First, speak with your doctor — you should not start relying on plants or stop your medicines on your own. You’ll need to work closely with your diabetes health-care provider, and you’ll need to do some research and monitor yourself. Still, millions of people are using plant medicines, and a number of them have written to Diabetes Self-Management to tell us that they’re working.
Diabetes is a serious disease requiring professional medical attention. The information and recipes on this site, although as accurate and timely as feasibly possible, should not be considered as medical advice, nor as a substitute for the same. All recipes and menus are provided with the implied understanding that directions for exchange sizes will be strictly adhered to, and that blood glucose levels can be affected by not following individualized dietary guidelines as directed by your physician and/or healthcare team.
These seeds, used in Indian cooking, have been found to lower blood sugar, increase insulin sensitivity, and reduce high cholesterol, according to several animal and human studies. The effect may be partly due to the seeds’ high fiber content. The seeds also contain an amino acid that appears to boost the release of insulin. In one of the largest studies on fenugreek, 60 people who took 25 grams daily showed significant improvements in blood sugar control and post-meal spikes.
Herbal prescriptions for diabetes are formulated or prescribed based on the patient’s predominant symptoms. For instance, a patient presenting primarily with excessive thirst (lung Yin deficiency) might be given a single herb, such as radix panacis quinquefolii; or a combination of herbs in a patent formulation such as yu chuan wan, which is used in general to treat diabetes of mild to moderate severity and specifically to treat excessive thirst due to Yin deficiency,12 and ba wei di huang tang (“eight-ingredient pill with rehmannia”), which was originally used to treat people exhibiting weakness, fatigue, and copious urine soon after drinking water.13
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).