In contrast with Diabetic Ketoacidosis, Nutritional Ketosis is a metabolic state that exists in the presence of an adequate amount of insulin to transport glucose from the diet’s limited carbs out of the bloodstream and into the cells that may require them. In this scenario, glucagon driven high blood sugars don’t exist, as is the case with Diabetic Ketoacidosis. The ketones measured result not from a cascade of emergency biological survival mechanisms run amok, but from purposefully modifying your dietary fat, protein and carbohydrate proportions with the specific goal of modestly increasing your fatty acid release and experiencing the benefits that come with it.
Synopsis of Previous Posts
I’m posting these installments about a week apart each, and I’ve never been accused of using one word when I could get away with ten, so in case you’ve lost your place, here is a quick review. Skip to the next header if you are reading these in series.
In the first post, Ketone Danger: “Aren’t ketones dangerous to diabetics?” I reviewed the origins of this common misconception through the lens of our ever evolving scientific understanding about what exactly is diabetes, and all of the underlying metabolic factors. In summary, before we even knew about insulin, or even understood that T1 and T2 diabetes were separate diseases, we knew that ketones were a sign of impending doom in young, slim people who spilled sugar in their urine. That caution has persisted as a generalized fear of ketones, even where there is no cause for concern and indeed ketones may indicate a healthy metabolism. It is with the relative security our ability to treat the condition with insulin that we are able to put the role of ketones in perspective, but ‘common wisdom’ has not yet caught up with verifiable fact.
In the second post, Diabetic Ketoacidosis: A Study in Metabolic Extremes, we reviewed the specific conditions required to start the not so merry-go-round, metabolic spiral of DKA. We concluded that, just as you need water to live, but can drown or drink so much of it that you disturb your electrolyte balance sufficiently to die, ketones can kill you if you allow a storm to build up by not taking enough insulin, either through negligence, unwise choices or lack of preparation.
The most important take away from the second post is that even if you don’t take enough insulin to cover all your carbs but just enough to keep ketone production mildly elevated (IOW, if you only meet the requirement of taking enough insulin to keep glucagon and fatty acid release moderate), then the worst that can happen is a high blood sugar and dehydration. Not good outcomes, mind you, but not DKA either.
The Matter at Hand
In this last post in the series I discuss the metabolic state known popularly as ‘Nutritional Ketosis’. So let’s start with a definition using everyone’s favorite online research resource, Wikipedia:
Ketosis is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis where blood glucose provides most of the energy. It is characterized by serum concentrations of ketone bodies over 0.5 millimolar, with low and stable levels of insulin and blood glucose.
Nutritional Ketosis is characterized by a slow, persistent burn of the body’s fatty acid stores, and is brought about by limiting your need for insulin by maintaining a diet which is very low carbohydrate, with moderate amounts of protein and the rest of your daily caloric requirements met with dietary fat.
Why Advocate Nutritional Ketosis?
So, why do I recommend nutritional ketosis for diabetics vs. the dietary recommendations from the American Diabetes Association (ADA)? For comparison’s sake let’s start with the ADA’s main goals as put forth in their Nutrition Recommendations and Interventions for Diabetes, last published in 2008:
- Blood glucose levels in the normal range or as close to normal as is safely possible
- A lipid and lipoprotein profile that reduces the risk for vascular disease
- Blood pressure levels in the normal range or as close to normal as is safely possible
All goals listed above are exactly what we should expect for any dietary regimen. Where we differ, however, is in the standards that these goals are measured against, and the effectiveness of the methods for satisfying those standards. Presently, I’ll break down each from both perspectives.
1. Blood glucose levels in the normal range or as close to normal as is safely possible
The ADA’s recommendation to satisfy the standard, “as close to normal as is safely possible” is a HbA1c of 7%, which translates to a mean blood glucose reading of 151 mg/dL. Normal is roughly half of that, but the issue of safety comes up for Type 1s or insulin prescribed Type 2s when manually dosing instead of relying on our bodies regulate doses organically.
Our needle supplied boluses load up in our interstitial fluid and slowly leak into circulation on their way to moving glucose into cells and lowering the glucose in circulation. Ideally, you calculate and inject your bolus before the plate of food arrives, and peaks in a matter of hours. If you inject or pump insulin, you have to factor into your dosing calculations:
- expected and recent activity levels which make you more insulin sensitive and implies less need for insulin to cover an equal amount of carbs
- the differing effects of the macronutrients you expect to eat on digestion rates (fats slow down the absorption of carbs, low-glycemic vs high-glycemic carbs, etc)
- the possible effect of gastroparesis or transitory digestive issues which slow stomach emptying and change insulin timing
- the stacked effect of recent correction boluses not having yet peaked or run their course
- possible changes in the amount of carbs you end up eating:
- the food arriving not being palatable enough to drive your appetite
- the food arriving differs in carb or protein content from the expectation you had when calculating your bolus
- the food arriving looks so good that you just can’t help yourself to seconds and thirds
- an argument, distraction or timing issue forcing you to abandon the meal before you finish it
- the freedom to be fickle, for Pete’s sake!
To contrast, a non-diabetic’s pancreas secretes insulin directly into the vena cava (a major blood vessel that runs by your pancreas) as they eat. Its availability to cells is relatively immediate and peaks very quickly. The non-diabetic’s pancreas doesn’t estimate the number of carbs eaten, and deliver an all-at-once bolus straight into circulation, but engages in a minute by minute negotiation with the needs of the body, adjusting continuously and unconsciously to all the factors mentioned above.
Obviously, with the dangers represented by low blood sugars – either chronic or episodical, there is ample reason to target blood sugars around twice the normal range if you are eating enough carbs to call for large doses of insulin and need the overhead for large miscalculations. Many Type 1s will agree with me when I say that forcing yourself to eat when you’ve miscalculated and are experiencing the desperation of an anxious and sweaty low, but feel like you can’t possibly stomach another bite is one of the more depressing realities of caring for yourself.
Many of us on the ADA’s diet find ourselves riding a roller-coaster of highs and lows – a point made throughout the very informative, if a bit dogmatic, Dr Bernstein’s Diabetes Solution The less insulin your dietary choices require you to take, the less chance you have of miscalculating your dose, overshooting and experiencing lows, then over compensating in a biologically fueled overwhelming urge to dig yourself out of a low by polishing off a tube of Pringle’s and going high again.
But what happens when you are on a ketogenic diet and averaging from 10 – 16 grams of carbs per meal? Well, when your insulin requirements are less than 2 – 3u per meal, a miscalculation is usually measured in fractions of a unit. I often find myself recovering from a miscalculation by merely setting my pump’s basal rate temporarily lower. The safety net afforded by keeping your insulin requirements low mitigates the need to keep your blood sugars as high as the ADA is targeting.
2. A lipid and lipoprotein profile that reduces the risk for vascular disease
I’ve chosen to put these points in the order that the ADA presented them, but in truth, wanted to put this first in the list because this is what drives the high carb ratios in their recommended diet. They are taking their lead from the American Heart Association’s dietary recommendations for preventing Cardiovascular Disease (CVD). From that perspective, dietary fat is the driver of obesity and CVD, so they do their best to minimize the amount of various types of dietary fat. Of course there are 9 calories per gram of fat versus the 4 calories per gram of carbohydrates or protein. As the percentage of one goes down, that difference must be compensated by increasing the percentage of one or both of the remaining macronutrients. Since high protein is thought to have deleterious effects on the kidneys, the only option for keeping a diabetic’s daily caloric intake sustainable when following this diet is to double the amount of carbs eaten for every gram of fat eliminated.
I could make this post much, much longer if I were to go into detail why the AHA and ADA’s rationale on limited fat intake are castles built on sand, but I will save that for a further post so your eyes don’t glaze over. Suffice to say for the purposes of this post that low dietary fat, high carb diets are actually high net fat diets in disguise. When you eat more carbs than you need to satisfy your immediate caloric requirements, and your body is doing everything it can to bring your blood sugars down to a normal range, your body can only store so much sugar as glycogen – a form which is easily converted back into sugar when needed. The rest gets turned into fat in the liver through a process called lipogenesis (lipo- meaning fat, and -genesis meaning to create). The high amounts of carb driven insulin in your blood stream at the same time locks that newly generated fat away in your fat tissue. What’s worse, the fat created by your liver through lipogenesis is smaller and denser LDL than would come from digesting dietary fat. This is the most dangerous type of fat from a cardiovascular health perspective. The high amounts of glucose in your blood stream has an effect where it distorts the shape of your blood vessels, and opens up fissures in them where these very small LDL particles can lodge and line your arteries with plaque, causing the very disease state that the AHA and ADA are trying to help you avoid.
Don’t take a lowly blogger’s word for it. Independent research exposing this reality has blossomed ever since ancestral diets started coming back into vogue, and specifically since the seminal work by Gary Taubes, Good Calories, Bad Calories helped to shift attitudes in the research community. If you really want to thoroughly understand the role of insulin in driving obesity and heart disease, and are not put off by my clumsy attempts at erudition, I cannot recommend this book, or Mr. Taubes’ more bite sized, Why We Get Fat enough.
3. Blood pressure levels in the normal range or as close to normal as is safely possible
Have you ever heard the criticism of low carb diets that goes something like, “Sure you lost six pounds in a week, but that’s just water weight”? Well, I’m here to tell you that there is an element of truth to this. That a lot of the weight you lose in the first couple of weeks of a ketogenic diet is in the form of water, not fat is true. It is less of a water loss than it is a water correction and that’s a good thing.
You see, the last ten thousand years of relative plenty that came with the agricultural age is not a diet to which the human metabolism is genetically adapted. We evolved to hunt, scrape and scavenge together our existence from wild game and very fibrous, low yield wild edibles, but are running around these days always topped off with glycogen from eating crops that were genetically bred and manipulated into be bountiful sources of carbs over thousands of years. Most of the food items we find in the supermarket these days would be unrecognizable to you if you saw the form they came in pre-agriculture. Indeed, most of it would be scarcely edible.
For every gram of glucose stored in glycogen, three or four grams of water gets stored as well. When you go low carb and lose the glycogen, you end up shedding a lot of water weight in the process. You also shed a lot of salt along with it. We simply weren’t made to walk around chronically bloated with excess salt and water in our bodies.
Well guess what you lose when you shed all that excess, unnaturally retained water and salt? That’s right, blood pressure. You’ll actually that find many people on ancestral or ketogenic diets who also engage in intense physical exercise (like many in the CrossFit community) supplement their diets with salty foods simply to keep up adequate blood pressure for their high levels of exertion.
The people at the ADA and AHA, all want what’s best for you. Of that I’m absolutely certain. Unfortunately years of market forces, bad public policy, and frankly, poorly conducted research has made the information that they are working from murky and unreliable. We have marched in lock step with low-fat, high carb dietary recommendations since the 1950’s and it has bought us a level of poor health, metabolic syndrome, obesity and heart disease unprecedented in human history.
I am not making these claims alone. I have referenced in this series of posts the works of Gary Taubes, Jeff Volek, Dr. Richard Bernstein, Dr. Peter Atia, Dr. Steve Finney, and Drs. Eric Kossoff, John Freeman, and Zahava Turner. Years ago, researchers interested in exploring the application of truly low carb diets to obesity, CVD and metabolic disorders like diabetes were actively discouraged by a lack of sources for funding, and an institutional bias against what was seen as a faddy diet schemes that flew in the face of “established science.” That bias is eroding thanks to the tireless advocacy of the above mentioned people and many more who I will refer to throughout the run of this blog. While just a few of these experts have given much thought to using a ketogenic diet to control Type 1 Diabetes, most advocate it for Type 2s, and all will back up the assertions I’ve made on a ketogenic dieter’s reduced risk of cardiovascular disease, lower blood pressure and lower blood sugars in general.
In my almost 22 years as a Type 1, I have never enjoyed better mean glucose levels, clarity of thought and peace of mind than I have eating a ketogenic diet. Our choice as diabetics is to follow the ADA’s guidance and be satisfied with the outcomes, or to lead they way to better outcomes by educating ourselves, throwing away what hasn’t been working for us, trying new approaches and listening to our bodies.
 The ADA materials actually recommend a lower carbohydrate diet, but you’ll find that “Low Carbohydrate” doesn’t have a standard measurement in medical and scientific circles. The only standard you need satisfy to call a diet low carbohydrate is to eat less carbs than a populations’ average. You’ll see this term distort the conclusions of many a scientific experiment, where “Low Carbohydrate” often counts as less than 55% of the subject’s daily caloric intake. On a ketogenic diet, even 10% can be too high.↩