Diabetic nephropathy (kidney disease second to diabetes leading to kidney failure and associated complications) has been a major problem for western medicine. Those with type 1 generally begin symptoms after 5 years of the disease and those with type 2 generally begin showing symptoms after 12-15 years. Estimates vary but most organizations report that 1/4 to 1/3 people with diabetes will get diabetic nephropathy at some point during the progression of their condition.
Kidney failure (requiring an eventual transplant) is generally diagnosed from oedema, weight gain (second to oedema from fluid retention), nausea and vomiting, fatigue, frequent headaches and decreased appetite.
Medications such ACE inhibitors and ARBs can slow down the degradation but evidence currently indicates that certain combination therapies actually speed up kidney failure and lead to poor outcomes so please consult your physician and your pharmacist!
Poplawski et al 2011 proposed that diabetic complications and age-related pathologies can be traced back to glucose metabolism, glycolytic enzymes and glucose enabled gene expression. If this is true, then by simply minimizing glucose intake and glucose metabolism many age-related and diabetic related complications can be controlled and minimized.
2 types of mice bred for type 1 diabetes were used in this experiment, with n= 28 for each genotype. At 20 weeks all had urine confirmed diabetic nephropathy At this time both genotypes were split into 2 groups. The control group continued to eat the standard diet for this animal (64% carbohydrate, 23% protein, 11% fat) while experimental group was placed on a ketogenic diet (5% carbohydrate, 8% protein, 87% fat).
Ketosis is a metabolic state where the body uses fat rather than sugar as its primary fuel. This type of diet has been used to help epileptics since the 1920s. The body releases huge quantities of fats in the form of ketone bodies. The liver packages fatty acids for transport, primarily to the heart and the brain (two organs which must continue functioning). In the event of fasting or low caloric intake, after 3 days, the brain switches from 99% glucose burning to 75% glucose burning and 25% ketone. If the low caloric or low glucose diet continues, after 40 days ketones can reach as high as 70% of the calories used for brain metabolism. Clearly, in such a metabolic state, glucose is playing little direct role in cellular metabolism.
After 8 weeks on the ketogenic diet, the experiment was terminated. It was found that at the time of termination, not only had the kidney failure stopped in the ketogenic mice but had begun to reverse! This indicates that genetic, molecular and cellular mechanisms activated during ketosis may in fact play a huge role in preventing age-related degeneration and diabetic degeneration. Genes that were regulated by the diet included; Casp8, CDKN1a, Duox1 and 20 others that play metabolic and immunologic roles in the body.
Ketogenic diets in humans have not only been used for epilepsy but evidence indicates benefits to autisms, depression, ALS and Parkinson’s. Many have puzzled over the seemingly wide variety of conditions this simple diet seems to help mediate.
It now seems clear that genetic and molecular mechanisms run through a ketogenic metabolic process work differently enough from a glycolytic metabolism that it changes inter and intra cellular environment enough to both change organ function and life expectancy.
It is too early at this time to recommend that everyone go on a ketogenic diet (please don’t). Also, without some carbs, cardiovascular work would suck even more but keep an open mind about fat in your diet and its place. It appears that a high quality of healthy fat after a 3 day adaptation period may play a very beneficial role in longevity and organ functionality!