Will a Low-Carb Diet Damage My Kidneys? Ketogenic Diet and Diabetic Nephropathy

Will a Low-Carb Diet Damage My Kidneys?

Anyone who has low-carbed for any length of time has heard the litany of dire health predictions: “You’ll get heart disease!” “It will weaken your bones!” “You won’t have any energy!” Etcetera, etcetera, etcetera.

One of the most persistent among these is the threat of kidney damage. Never mind that repeated studies have demonstrated this not to be the case. Never mind that decades of ketogenic diets used for controlling intractable seizures in children have resulted in remarkably few kidney problems and that those few were largely kidney stones reported to be caused by the restriction of fluids on that admittedly extreme version of the diet, and were cleared up by liberalization of fluids. No, no, we’re all destroying our kidneys.

This made a recent study all the more interesting. In April, the medical journal PloSOne published the results of a mouse study of the effects of a ketogenic diet on diabetic nephropathy – the diabetes-caused kidney damage that is the leading cause of kidney failure, and the most common cause of death in diabetics between 50 and 70 years of age. Specifically, the researchers wanted to know if one particular ketone, called ketone 3-beta-hydroxybutyrate (3-OHB), was actually protective of kidneys. Here’s the deal:

They took three kinds of mice: “wild type mice,” whom I assume served as controls, and two kinds of mice bred to be predisposed to diabetes, one group to type 1 diabetes, often called juvenile-onset diabetes, the other to type 2, or adult-onset diabetes. All of the mice were fed a standard chow for the first 20 weeks of their lives, giving the diabetes-prone mice time to develop diabetes. They monitored the diabetic mice’s urine for something called the albumin-to-creatinine ratio, the indicator that the diabetic mice’s kidneys had been damaged. (The albumin-to-creatinine ratio has to do with the passing of protein in the urine.) The scientists then placed half of the mice in all three groups on a ketogenic diet, with a macronutrient ratio of 5% carbohydrate, 8% protein, and 87% fat. The rest of the mice continued a standard chow diet, with 64% carbohydrate, 23% protein, and 11% fat.

What happened in the study?

Well, first of all, two of the diabetic mice on the chow diet died; none of the mice on the ketogenic diet did. Since those chow-fed mice died within two weeks of starting the study, the researchers were worried they might not have any chow-fed diabetic mice left by 8 weeks in, the projected duration of the study. Because of this, all of the chow-fed mice were “sacrificed” – scientist-speak for killed – by two weeks into the study. The ketogenic mice all lived for the remaining 6 weeks of the study.

At the eight-week mark, the scientists collected urine from the ketogenic group, who then met the same fate as their chow-fed pals. Their kidneys were collected, as well. The kidneys and the urine were then studied.

Results? Let me quote: “Remarkably, within 2 months, diabetic nephropathy was completely reversed as indicated by urinary albumin/creatinine ratios.” However, the albumin/creatinine ratio didn’t change at all in the non-diabetic mice, which indicates that they were not developing kidney damage while the diabetic mice were improving. The diabetic mice on the keto diet also had a 50% drop in blood glucose, while the non-diabetic mice showed just a slight drop in blood glucose.

But what about those kidneys?

They were examine closely. There was a partial reversal of histological changes – that is, tissue changes on a microscopic level. This led the researchers to conclude that functional changes in the kidneys – the ability of the kidney to properly filter the blood – happen more rapidly than tissue changes.

More interesting details: Remember we were looking at one particular ketone, 3-OHB? The study states: “As expected, the ketogenic diet produced elevated blood 3-OHB in all groups, particularly in the diabetic mice.” So apparently the protective ketone actually was raised more in the mice whose kidneys were damaged. Isn’t that elegant? Also mentioned was that the non-diabetic mice lost weight on their ketogenic diet, while the diabetic mice did not, despite eating fewer calories. Discouraging, I know, but I’d rather be chubby with healthy kidneys than chubby and on dialysis. Just another demonstration that yeah, there are factors other than diet that influence weight, and not all of them are under our control.

Another interesting quote from this study: “A key issue raised but not resolved in the present study is the mechanism by which the ketogenic diet reverses nephropathy and gene expression profiles associated with nephropathy. One potential mechanism is that the reversal was simply due to a reduction in blood glucose. However, since previous studies demonstrated that good glucose control prevented, but did not reverse diabetic nephropathy and since diabetic complications are thought to be caused by increased cellular metabolism of glucose, we hypothesize that at least part of the restorative effect was mediated by reduction of glucose metabolism.” In other words, they think the reversal in damage happened because these mice were running their metabolisms on fat and ketones, not glucose. We also learn from this that it is thought that diabetic complications are caused by increased glucose metabolism – that running a glucose-based metabolism may, in itself, be damaging.

The study goes on to say, “Since ketones and the ketogenic diet are neuroprotective in a wide range of conditions, a phenomenon we have corroborated in the present study, it seems highly likely that the ketogenic diet will be protective in diabetic neuropathy and possibly retinopathy as well.” So we’re looking at the possibility – speculative for now – that a ketogenic diet may also prevent nerve damage and blindness in diabetics. Wow.

It’s important to remember that this is a mouse study, that mice are not people and people are not mice, and that all of this is simply a really encouraging pointer to new research. However, this one final detail thrills me. You may have heard that caloric restriction is the only clinically proven way of extending lifespan. The researchers here say “One manipulation that produces a chronic elevation in 3-OHB levels is caloric restriction, and we have hypothesized that this elevation in 3-OHB may mediate many of the protective effects of dietary restriction.” Since caloric restriction has been shown to effectively slow aging, prevent disease, and extend lifespan in a wide range of animals, it’s not crazy-wild to speculate that a ketogenic diet may do the same. (Dr Cynthia Kenyon a researcher at the University of California, San Francisco, has pioneered work indicating that carbohydrate restriction may, indeed, extend lifespan. https://www.carbsmart.com/can-low-carb-slow-the-aging-process-by-dana-carpender.html) Sure sounds more appealing than going hungry for the rest of my life. The old joke about calorie restriction for life extension is the obvious “It just seems longer.” But if you don’t have to go hungry, it’s a whole new ball game, now isn’t it?

(I have long speculated that quite a lot of the reason caloric restriction worked is that when you’re eating, say, two-thirds of the standard calorie intake, there’s simply no room at all for junk carbs.)

One more point to keep in mind about this study: It was, indeed, of a hard-core ketogenic diet, deriving 87% of calories from pure fat. This is not the “high protein” diet people assume a low-carb diet to be. Just another indication that the whole idea that fat is bad for you is sheer bunk, and another endorsement of the idea that a low-carbohydrate diet should derive the bulk of its calories from fats.

© Dana Carpender. Used by permission of the author. What do you think? Please send Dana your comments to Dana Carpender.