An error occurred while setting your user cookie. Please set your. browser to accept cookies to continue. This cookie stores just a. ID; no other information is captured. Accepting the NEJM cookie is. At this stage we were still hunter-gatherers, out looking for food rather than growing and rearing our own supplies. Modern day hunter-gatherers such as the San of. As The Eating Academy approaches its first birthday in about a month, I figured it was as good a time as any to put together some thoughts on a subject I get asked. These were the keys to my transformation: 1. I stopped dieting and started nourishing my body. I learned through my research that my body was chronically starved for. Ketosis – advantaged or misunderstood state? In part I of this post I will see to it (assuming you read it) that you’ll know more about ketosis than just about anyone, including your doctor or the majority of “experts” out there writing about this topic. Before we begin, a disclaimer in order: If you want to actually understand this topic, you must invest the time and mental energy to do so. The first confusing thing about ketosis is that ketone bodies are not all – technically — ketones, whose structure is shown below. Technically, the term ketone denotes an organic molecule where a carbon atom, sandwiched between 2 other carbon atoms (denoted by R and R’), is double- bonded to an oxygen atom. Conversely, the term “ketone bodies” refers to 3 very specific molecules: acetone, acetoacetone (or acetoacetic acid), and beta- hydroxybutyrate (or beta- hydroxybutyric acid), shown below, of which only 2 are technically ketones. To understand why or when the body would do this requires some understanding of how the body converts stored energy (the food we eat or the energy we store in our body, i. To put this comment in perspective consider the following: though our brain represents only about 2% of our body mass, it accounts for about 2. It depends on a few things that impact both the “source” and the “sink” of glucose. But, in a state of starvation we’ve only got about one to three days before we’re in trouble. Obviously our species wouldn’t be here today, blogging for example, if this were the end of the story. But, to understand how we survived requires one more trip down biochemistry memory lane. This is another rendition of the figure above showing the Krebs Cycle, but here you can see where B- OHB and acetoacetate enter the picture. The reason a starving person can live for 4. Krebs Cycle in the mitochondria of our neurons. In fact, the more fat you have on your body, the longer you can survive. In fact, the late George Cahill did an experiment many years ago (probably would never get IRB approval to do such an experiment today) to demonstrate how ketones can offset glucose in the brain. Subjects with very high levels of B- OHB (about 5- 7 m. M) were injected with insulin until glucose levels reached 1 m. M (about 1. 9 mg/d. L)! If this distinction is not clear, I’d suggest giving this earlier post a quick skim for a refresher. Let me reiterate, it is physiologically impossible to induce DKA in anyone that does not have T1. D or very, very, very late- stage T2. D with pancreatic “burnout.”Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2. Atkins diet how harmful it was because of DKA. If you’re reading this, sir, please forgive me. You deserved a smarter doctor. In Part II of this post I’ll tackle the questions I know folks still have on their mind (below).
Until then, re- read this post to make sure you really understand this physiology.
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