TCC The Science of Fat Loss Series Part 4 – The Fed State

You’d think by now scientists would have most things figured out. But you’d be wrong.

A lot of nutritional research has only really happened in recent times. Prior to this, everyone just accepted “conventional wisdom” when it came to all things diet. Little gems such as Fat Is Bad, and Cholesterol Is Bad – amongst others – weren’t based off any in depth controlled research. At best they were made off skewed correlational data.

This also means a lot of assumptions were also made about fat loss. And a lot of generalisations about what happens in the body.

Keep that in mind when reading the following section.

Even though it is one of the most straight forward parts of our discussion, it is a critical transition from us from understanding what is happening at the cellular level in fat loss to the more important macroscopic level that we have control over.

In other words, how the hell do these cellular states get influenced by what we do?

We have looked in some detail as to how your fat cells lose fat and how your fat cells gain fat. What we really need to start asking now is WHAT conditions these states occur in? WHEN do each of these states occur? And HOW best can we go about manipulating it to our advantage?

When scientists talk about different “states” the body can be in, they will generally refer to the Fed State and the Fasting State. The Fed State is obviously what is happening in the body straight after eating a meal. The Fasting State is when all this has settled down and you are in between meals. Bear in mind, when scientists talk about the Fed State, they are always generalising a meal that contains carbohydrates, proteins and fats in large enough amounts. Text books will rarely, if ever, talk about the different composition of meals and the differences these have on those states. This is where it has only been in modern research that scientists began looking at the different composition of diets on body fat levels i.e. low carb vs high carb, etc.

As mentioned, a “meal” according to the following statements are always comprised of a mixture of protein, carbohydrates and fats in ample amounts. And text books will then look at the different fates of these macronutrients based purely on a timeline related to the meal i.e. After a meal, between meals, overnight, while exercising.

This is a very basic way of looking at what is happening. And when looked at purely from this perspective it is easy to see why scientists usually only get caught up in “calories in calories out.” It completely ignores the “state” your body is in at the time – metabolically and hormonally – and how this can actually affect the fates of the different macronutrients also.

In these discussions, you won’t hear much about the activation of the enzymes that govern fat storage and fat loss. aka HSL and LPL from previous parts. That is because, again, context is everything, and for some reason researchers and scientists are great at looking at pieces of the puzzle in isolation, but tend to miss the “forest from the tress”. That is something we will endeavour to do later ourselves.

However, having a basic understanding the Fed State and Fasting State will form the underlying basis on how we can best create the ultimate fat loss environment. And how to avoid overdoing the fat storage environment.

This week we will look in some detail at the Fed State. Followed next week by the Fasting State.

The Fed State (aka Fat Storage Mode)

After you consume and digest a meal, glucose and amino acids are transported from the intestine in to your blood. The fats you eat don’t go through the same line of processing though, instead they are packed in to special packages called chylomicrons and are actually transported to your blood via the lymphatic system. (Remember from your high school chemistry how fat and water don’t mix very well? Your body needs to coat the fat in special proteins so it can be transported through your blood.)

Glucose and Amino Acids HAVE to go through your liver first. Your liver is your blood filter and one of its primary goals is to maintain your blood glucose levels. Fats bypass this process.

So, now you have a whole bunch of Glucose, Amino Acids and Fats injected in to your system.

In response to an increase in blood sugar, you body will increase levels of Insulin. The fed state is characterised by this release of insulin.

We’ve already learnt that insulin is one of the main regulators of your fat cells but it is also one of the most important regulators of cell metabolism in other parts of the body also. The other regulating hormone in opposition to insulin in cell metabolism, is a hormone called Glucagon.

Now, if you remember correctly, we found out last week that it was actually Adrenalin that was the main opposition hormone to insulin. And yes, this is still true as far as your FAT CELL goes. But, Glucagon has no effect on human fat cells. When it comes to other cells, like your liver, Glucagon is actually the opposing hormone to insulin.

Insulin gets secreted by your pancreas and is stimulated not only by blood glucose but also by your Parasympathetic Nervous System (meaning you don’t always need just an increase in blood glucose to get an insulin response). Insulin starts getting released even as soon as you start eating something sweet. Your body has learned over the years, if you have something that tastes sweet, this usually means it has a crap load of sugar. Your body then prepares itself for this glucose onslaught by releasing a little bit of insulin in preparation. You have probably heard or read in an article about dieting before that your body still releases some insulin even though you might be drinking a no sugar soft drink.

This Parasympathetic Nervous System response is also another reason why even if you try to completely eliminate carbs from your diet, you will never actually eliminate insulin.

In this way though, for the scientific definition, INSULIN SIGNALS THE FED STATE.

The high presence of glucose itself drives an increase in glycogen storage. But it also drives insulins release. Again, another example of where storage of something in the body is not only driven by the amount of substrate available, but also the hormonal environment.

Insulin stimulates the storage of fuels. It tells your body to store carbohydrates in both your muscles and liver. It also stops the liver from making its own glucose. If your liver levels are full, it will actually cause your liver to break down its stored glucose and form fatty acids. It will also drive glucose in to your fat cells to make the glycerol backbone. This is why insulin is called the storage hormone. It tells your body to store EVERYTHING

The Fed State:

The immediate energy requirements are being met by the food you have just eaten.

Carbohydrates are used by almost all tissues preferentially. If the body is at rest and fed, metabolic activity will be directed towards storage.

Amino acids absorbed from the gut will be used largely for protein synthesis with a small amount used directly for ATP synthesis depending on the body’s energy requirements.

Similarly, fatty acids will be stored predominantly with a small amount used for ATP production.

These storage processes are all stimulated by insulin.

If you went by this information, you would think the Fed State is a terrible thing to be in, as it would promote fat storage. But, hey, you still have to eat right?

When you look at things from this perspective, and include the basics of the calorie theory. You could appreciate why researchers restrict themselves to the argument of “it’s all about calories in / calories out”.

Hopefully, you can begin to appreciate the limitations of just looking at things from such a basic perspective though. As you will find out soon, there are so many other factors and so many other hormones that influence the flux of your fat cell beyond just the basic substrate availability and insulin release.

It is, however, important for you at this stage to understand in order to appreciate everything that we will cover later on.

In future posts, we will begin to explore everything that makes up the Ultimate Fat Storage state and what makes up the Ultimate Fat Burning State. What happens during the Fed State will make up part of that discussion, but it won’t be defined completely by it.

Key Points to Remember:

1) The Fed State = storage mode = fat storage mode

2) The Fed State by the scientific version is after a meal and is characterised by insulin release. (Which, by this definition, usually involves more than enough carbs for what your body can deal with at that time.)

Next instalment in the series will explore what happens in between meals and overnight and why the Fasting State is also known as the Fat Loss State.

Coming Up in Part 5 – The Fasted State

Ben Minos has Bachelor degrees in both Physiotherapy and Exercise Science (Human Movements). He has worked as a Personal Trainer for 20 years and a Physiotherapist for close to 15. Ben has authored a book on nutrition titled Calories Don’t Count, available through iBooks, Amazon and most online retailers. He has also authored many articles for Ironman Bodybuilding Magazine and also co authored Australia’s first Kettlebell instructor certification course. He has competed in Natural Bodybuilding over a number of years, as well as prepared numerous clients for the stage.

TCC Science of Fat Loss Part 3.2 (Addendum 2)

Important points to make before we continue (Part 2)…

The process of storing and releasing fat is in a constant tug of war inside your fat cells. It’s not like when one process is dominant the other is completely switched off. It just comes down to which one is MORE dominant.

Your Fat is in a Constant State of Flux

This process of always being broken down and rebuilt is called being in a state of flux.

Scientists call the flux cycle of your fat cell the  Fatty Acid / Triacylglycerol cycle

If more fatty acids are bound to glycerol than are free, fat will accumulate. If more are free than bound, your fast cell will decrease in size.

Think of it like trying to fill up a bag of sand while someone is shovellibg it out the other end. If you put more in the bag than gets emptied, your bag will be bigger at the end of the day. If you put sand in slower than the other person is taking it out, your bag will be less full at the end of the day.

This means that to lose fat, you have to influence this state of flux. You have to spend more time emptying the sand bag than filling it.

Control this flux, control your fat.

In future series, we will explore what happens after and between meals, what hormones affect this flux and how ultimately you can create an environment that best controls this flux to work in your favour.

A Few Points On Insulin

Insulin. The double negative.

You learned in previous articles that insulin is the main regulator of your LPL. The fat storage enzyme.

Insulin also works as a very powerful inhibitor of HSL. If insulin levels are high, it not only tells your fat cells to store fat, it prevents your fat cells from releasing fat. The inhibitory effects of insulin are also greater than the excitatory effects of certain hormones that try and stimulate fat release!

This makes sense though. Insulin is a response to blood sugar levels. If blood sugar is on the rise, this means all your current energy needs are easily and excessively being met by glucose. You wouldn’t want your fat cells to release anything. Your body would have nothing to do with it.

This means, if you have chronically elevated levels of insulin such as what occurs in insulin resistance, like in Type II diabetes, you are basically in a metabolic environment that is built for fat storage.

In real world terms, this means it’s easier for the lean to get leaner and the fat to get fatter. If you are in this metabolic situation your body does NOT process the macronutrients – especially carbohydrates – the same way. You cannot eat the same amount of sugar as your fitspo on instagram. It simply won’t work for you the same way.

Hormone Resistance

I’ve alluded a couple of times to different hormones having an affect on your fat cells. Insulin obviously has come up a few times and I have also just mentioned insulin resistance in the context of Type II diabetes.

How receptive a cell is to a signal can greatly influence how much of a hormone needs to be released. You know when someone in a room just keeps talking and talking and talking and you start to tune them out? Your cells do the same thing.

In the case of insulin, for example, if you constantly eat foods that demand a large chronic insulin output, your fat cells start to become full. When this happens, they then start to “tune off” and decrease their sensitivity to insulin. If you keep having foods that “demand to be heard”, your body will then start trying to speak louder to them, by releasing more insulin.

In this way, insulin resistance means that your body has to release a greater amount of insulin to get the same affect. Someone who doesn’t have insulin resistance, doesn’t have this problem. Their body will only release a smaller amount of insulin as their cells are listening attentively.

Insulin resistance is always a pre cursor to Type II diabetes and is one of the issues involved with people who become obese. Not in all cases, but most of them.

Your sensitivity to insulin can change over time depending on factors such as your diet and exercise. This is one of the reasons why scientists are looking at fasting as an option for treating obesity in recent years. One of the ways in which fasting can help is not only because it drops someones “calorie” intake, but because it helps to improve insulin sensitivity and glucose tolerance. You go “cold turkey” so to speak and your insulin resistance starts to reverse and glucose tolerance improves.

Keep in mind, this isn’t an either you’re resistant or not resistant type of situation. It works on more of a spectrum. Genetics definitely has a role, but you can also alter where your body sits on this spectrum.

How receptive you are to a hormone can be a powerful influence on your results. It also governs how much of a hormone your body has to release in order to get noticed. Improve your cells receptivity to hormones, you will change how your “calories” need to be processed. This will go for ALL of the hormones we will discuss in later parts.

You Will NEVER Be No Carb

Can’t stand when people learn a few basics on insulin and then magically make the leap of faith to eliminating carbs as being the answer.

“Eliminate carbs. Eliminate insulin! Easy! Then I can eat all the fat I want!”

Yeah…doesn’t really work that way

Your body can always convert excess glucose to fat. But you can never convert fat back in to glucose. It’s impossible for your body to convert fatty acids in to glucose. It must be burned as fat.

You can, however, manufacture your own glucose. Your body does this by using amino acids (from diet or body tissue). And certain organs and your brain can even use ketone bodies (a by product of fat breakdown) for energy

BUT!! Also remember the Glycerol backbone!

Remember when your body released fatty acids, it couldn’t re-use the glycerol backbone? It had to be sent to the liver for conversion?

This means, even if you go no carb, your body will get some glucose from the glycerol backbones, and also from gluconeogenesis from amino acids.

Answer? You can control carb intake. You can never eliminate carbohydrates from your system. You can control insulin. You will never eliminate it from your system.

Not saying that controlling carbohydrate it is not an effective way to lose body fat, just clearing up the misconceptions people have about the process in which it works.

Coming Up In Part 4 – What Happens After You Eat?

Ben Minos has Bachelor degrees in both Physiotherapy and Exercise Science (Human Movements). He has worked as a Personal Trainer for 20 years and a Physiotherapist for close to 15. Ben has authored a book on nutrition titled Calories Don’t Count, available through iBooks, Amazon and most online retailers. He has also authored many articles for Ironman Bodybuilding Magazine and also co authored Australia’s first Kettlebell instructor certification course. He has competed in Natural Bodybuilding over a number of years, as well as prepared numerous clients for the stage.

TCC Science of Fat Loss Part 3.1 (Addendum 1)

Important points to make before we continue (additional to part 3)

It’s Not Just About The “Calories”!!!

One of the most important things to remember when discussing how fat is stored and how fat is released is that the regulation of your fat cell isn’t just under substrate control.

It’s not just controlled by the amount of fat or carbs or protein that is present. Or, in other words, it’s not just the calories. There are more than a few factors that regulate your fat cell. So what regulates the accumulation and mobilisation? As stated a few times now, the enzymes that regulate the fat cell are influenced by the hormonal status. Your hormonal status can be influenced by your nutritional status, but it isn’t solely governed by it.

Let me say that again

Your Hormonal Status Can Be Influenced By Your Nutritional Status, But It Is NOT Solely Governed By It

Alternatively, when you look at the conditions that everything happens in, and the hormonal regulation of your fat cells, you will see it’s not just a simple matter of “eliminating insulin”. Which as I’ve said before, unless you plan on making yourself a Type I diabetic, is a physiological impossibility.

There is NO ONE THING that is the only factor that controls your fat cell. That’s part of the reason why everyone who bangs on about the calories is partly right. And everyone who bangs on about insulin, is also kind of right. But none of them are completely right. And it’s their own narrow mindedness that blinds them from looking at the whole equation in context.

And again, just because I say the “calories” don’t matter, doesn’t mean that the amount of substrate present isn’t a factor either. You simply cannot EVER think you can influence one of these factors and get away with everything else. The most obvious is when people go low carb and then think they can eat all of the fat they want without consequence. It just doesn’t work that way.

Whenever you ask yourself a question, always think of the context it is happening in. Look at not only the substrates that are available at the time, but also the hormonal environment it is happening in and also the substrates effect on that hormonal environment. If you do this correctly, you will be able to answer whether or not fasted cardio is a good idea, or if insulin getting released from amino acid intake has the same effect on fat storage than an insulin response from carbohydrates.

The upcoming posts will look at the many hormones that actually do influence your fat cell flux. Which are storage hormones, which are hormones that promote release. You will see that only a few of them are actually substrate control. In other words, your “calories in” only affect some of them, not all of them.

Up Next – Part 3.2 Addendum 2

Ben Minos has Bachelor degrees in both Physiotherapy and Exercise Science (Human Movements). He has worked as a Personal Trainer for 20 years and a Physiotherapist for close to 15. Ben has authored a book on nutrition titled Calories Don’t Count, available through iBooks, Amazon and most online retailers. He has also authored many articles for Ironman Bodybuilding Magazine and also co authored Australia’s first Kettlebell instructor certification course. He has competed in Natural Bodybuilding over a number of years, as well as prepared numerous clients for the stage.

TCC Science of Fat Loss Series Part 3 – How Fat Is Released

How is Fat Released?

In Part 2 of the Science of Fat Loss Series, we looked at how your body stores fat (Lipogenesis). This week we will look at the cellular process on how your body releases fat (Lipolysis).

As you learned in Part 2, fat is stored by tying 3 fatty acids to a glycerol backbone. This process is catalysed mainly by an enzyme Lipoprotein Lipase or LPL for short. This enzyme is in turn regulated by hormones. The main hormone being insulin.

Remember also, that once fat is in this TAG form, it is too big to escape from the cell and is trapped inside your fat cell.

The process of releasing fat from your fat cell is obviously quite similar to this, just on the opposite side of the coin. If you want to release fatty acids from your fat cell, you first have to cleave them off the confines of the glycerol backbone.

Again, it is an enzyme that is in control of this process. The main enzyme this time, is an enzyme called Hormone Sensitive Lipase. Or HSL for short.

If HSL is activated it goes about cleaving off fatty acid tails from the glycerol backbone. Once these fatty acids are free, they are then able to run and escape from the fat cell and return in to circulation, ready to be taken up by another cell and used up for energy.

And, just like before, the main regulator of this enzyme is actually hormones. The main hormones being what are called catecholamines. You’ve probably heard of adrenalin, well this hormone belongs to this group. In this way, adrenalin is the main antagonist to insulin. If your body releases adrenalin, say in response to exercise, this hormone switches on HSL enzyme and fatty acids are singled to be released from your fat cells.

Also, once again it is important to remember, adrenalin is not the only regulator of this enzyme, but it IS the main one.

All the other hormones involved in regulating these processes will be discussed in detail in later parts of the series.

This is one of the reasons why HIIT works so effectively in stripping body fat. The surge of adrenalin that is released in High Intensity Training serves to signal your body to release more fatty acids than just steady state alone.

Don’t forget the Glycerol Backbone!

The fate of your glycerol backbone is a curious one. Once fat is released from the glycerol backbone, your fat cells actually lack the ability to lock another bout of fatty acids to the same glycerol molecule. It has to get released in to the blood stream and transported back to the liver for processing to turn it back in to glucose.

Translation? You can’t store fat without a fresh supply of glucose. You will need a fresh supply of glucose if your fat cells are going to be able to make another glycerol backbone for more fatty acids to get bound to.

Again, keep it in context though. You need to ask where is this fresh supply of glucose coming from? Obviously it can come from the glucose you eat. Or, theoretically, it could also come from glucogenic amino acids that have been converted in to glucose from the liver. But, this in an of itself is a pretty laborious task in the context of fat storage and fatty acid synthesis. Not impossible though.

One thing we haven’t discussed in detail at this stage is the circumstances in which each of the processes occur in. These will discussed in coming posts focusing on what happens after you eat a meal and what happens between meals. We will also discuss the different hormones involved in these processes and how what you eat can influence these directly and indirectly.

Take Home Points:

– For fat to escape, you have to unlock the fatty acids from the glycerol backbone

– This process is catalysed by the enzyme HSL

– This enzyme is regulated by hormones. The main regulator being adrenalin.

– The fatty acids are then free to move out of the cell as they please and return in to circulation to be used by another cell

– The glycerol backbone cannot be re-used by your fat cell and must travel back to the liver for processing back to glucose

You can now maybe start to appreciate why lower carbohydrate diets have been found to work better than high carbohydrate diets, even when calories are kept the same. You can also see why carbohydrates have been victimised over recent times in relation to this.

Carbohydrates are not only are the main macronutrient that affects insulin output, it is also responsible for the glycerol backbone. Also, an excess of carbohydrates are easily converted to fatty acids. In this way it directly provides the substrates necessary for fat storage, both the backbone and fatty acids.

This is not to say I am advocating very low carbohydrate diets. I’m not making any inferences at the moment as to what is the best way to strip fat. Only discussing the exact events that occur and touching on the circumstances in which they occur in.

If you missed Part 2 – How Fat is Stored click here

Coming Soon – Addendum Part 3.1 Important Information Before We Go On (Part 1)

Ben Minos has Bachelor degrees in both Physiotherapy and Exercise Science (Human Movements). He has worked as a Personal Trainer for 20 years and a Physiotherapist for close to 15. Ben has authored a book on nutrition titled Calories Don’t Count, available through iBooks, Amazon and most online retailers. He has also authored many articles for Ironman Bodybuilding Magazine and also co authored Australia’s first Kettlebell instructor certification course. He has competed in Natural Bodybuilding over a number of years, as well as prepared numerous clients for the stage.

TCC Science of Fat Loss Series Part 2 – How Fat is Stored

In part 2 of the series, we will look specifically at how exactly fat gets stored within your fat cell. Bear in mind, at this stage, we are looking at the specific biological events that occur and how they occur. It is not necessarily looking at the conditions they occur in. Although some will be touched upon here, the discussion of that will come in later parts of the series.

For the sake of understanding, some parts of the pathways that aren’t as important to our discussion will be simplified to avoid confusion.

Lipogenesis (meaning generating stored fat) occurs inside your fat cell. It can also occur in your liver, but we’re focusing just on the fat cell for now.

Fat is stored inside your fat cell as Triacylglycerol or TAG for short, which is 3 fatty acids handcuffed to a glycerol backbone. Whenever I mention TAG, just think the stored fat.

When you have “Free Fatty Acids”, or FFA, they are literally free to move in and out of your fat cell as they please. If, however, you get 3 FFA and handcuff them to a Glycerol backbone inside the fat cell, the whole complex is now too big to escape the fat cell and is “locked” inside as fat.

So remember:

– FFA = free fat, comes and goes as it pleases

– TAG = stored fat, 3 fatty acids locked to glycerol backbone.

Don’t let all the big science names scare you off. I’ll use acronyms for a lot of them, just like scientists often do. Mainly because the name itself isn’t important. Understanding the concept is.

What this means is the base ingredients you need for fat storage are:

1) 3 Free Fatty acids

+

2) Glycerol Backbone

Two questions then become important.

1.Where do these ingredients come from?

2.How do they get locked together?

1. Where do these ingredients come from?

Free Fatty Acids

The fat you eat:

The fat you eat and the fat you store are NOT the same thing. When you eat fat, it has to undergo digestion and then gets re-synthesised for transporation. Because fat and water don’t mix it has to get transported through the blood in a special coating of proteins. This coating doesn’t last long though, only about 8 hours. Depending on your energy demands at the time and a few other factors, the fat can then either 1) enter cells of your body to get used for energy, or 2) potentially get stored in your fat cells for later. Once inside your fat cell, they enter the free fatty acid pool. In this form they are “free” to come and go from the fat cell as they please.

The fat you make:

It may be a surprise to a few of you, but very little synthesis of FFA occurs inside your fat cells. FFA are mainly synthesised by your liver. If your carbohydrate intake exceeds your body’s energy needs at that time (and after your glycogen stores are saturated), glucose can be used for fatty acid synthesis in the liver.

So, in this way carbs that don’t need to be used at that point in time can be stored as glycogen in your muscles and liver. After these glycogen stores are topped up, any excess carbohydrates are converted to triglycerides primarily by the liver and transferred to your fat cells for storage.

Important point to remember!!

Fatty Acid Synthesis DOES NOT equal fat storage!!! You are just looking at putting this excess energy in to a “holding pattern” for the time being because you don’t need it right at that point.

It’s only when the fatty acids are transported and locked to the glycerol backbone inside your fat cell that it becomes stored fat.

Theoretically, any substrate – carbs, fats or proteins – can be converted to fatty acids, but the pathways and metabolic processes can be quite different and cumbersome for some more than others. We will cover some of these areas in a later series.

Glycerol Backbone

The glycerol backbone, as the name suggests, is only manufactured from glucose. So anything that works to transport glucose in to the fat cells will contribute to the accumulation of fat. And what is the main component responsible for driving glucose in to your cells? Insulin. What’s the main substrate that drives insulin release? Carbohydrates. There are a few amino acids (i.e. proteins) that can also elicit an insulin response. This will be discussed another time. Again, not making any inferences just yet here. Just describing the circumstances that take place.

Important reminder:  At this stage of the process, having these ingredients does not mean it will be stored as fat in your fat cell. For that to happen you need to actually store it as TAG inside your fat cell.

2. How do they get locked together?

This is the most important question of all. How does your fat get stored as fat? What is actually responsible for locking the 3 FFA to the Glycerol backbone? Once you have got these ingredients, how do you actually lock these things together inside your fat cell?

The key lies in certain enzymes that exist inside your fat cell. Enzymes are like little ignition catalysts inside your cells. They kind of spark the chemical reactions in to life. The most important enzyme in this process is Lipoprotein Lipase. Or LPL for short.

In a nutshell, if you activate LPL, this will go around the cell and start handcuffing all the FFA it can find to glycerol backbones.

So, your fat doesn’t start getting fat until this step occurs. Activating LPL is the critical step in storing fat inside your fat cells. The key to figuring out fat storage then is figuring out what drives LPL activation.

This critical step is NOT under the control of substrates (or ingredients) though. The main triggers that fire LPL is in fact hormones. And insulin is the main hormone responsible for this process.

In this way, Insulin is actually the main regulator of your fat cell. It drives free fatty acids and glucose in to the fat cell. It also ignites the LPL hormone to start handcuffing the glycerol backbone to the FFA’s. Its net effect is to enhance fat storage AND block mobilisation (more on that in the next part).

To summarise here: The enzymes that control fat storage are under hormonal control. Not substrate control. Some substrates can affect certain hormones. The most obvious one is carbohydrates effect on insulin. The other hormones and circumstances that affect them will be covered in Part 7 and 8.

Just because you have excess substrate, it doesn’t necessarily mean it will get stored as fat inside your fat cell. Or in other words, just because you have all the ingredients doesn’t mean you’ve made it in to a cake.

You cannot, however, ever eliminate insulin completely. So thinking you can eat all the fat you want just because you’ve dropped some carbs out is also based on pseudoscientific half truth’s.

One final point before we wrap today:

One of the worst things about your fat cells is your bodies ability to store fat is limitless. The is a limited amount of carbohydrates your body can store. It has no efficient form of stored protein (besides what is structural and what is in the “free amino acid” pool). There’s theoretically no limit as to how much you can store. Beyond your mortality any way. Literally EVERYONE has the capacity to become obese. Isn’t that a pleasant thought to sign off with…

Take home points:

– The ingredients needed to store fat are 3 fatty acids and a glycerol backbone. These can come from your diet or be manufactured by your body

– Fat is stored as TAG inside a fat cell only when 3 fatty acids are locked to a glycerol backbone

– Lipoprotein Lipase is the enzyme that acts as a catalyst for this reaction to take place

– Substrates are not directly responsible for driving this reaction. Hormones are responsible for activating the LPL enzyme

– The main regulating hormone is insulin. It is not the only hormone. But it is definitely the most powerful one.

Questions you should start thinking about are:

What would happen if you didn’t supply as many ingredients? ie decreased your “calories” so to speak

What would happen if you had less carbs?

What would happen if you still had some insulin response but less carbs available to make anything out of?

We’ll explore these circumstances and how they take place another day.

Coming up in Part 3: How Your Body Loses Fat

Miss Part 1? Click Here

Ben Minos has Bachelor degrees in both Physiotherapy and Exercise Science (Human Movements). He has worked as a Personal Trainer for 20 years and a Physiotherapist for close to 15. Ben has authored a book on nutrition titled Calories Don’t Count, available through iBooks, Amazon and most online retailers. He has also authored many articles for Ironman Bodybuilding Magazine and also co authored Australia’s first Kettlebell instructor certification course. He has competed in Natural Bodybuilding over a number of years, as well as prepared numerous clients for the stage.