In my last post, I discussed the “fat on the inside” of people with diabetes. One of the most insidious places for this fat to live is in the liver! Science is now showing the relationship between liver fat and diabetes, and the potential cure for both — fasting!
Diabetes and non-alcoholic fatty liver disease (NAFLD) are closely linked, with studies showing that NAFLD is present in up to 70% of patients with Type II diabetes.
While the association between diabetes and fatty liver disease is well known, the relationship between the two has been unclear in Western Medicine. Which comes first – diabetes or NAFLD? A study of a Korean population published in 2011 sought to investigate this question and found that the presence of fat in the liver was a good predictor of Type II diabetes risk:
Nonetheless, fatty liver detectable by ultrasound identified individuals with worse metabolic profile and greater risk for T2DM [Type 2 diabetes mellitus], regardless of baseline fasting insulin concentration. Therefore, our findings suggest that fatty liver, although associated with insulin resistance, is also an independent predictor of T2DM.
A newer analysis of Chinese patients published in 2017 demonstrated a bidirectional relationship between fatty liver disease and diabetes.
In conclusion, the present prospective cohort study provides evidence that the association between NAFLD and T2DM is bidirectional. Future studies are needed to investigate the potential mechanisms.
The irony is that despite the growing evidence of a causal relationship between diabetes and NAFLD, the current treatments don’t really address fat accumulation in the liver! Diabetes drugs use different mechanisms, such as getting your liver to produce less glucose, getting your pancreas to create more insulin, or even getting you to pee out sugar from your blood excreted through your kidneys. However, they don’t address what appears to be a root cause.
To that end, a recent study out of Germany has identified a specific protein responsible for controlling the absorption of fatty acids in the liver and associated blood sugar levels!
Subsequent simulation tests showed that GADD45β is responsible for controlling the absorption of fatty acids in the liver. Mice who lacked the corresponding gene were more likely to develop fatty liver disease. However when the protein was restored, the fat content of the liver normalized and also sugar metabolism improved. The scientists were able to confirm the result also in humans: a low GADD45β level was accompanied by increased fat accumulation in the liver and an elevated blood sugar level.
How do you restore the protein levels to normal? By stressing the liver cells through FASTING!
“The stress on the liver cells caused by fasting consequently appears to stimulate GADD45β production, which then adjusts the metabolism to the low food intake,” Herzig summarizes.
While the follow-on to this research is to find other ways to stimulate the protein production through drugs, the easier mechanism I see now is through fasting!
This is why I am taking my journey!