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Ketosis – advantaged or misunderstood state? Part I) - 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 about with great frequency.  (For those wondering when I’ll get to Part X of The Straight Dope on Cholesterol, the answer is, “hopefully before the end of the year.”) A few months ago I was planning a post along the lines of “the 1. I’m now thinking that might be putting the proverbial cart before the horse.  So, let’s start with a more fundamental set of questions.

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.  You really have to get into the details.  Obviously, I love the details and probably read 5 or 6 scientific papers every week on this topic (and others).  I don’t expect the casual reader to want to do this, and I view it as my role to synthesize this information and present it to you.   But this is not a bumper- sticker issue.  I know it’s trendy to make blanket statements – ketosis is “unnatural,” for example, or ketosis is “superior” – but such statements mean nothing if you don’t understand the biochemistry and evolution of our species.  So, let’s agree to let the unsubstantiated statements and bumper stickers reside in the world of political debates and opinion- based discussions. For this reason, I’ve deliberately broken this post down and only included this content (i. Part I. What is ketosis? Ketosis is a metabolic state in which the liver produces small organic molecules called ketone bodies at “sufficient” levels, which I’ll expand upon later.  First, let’s get the semantics correct. The first confusing thing about ketosis is that ketone bodies are not all – technically — ketones, whose structure is shown below. Watch Dragon Crusaders IMDB.

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. Showtime Full Young Guns Online Free there. 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.  (The reason beta- hydroxybutyrate, or B- OHB, is not technically a ketone is that the carbon double- bonded to the oxygen is bonded to an –OH group on one side, technically making B- OHB a carboxylic acid for anyone keeping score.)Now, back to the real question at hand.  Why would our body make these substances? 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.

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2. 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.

For a refresher on this process, please refer to the video in this post, specifically the section from 2: 1. The ATP issue. As you may recall, about 6.

ATP (“energy currency”) to do 2 things: allow ion gradients to function and allow muscular relaxation.  So, obviously we can’t tolerate – literally even for one minute – insufficient ATP production.  In fact, one of the most potent toxins known to man (cyanide) exerts its effect on this process by inhibiting the electron transport chain which generates the bulk of the ATP our body produces.  Even the most transient interruption of this process is fatal. Take home message #1: No ATP, even for 1 minute, equals no life. The brain issue. The brain is a particularly greedy organ when it comes to energy requirement. 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. In children, by the way, this may be closer to 4. So, beyond the ATP issue, above, there is a substrate issue with the brain as neurons derive most of their energy from glucose.  While there is emerging evidence that neurons can also oxidize fatty acids directly in small amounts and may even prefer lactate (over glucose), these two substrates do not approach the levels of consumption by neurons that glucose does.  So, for the purpose of this discussion, let’s just focus on the need of the body to provide glucose to the brain.

You’ll recall, from the point I made above, that my brain requires about 4. You’ll also recall (from the video, above) that I can store about 1. While I can store much more in my muscles, (on the order of about 3. In other words, muscle glycogen is a stranded asset of glucose in the body to be used only by the muscle. So, if I’m deprived of a dietary source of glucose, I depend solely on my liver to release glycogen (a process known as hepatic glucose output, or HGO).

How long can HGO supply my brain with sufficient glucose? L.I.E. Movie Watch Online. It depends on a few things that impact both the “source” and the “sink” of glucose.  Other competing sinks for glucose (e.

But, in a state of starvation we’ve only got about one to three days before we’re in trouble.  If our brain doesn’t get a hold of something else, besides glucose, we will die quite unceremoniously. Take home message #2: No glucose for 2. The Krebs Cycle. This poses a real evolutionary dilemma.  We need an enormous amount of energy just to not die, but the single most important organ in our body (also quite energy hungry in its own right) can’t access the most abundant source of energy in our body (i. 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.  In the figure below (also included and described in the video) I gloss over a pretty important detail. How, exactly, does our body take pyruvate (from glucose) or acetyl Co.

A (from fat) and generate so much ATP? The answer lies in the beauty of the Krebs Cycle, which feeds into a process called the electron transport chain (or ETC), I alluded to above.  Since the adage ‘you can’t get something for nothing’ is as true in biochemistry as it appears to be in life, to get all that ATP (i. What the ETC does give up, as its name suggests, is electrons.  Through a series of redox reactions the ETC trades the stored energy held by electrons going from higher to lower energy states in exchange for the chemical energy stored in the bonds of the third phosphate group on an ATP molecule. To think of it another way, if you start with stored energy – glucose or fat, for example, which if burned in calorimeter will give off varying amounts of heat – and you’re willing to convert their carbon, hydrogen, and oxygen molecules into another form with less energy – water and carbon dioxide which, if burned, produce very little heat – it’s a fair trade!  The ETC is simply the vehicle that allows our body to make the switch.

In a car, by contrast, it’s much simpler.  The engine combusts the hydrocarbon (e. If you take a look at the figure, below, you’ll get a sense of the moving pieces involved in this cyclic transfer process.  Molecules shuffle back and forth, around the cycle, and kick off spent carbon (carbon dioxide, termed “waste”) and reducing agents (e. NAD+ to NADH) for the ETC. Under conditions of abundant glucose (and sufficient insulin sensitivity) the brain is primarily converting glucose to pyruvate (left side of figure).  Pyruvate is then shuttled into the mitochondria and converted into acetyl Co. A with the help of a very important enzyme called pyruvate dehydrogenase (PDH).  I’m going to come back to this enzyme, in part II of this series, because this is where the story gets very interesting.  Acetyl Co. A (which is also a direct byproduct of fatty acid breakdown) is then combined with oxaloacetate and so begins the Krebs Cycle, which generates all the reducing agents to feed the ETC and generate massive amounts of ATP.