AI1 shows effective amylase binding abilities in vivo in mammals.
Alpha-AI1 seems to have highly unpredictable effects on in vivo carbohydrate metabolism as the activity of the binding process is influenced highly by pH, temperature (when away from optimum pH) and coingestion with particular ions as Nitrate, chloride, bromide, iodide, thiocyanate, and calcium ions all increase the ability for Alpha-AI1 to bind to amylase, whereas potassium, magnesium, sulfate and sodium showed no effect. As well as other indirect effects like an increased secretion of amylase from the pancreas in response to slower intestinal transit time.
Phase 2 is a brand name for a specific processed extract of Phaseolus Vulgaris.
Subpar extracts of Phaseolus vulgaris can result in a very high phytohaemagglutinin (PHA) content, which would reduce the high safety threshold of white kidney bean extract significantly. They also have been reported to have much lower intestinal action on the amylase enzyme.
Phase 2 undergoes a process that inactivates the PHA content and increases the activity of Alpha-AI1 and is used in the majority of human studies.
Via inhibition of Alpha-amylase, Alpha-AI1 prevents long chain carbohydrates from being taken up in the small intestine for nutritional value to the human. This causes said starches to pass through to the colon where they have the potential to be fermented by bacteria. In this manner, Alpha-AI1 can make ingested carbohydrates act like a probiotic.
When fermented, these carbohydrates can release short-chain fatty acids including propionic acid, butyric acid, and acetic acid. These short chain fatty acids are thought to be involved in reducing the risk of colon cancer (as has been shown in experimentally induced animal models) as well as having other benefits, such as modulating insulin/glucagon release and acting as a low grade systemic Histone deacetylase(HDAC) inhibitor.
It has been noted in humans to effectively decrease amylase activity.
Initially, studies in animals noted that raw bean consumption was able to ameliorate weight gain and later studies found that it could wholly be accounted for by a combination of reduced food intake and increased starch excretion, suggesting that the mechanism of action in vivo is due to malabsorption and that in vitro studies carry over.
The acute toxicity of Phase 2 has been established as greater than 5g per kg of body weight in rats, a dose well above recommended human consumption, leading white kidney bean extract to have an excellent safety profile.
Chronic intake over the span of 28 days in doses up to 2500mg/kg bodyweight have been concluded as safe in lab animals additionally.
Alpha-AI1, specifically in the patented form of Phase 2, seems to be effective in inducing starch malabsorption and thus induce weight loss by ways of mimicking a caloric deficit. Human studies all show benefit in supplementation with the highest starch containing meal, although the degree of benefit seems highly variable.