TCC The Science of Fat Loss Series Part 7 – How You Get Fat

What is the ideal fat storing environment?

Although some of you may ask, why am I covering fat storage when all you want to know about is fat loss? Well, it kind of makes sense, if you don’t want to get fat, you should avoid the things that get you fat.

Let’s look beyond calories again, and look at what is really going on inside the body at the cellular, hormonal, metabolic and enzymatic processes. Some of these things are influenced by the amount and type of macronutrients directly, others indirectly, others are governed by things completely separate to these altogether.

Remember how “The Fed State” was characterised by an insulin response. And in the scientific definition, this was typified by a carbohydrate rich meal. Already, most of you should know you can manipulate macronutrient make up of a meal so this doesn’t have to be the case, but let’s take a look at the actual Hormonal Response to The Fed State.

Hormonal, Metabolic, Enzymatic Response to Eating i.e. “The Fed State”

Rise in Insulin – mainly influenced by blood glucose levels

Activation of Lipoprotein Lipase (LPL) – the fat storing enzyme

Rise in Leptin – your fat cells talk to your brain telling you you’re full

Decreased Grehlin – you stop sending “hunger” signals to your brain

Increased Thyroid – metabolism speeds up (there is no evidence that having 5 meals per day is any more beneficial for metabolism than, say, 3. So the old way of thinking that smaller meals throughout the day is better for the metabolism has been pushed to “urban legend” status. This doesn’t mean there aren’t other benefits to spaced out feedings – see Muscle Protein Synthesis post – just saying it’s not done for basal metabolic rate improvements)

Decreased Growth Hormone – You can’t have everything all at once. Just because this beneficial hormone gets suppressed during this eating period, doesn’t mean it doesn’t get released at other, more beneficial, times. There is also evidence that GH can be augmented with amino acids Arginine, Ornithine and Lysine. The only problem is, the jury is still out whether these work that well when taken orally.

Increased Serotonin – this is why some strength coaches recommend a small carbohydrate meal just before bed time. Increased serotonin levels from this can help with quality of sleep.

As you can see, there are some good and some bad things that occur when you eat a meal as far as your fat loss efforts go. Needless to say, not eating doesn’t work as a sustainable way for fat loss.

Is there any way we can manipulate say the composition of a meal in order to optimise this outcome?? You bet.

You can get the positives out of the fed state and offset the negatives. It just depends on how you structure the composition and timing of your meals. This will be covered in the next part of the series. I think you can already take an educated guess as to what this might be though.

We will look at the optimal meal composition to maximise the good hormones and mitigate the bad hormones next instalment.

One of the big things to remember when talking about these hormones. It’s not only the output of these that are important, it is also your cells receptivity to it. How sensitive they are to its effects. The other important point is the interaction a lot of these different hormones have with each other.

Let’s take insulin, for example. You can elicit a NORMAL insulin response. The biggest problem with insulin normally arises from CHRONICALLY ELEVATED LEVELS OF INSULIN. Usually from over consumption of carbohydrates and even worse with the over consumption of the wrong type of carbohydrates. You can also get elevated levels of insulin as a result of the development of Insulin Resistance. With Insulin Resistance, your body no longer has the same effect at a lower dose, so it has to increase insulin output to try and exert even a small effect. Now you’ve turned in to an insulin junkie. Needing a bigger and bigger hit, just to get a small “high”.

To make matters worse, Insulin Resistance quite often coincides with Leptin Resistance. So, now you eat things that aren’t good for you, your blood sugars are way too high, your insulin levels are way too high, BUT YOU DON’T FEEL FULL!! And we wonder why obese people over eat?!?

Glucose tolerance and Insulin Resistance is highly variable from one person to the next. There are diet, exercise and also genetic factors involved. How you respond to a certain level of glucose is going to be different than mine. BUT. This is also a fluid and shifting process for each individual. One that you can actually exert an influence over. You can start affecting insulin sensitivity in as little 2-3 weeks if you really wanted. You can also start reversing these symptoms in that time frame too.

If you just said to me “the only way you get fat is if you eat more calories than you burn”, then you can see now how you start looking like a petulant child learning at a grade 2 level. Think about every level in the list above. And then think about all the things that can go wrong with not only the output of said hormones, but also how the body is receptive to them. Do you think it would change things if a person had:

– Insulin resistance?

– Leptin resistance?

– impaired Thyroid function?, etc

HOW your body process and responds to the calories is a huge factor.

It should seem obvious, but…if you eat a high fat high sugar diet, you’re going to have a bad time. Shocking right?!! I know! Imagine that. What people telling us over and over again for years might actually be true. I don’t give a crap about what diet dogma you subscribe to, you can’t get around these factors. And you will see, there is not one diet approach in the world that advocates a high fat / high carb diet. It’s used to be Atkins or Pritiken. Zone or South Beach. These days it’s Paleo. Now the pendulum is starting to swing back again. What I’m trying to say is, you can dress it up and sex it up any way you want to. At the end of the day they ALL fall back on the same physiological principles. You are never EVER going to escape these.

Hormonal Response to Chronic Stress

As discussed in previous posts. Stress affects a great deal of the hormones involved in fat accumulation and fat loss. As a general rule. Chronic stress leads to an increase in all of the “bad” hormones. And a depression of all of the “good” ones.

Increased Cortisol

Decreased Growth Hormone

Decreased Thyroid Hormones

Decreased Testosterone

Increased Grehlin (makes you hungry)

Decreased Serotonin (makes you feel hungry and crave carbs, not to mention pain in the ass cranky)

Increased Insulin resistance / Decreased Glucose Tolerance

This obviously leads to greater fat deposition, increased hunger, muscle loss, and a slower metabolism.

Hormonal Response to Lack of Sleep

What happens to your body when you don’t get a) enough sleep? b) enough quality sleep?

Increased Cortisol

Decreased Growth Hormone

Decreased Serotonin

Decreased Testosterone

Decreased Leptin (feel hungry)

Increased Grehlin (again, you feel hungry)

Increased Insulin Resistance / Decreased Glucose Tolerance

As you can see. The responses from chronic stress and a lack of sleep are pretty much exactly the same. I need to look in to it further, but I’m currently unsure of the compounded impact of both of these occurring at the same time. For example, if you are in a highly stressed job or going through a difficult emotional period AND you are not sleeping, whether this has an even greater detrimental effect on your system than either one on their own. It’s common sense though, you rarely if ever have one without the other though. As most people can easily attest to.

Here it is!! How To Get FAT In 3 Easy Steps!!!!!

What is the perfect $#IT storm then for you to get fat??

1) Eating Too Much High Sugar High Fat Food

High carb / high sugar diet. High fat / high carb. HSHF or HCHF diet. Whichever way you cut it, there it is. Why does “processed” foods get such a bad wrap? Because this is exactly what it’s made up of.

Too much fats, too much carbs leads to “fuller” fat cells and insulin resistance.

Chronically elevated levels of insulin are a combination of too high insulin from too much carbohydrates and too much refined carbohydrates. It is also a result from insulin resistance. Insulin resistance can also result from over eating fats. So, just because you cut out your fruit doesn’t mean you can load up on all the butter and bacon you like and not have a problem. It’s stupid, it’s non sensical. It’s also unfortunate that some people still advocate this type of approach.

Now. Walk through any supermarket aisle and start looking at all packaged foods. Breakfast cereals, biscuits, chocolate, chips, whatever. Now look at the nutritional information and pay close attention to the “per 100g” part.

I will guarantee you it will look something close to:

Carbohydrates – 60g

Fats – 10-30g

Proteins – not much because we can’t get the food to taste good with it

Sugar. Fat. Salt. That’s what makes food taste good, feel good in your mouth, and make you want more.

2) Stress OUT about EVERYTHING

If I have to seriously write again why stress leads to fat gain, muscle loss, being a turd to live with and generally a shell of a human being, then you haven’t been keeping up.


3) Cut Down on Your Sleep

See above.

For every new parent out there that I haven’t had a chance to talk to. You’re going to get fat. You’re going to lose muscle. You’re going to suck at life for a while. For all of you people that don’t have an excuse. Shame on you, you should know better.

Now you know why “adrenal fatigue” is such a buzz word for the day.

Key Points:

1) Don’t eat too many carbs and fats

2) Stress is bad

3) Losing sleep is bad

Good. Now we’ve covered everything that makes you fat. We can now look at what you can do about it. 10 points to the people who can figure out what that’s going to be.

Coming Up in Part 8 – The Ultimate Fat Loss Environment

Calories Don't CountBen 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 iBooksAmazon 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 6 – Hormonal Control of Fat, Appetite and Hunger

Belly FatIn the last couple of posts, we looked at what happens after a meal and between meals purely from a substrate level response. Which somewhat contrasts what we learned in the first few parts, where we discussed what was happening from a cellular level and the enzymes that control fat being under hormonal control.

Remember from very early on in the series how we looked at the enzymes LPL (fat storage enzyme) and HSL (fat releasing enzyme). We learned these enzymes are mainly regulated under hormonal control. We also learned that insulin not only stimulates LPL but also inhibits HSL to promote fat storage. The main antagonist to this process being adrenalin.

Now we get to the exciting part of the series. The part where we start filling in the gaps. Now we start looking at what you eat and what you do and how it influences the hormonal environment as well. And how these hormones affect fat loss – or gain – at the cellular level. We are now moving on from the substrate level of control, to now also include the metabolic, enzymatic and hormonal control.

This is definitely NOT a comprehensive list. But it does serve to highlight some of the main players involved in this whole process. This instalment we are introduced to the main players, what their role is. In the next two posts we will categorise them in to which ones promote fat storage and which ones promote fat loss.

I will try and keep things as simple as possible. You don’t have to remember all the details, just as long as you understand the basic principles. Remember, hormones are messenger molecules, they tell your body to do things. These hormones operate simply to signal your body for a reaction to something that has taken or is taking place. Most of these are usually under strict regulatory control. Any thing too high or too low is often undesirable and can have consequences to your health. Also be aware, these hormones usually have an “opposing” hormone, and / or they work with others in different feedback loops. That levels start to rise or drop too far, this usually signals for something else to take place. Some hormones also affect the output of others as you will see.

Hormones that control Appetite and Metabolism:

Insulin – released by your pancreas in response to blood glucose and parasympathetic nervous system response. It is a storage hormone that promotes fat storage and prevents fat loss. This is the main regulator of your fat cell influencing not only fat storage but also inhibiting fat loss.

Grehlin – as you eat and your stomach gets full, your stomach starts releasing this hormone to tell your brain you are full. Think of Grehlin as your short term control of your appetite. If your stomach feels full, you are not hungry. This is one reason why eating high volume, nutrient dense, less energy dense foods help you feel fuller, without all the “calories”.

Leptin – remember how we learned that your fat cells act like an endocrine organ? Well this little baby is one of those hormones your fat cells release that has important implications in your fat loss efforts. Leptin is release by your fat cells and “talks” to your brain. In an oversimplified version, think of Grehlin as controlling short term appetite, but Leptin controlling your appetite over the long haul. The bigger your fat cells get, the more leptin they release. This Leptin tells your brain you don’t need to eat as much, in a sense it is telling you your fat cells are full. Leptin is a good way for your body to naturally suppress its appetite. Likewise, if you lose a whole bunch of body fat, your fat cells start to get “hungry” and they will tell your brain you need to eat more to fill them back up.

Leptin not only controls appetite, but it also has a direct effect on your metabolism and immune system as well. One of the biggest issues with people who are overweight is they start to become resistant to leptin.

Important*** You can become resistant to some of these hormones if they are pumped out in your system all the time. We have already discussed Insulin resistance. Quite often, insulin resistance will go hand in hand with leptin resistance. This means that you will have a high output of insulin promoting fat storage, but, even though more leptin is getting pumped out of your fat cells, your brain doesn’t listen any more. So you don’t feel full!!! So you keep on eating. And you get fatter…And the process goes on. This is one of the reasons why it is easier for fat people to get fatter. They don’t have the same off switch any more. This is also one of the ways in which your hormonal environment can influence your behaviour. We are quick to tell people just to “eat less and move more”, but we fail to give respect to the internal hormonal environment also influencing their metabolism and their behaviour.

We are quick to point to things such as testosterone for making people “angry” but when it comes to people that are overweight it’s all of a sudden their “will power” that’s lacking.

One thing I will say though, behaviour influences this internal environment, which then influences behaviour, which influences…and so on. It comes back to that age old adage you have to control the things you have control over.

Thyroid hormones T3 and T4 – Most people have heard of it. The hormones released by your thyroid are powerful regulators of your metabolism. T3 is the active form, with T4 having to be converted at the target cell in order to be used. Either way, this little sucker is responsible for how your body regulates your energy output.

Sex Hormones:

Oestrogen – typically known as the “female” hormone, but it is present in both males and females. As well as influencing a whole host of body processes, we are mainly concerned with the fact it increases fat storage.

Testosterone – typically known as the “male” hormone, but again, is present in both males and females. It promotes fat loss and an increase in muscle mass.

Stress Hormones:

One thing to note here is there is a difference between acute stress and chronic stress. Acute stress, say from exercise, is good. Chronic, or long term, stress is bad. Both of following hormones are released by your adrenal glands located above your kidneys.

Adrenalin – the “short term” stress hormone. This gets released during your “fight or flight” response and signals your body to release glucose and fatty acids. This is the main antagonise to insulin and promotes fat being released. This is one of the reasons why High Intensity Interval Training has been found to be such an effective means of stripping body fat over steady state cardio. Steady state cardio doesn’t have the same effect on adrenalin output.

Cortisol – the “chronic” stress hormone. I’ve written a little about cortisol and its effects in previous posts. More is written about it below. Suffice it to say, this one isn’t one you DON’T want chronically elevated in your system. It promotes fat storage and muscle loss over the long haul.

Sleep Hormones:

Growth Hormone – this powerful hormone affects muscle mass and fat loss. It gets a spike about an hour or so after you fall asleep, so sleep quality is important. It is also affected by protein / amino acid intake, blood glucose levels and also the type and intensity of exercise you do.

Serotonin – suppresses appetite, regulates mood, and influences sleep quality. You know how someone feels better and can sleep better after a few carbs? This is one of the reasons. One of the biggest complaints you hear about people preparing for a comp is they are cranky and they don’t sleep very well. This is one of the reasons.

Melatonin – another sleep hormone that affects the output of some of the other hormones listed here. One of the reasons why a lack of sleep can also affect Thyroid output.

One of the most important things to note is that most of these hormones do NOT act in isolation. They form complex interactions with one or more systems simultaneously. A dysfunction in one system will most likely cause a dysfunction in another. One example of this is Cortisol. Chronically elevated levels of cortisol work to actually inhibit your Thyroid output which works to DECREASE metabolism. Cortisol also increases insulin resistance to again promote fat storage. When cortisol levels are elevated it will also disrupt sleep cycles which in turn will affect Growth Hormone output. Cortisol also negatively impacts testosterone levels and the immune system. It’s no wonder why cortisol is the buzz word in the health and wellness industry at the moment.

The Good News:

In an effort to optimise certain systems, you will inadvertently optimise a number of them at the same time. This is the great thing about the body. When you eat the right amount of foods, of the right composition and the right quality at the right times, etc. You will optimise all of these systems on multiple levels.

The Bad News:

If you want to screw up your system completely, the reverse is also true. As noted above, if you are under chronic stress (sometimes there are times in your life when this can’t be avoided) it will have a knock on effect on multiple systems of regulation. This can put the whole system in to turmoil.

In the next couple of posts we will explore the optimal environment to promote fat loss and also the optimal environment for fat storage. The obvious point is to want to optimise the fat loss environment and inhibit the fat storage one as much as possible.

Take a look at all of the above hormones that affect fat loss and fat storage. And tell me honestly how many of them are directly influenced by the amount of “calories” you ingest?

But it still comes back to energy in vs energy out right? It’s still something to this day I question myself over and over again. And the short answer is yes. And no.

One thing to keep in mind though, is all of this does happen in conjunction with the type and amount of substrate involved!!!!

The amount of “calories” in doesn’t account for where it goes and what it’s used for. Whether this energy in is used up, lost as heat, stored for later, stored as potential energy, or stored as a structural organ / muscle, etc. It doesn’t account for other factors such as Thermic Effect of Feeding (see some previous Courage Corner posts for this), and so on.

There are so many factors to account for!!!!

But again, it will all come back to just a few key things well in order to optimise ALL of them.

SPOILER ALERT!!!! Even just from that list above, what do you think you can influence by diet? By training? By sleep patterns? By stress management? By the end you will find there are really just 3 key things (well, maybe 4, or more…) you need to do well to optimise this whole scenario on every possible level.

How many diets do you know of or can you list for me that even in the past couple of years you have heard of that really only try and focus on ONE of these factors???

– IIFYM (If It Fits Your Macros) – Looks purely at the calorie intake as being the most important factor. In it’s proper form has some great merit. At worst it’s misinterpreted and used as an excuse to eat pop tarts and nutella.

– Intermittent Fasting – looks to reproduce the fasting state as the key to fat loss. Works on a couple of different levels, but again, falls short on a couple of factors.

– Low Carb / Insulin control – apparently you can just eliminate carbs to eliminate insulin and then eat all the butter and lard you like and not get fat…

– Adrenal fatigue whatever – don’t get me going again…

One of the latest ones seems to be all about the Thyroid, or carrots and ice cream or something…

And don’t even get me started on everything from the past 20 years. There’ll be some people in the industry now who won’t even remember what Atkins means. Or they think that Paleo means low carb.

THE INDUSTRY IS F#CKIN NUTS!!! It always has been. It always will be. When it comes to fat loss, people want the latest thing. People want a quick fix. People want a pill. People want something easy. What they don’t realise, is, just like every informercial. All that happens is some old piece of SH!T gets reworked and repackaged in to some new form of SH!T that we think somehow is going to revolutionise the industry.

Just like Crossfit apparently did by reinventing the exercise wheel. But hey, at least they gave us the kipping chin up and a way to murder a KB swing. Enjoy your F45 or whatever it is the kids are in to these days, there’ll be something new in 6 months.

I better stop now before I really get going…

Coming Up in Part 7 – The Ultimate Fat Storage Environment

Calories Don't CountBen 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 iBooksAmazon 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 The Science of Fat Loss Series Part 5.2 – What Have We Learned So Far?

Below is a summary of the main points we have learned on our journey so far. These are the things to keep in mind as we start tying this whole thing together.

What we have learned so far:

  • Fat cells are MAINLY regulated by hormones, not “calories”.
  • Fat cells are in a constant state of flux. This flux is regulated by enzymes. Hormones in turn regulate these enzymes.
  • The main regulator of your fat cell is insulin. The MAIN regulator. NOT THE ONLY regulator. Insulin signals fat storage and also inhibits fat breakdown.
  • The main antagonist to insulin for your fat cell is adrenalin (for the liver it is Glucagon)
  • The main substrate that influences insulin is carbohydrates.
  • Substrate availability also influences your fat cell flux both directly and indirectly. For example, glucose availability drives certain reactions inside your fat cells and glucose availability also influences insulin.
  • Fat cells are therefore under substrate AND hormonal control. Substrates availability can in turn affect SOME of these hormones but NOT ALL OF THEM.
  • The ideal storage environment is typified by what scientists call the “fed state”
  • The opposite to this is the “fasting state”. This is typical of a fat burning state but does not constitute the ideal fat burning state as far as recompositioning goes.
  • The other hormones involved in fat storage and fast loss will be explored in future posts. From this we will determine what is the ideal fat loss environment and how you can go about creating it.
  • ANY diet or weight loss plan you could ever go on in your entire life will work through regulating one or more of the hormonal, substrate and metabolic factors involved.

When people say “cutting calories always works”. This is not an incorrect statement. But what they fail to appreciate is that it’s not just the substrate availability that has been affected. By cutting calories you also inadvertently cut down the insulin response indirectly as well, which in turn also affects the fat cells. What they don’t tell you though is that it is widely accepted in the literature that cutting calories is actually an INEFFECTIVE means of treating obesity. This is widely accepted in the scientific community as numerous journals and textbooks make mention of it repeatedly. Obesity is a multifaceted issue and one that can’t be tackled with just simple calorie cutting.

The good news is: we can affect nearly ALL of these factors that affect the accumulation of body fat with some meaningful changes that are under your control. You will learn what all of these are very very soon.

Other helpful things we have learned (from these and other recent posts)

– After a fasting period (or a relative period of low carbohydrates) your liver will make its own glucose if it’s own stores are depleted.

– your liver will stay in this state of gluconeogenesis even after you ingest carbohydrates until it’s own stores fill back up. This “shunting” of ingested glucose ensures your muscles and your brain have “first dibs”

– fructose can only be processed by your liver. If you ingest fructose with glucose post workout, this will result in greater muscle glycogen replenishment as the liver will shunt the glucose to your periphery while trading care of the fructose.

– if you ingest whey protein with fast acting carbohydrates post workout there will be greater muscle protein synthesis and greater muscle glycogen replenishment than either one on their own.

– you can do this without affecting how fat is processed

In Part 6 we now FINALLY get in to juicy bits you have all being waiting for!!! The main hormones that influence Fat Loss!

Calories Don't CountBen 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 iBooksAmazon 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 The Science of Fat Loss Series Part 5.1 – Decoding the Puzzle

How Do We Start to Decode the Fat Loss Puzzle??

The control of your body fat is an interplay amongst many factors. As I’ve mentioned from the very beginning, it is not just substrate availability, or “calories” that drives this whole business. You simply have to also give credence to the hormonal and metabolic environment that this is all occurring in AT THE SAME TIME. To confuse matters even more, the substrate availability does contribute to the hormonal and metabolic environment BUT it is not solely governed by it.

For example: Carbohydrates have an effect on insulin. But you can also affect insulin sensitivity in other ways (like exercise), which will also have an effect on insulin output. Eating carbohydrates after a workout can be partitioned differently with relative metabolic processing than at other times, which can assist in refuelling muscle glycogen levels quicker.

Also, your food intake doesn’t affect adrenalin output, but this is the main antagonist to insulin’s effects on your fat cells.

Strange how scientists will discuss the enzymatic and hormonal control of your fat cells at the cellular level, then completely bypass this when they take a step back and talk about The Fed State vs Fasted State. Then only revisit it again when looking at endocrine factors that control metabolism and relative disorders states. Why they never look at the interplay of these processes from the BEGINNING is beyond me. Some do. But for most it gets lost in translation.

The Interplay:

People throw the word “metabolism” around everyday without an even basic understanding of what exactly this means. It’s not good enough to just say “the amount of calories we burn”. Your body will only change these processes if it needs to. For example, your Thyroid will contribute to an increase in your rate of calorie expenditure in response to the cold. This is so it can keep warm. The Thyroid can also have its production rate influenced by other factors, such as stress and even the amount of daylight you’re exposed to. These processes are NOT strictly under calorie control.

At it’s most basic basic level, think of your fat gain / fat loss environment being influenced by

  • Enzymatic control at the fat cell level
  • Which in turn is mainly regulated by Hormones
  • Which in turn is mainly regulated by:

          1. Substrate availability: Your calories. From both ingested and previously stored forms

          2. Hormonal receptivity, Hormone levels, Hormone cascade events: NOT just your calories.

          3. Existing Metabolic environment: What’s the current metabolic status and, therefore, fate of those “calories”

As you know from the previous two instalments, the metabolic “state” the body is in has a direct influence over the fate of each macronutrient. For example, you eating carbohydrates after a fasting period have a different fate and a different effect on the body than during a “Fed State”. This partitioning of these calories and their fate has important implications in fat burning and maximising the use of each substrate.

If anyone at this stage of the process is still willing to argue with me that it is “all about the calories” please stop reading and leave. There is nothing more I can do to help you. In fact, you are beyond help.

People have seemed to have been able to accept that HIIT works better than steady state for fat loss. Even though your fitbit calorie counter might not say so. But they can’t accept it’s not just all about the calories you eat. No. THAT somehow defies science.

Coming Up in Part 5.2 – What We Have Learned So Far?

Calories Don't CountBen 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 iBooksAmazon 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 The Science of Fat Loss Series Part 5 – The Fasting State

Last instalment we covered The Fed State, which is what is happening in the body immediately after you ingest a meal.

This week we will explore what happens between meals and during the overnight period. Something that is also known as The Fasting State. For scientists, this also equates to their version of The Fat Burning State.

The Fasting State (aka Fat Burning Mode)

A few hours after your meal, blood glucose levels begin to decline. Your body decreases its Insulin secretion and Glucagon secretion starts to rise.

Just as insulin signalled the Fed State. Glucagon signals the Fasting State. 

Glucagon is therefore the main antagonist to insulin. Wait, wait, wait. I know in previous instalments we discussed Adrenalin as being the main opponent to Insulin. And this is still correct. As far as your fat cells go! BUT. Glucagon has NO EFFECT on human fat cells. So, your fat cells don’t care about Glucagon. So what gives? This is the prime example of how scientists and their definition for certain states are extremely myopic and small minded when it comes to how the body works. All they are concerned about when discussing these states is purely blood sugar levels and blood sugar maintenance. Rarely do they discuss tissue specific responses in correlation with each other.

So, the main target of Glucagon is your liver. Glucagon signals the liver to start releasing some glucose to keep blood sugar levels stable. Your muscles though, are pretty selfish and don’t listen to Glucagon. Your muscles actually lack the enzyme to release stored glucose back out in to the blood stream. Once glucose is stored in your muscles it stays there until the muscle itself uses it up. It won’t release it back in to the blood stream for your brain to use! Think about the implications of this for a minute. We are constantly drilled in to your heads how important glucose is for your brain. That your brain mainly uses it as its primary fuel source and can’t function properly without it. And yet your body stores MOST of your carbohydrate stores (even up to 3-5 times greater) in a place where the brain will never have access to it! Your body obviously values the principle of “fight or flight” over the maintenance of blood glucose for the brain. This will have important implications later for the timing of your carbohydrate intake. Anyway, I digress…

During this period of lowering glucose, your body keeps blood sugar stable in 3 ways:

1) Your liver releases it’s stored glucose – any glucose that was stored in the liver after the previous Fed State will now start to be released in order to maintain a normal blood glucose level.

2) Your body releases more fatty acids – your body will start to release more fatty acids in order to have them available for an alternative source of energy in order to preserve blood glucose.

3) Your muscles and liver shift to use more fatty acids for energy – Just as your body made more fatty acids available, your muscles and liver switch their metabolic processes to now burn more fatty acids. This all has a “glycogen sparing” effect.

This is why it’s also sometimes known as The Fat Burning state. This is the type of environment where your body is releasing more and more fatty acids and your body switches to mainly uses the fatty acids as a fuel source. If you are in the Fasting State, you are usually in a Fat Burning state.

What happens once liver stores of glycogen are depleted? 

Remember, one of the primary roles of your liver is to maintain nice steady and stable blood glucose levels. So, what do you think your liver does if you haven’t eaten anything and it has run out of its own supply?? It starts making its own glucose! It’s a process called gluconeogenesis. This process mainly occurs in the liver, and it is for this reason your brain doesn’t get too panicky about the muscle not releasing any glucose! It knows the liver has got its back, and will make glucose for it if needed.

Where does your body get the raw materials to make glucose from?

It’s impossible for your body to make fat in to glucose, but it can use some of those glycerol backbones we’ve already spoken about. The other substrate it can use are amino acids. If you haven’t eaten any or enough protein, your body will start to break your muscles to get it. Obviously not a good state to be in if you want to keep your gains while stripping fat. This is one of the reasons why, if you are on a lower carbohydrate intake, you may have to increase your protein intake even more to compensate for this.

The ReFed State (after an overnight fast)

An interesting thing happens if your body has gone through a slightly longer fasting period, as what happens after an overnight fast.

If you wake up in the morning and have a meal, any fats you eat will still get processed the exact same way.

Curiously though, even if you eat carbohydrates, your liver doesn’t stop making its own glucose. At least not yet.

Any glucose you do eat is actually shunted away to your muscles for them to get “first dibs” on it. While this is going on, your liver actually keeps making its own glucose, but now it uses it to fill up its own glycogen stores. This also has some implications for nutrient timing to be covered later. It is also for this reason some people recommend partitioning half of your daily carbohydrate intake between the post workout meal and your first meal of the day.

Once your muscles have their fill. And the liver stores fill up. The liver starts making fatty acids again. Obviously, the magnitude of all of this is largely dependent upon HOW MUCH of each macronutrient you have eaten. Yes, amounts of macro’s still do matter.

The Fed State 2

Fasting diets

Just because scientists talk about the Fed State as being after a meal. They never stipulate exactly what the composition of that meal is. Read any text book and they will all talk about the Fed State as after you have insulin being released in response to a large enough carbohydrate meal.

Obviously, The Fed State is not an ideal metabolic environment to be in when you are trying to lose fat. Your body is in fat storing mode.

The Fasting State (at least metabolically mimicking this) is the state you want your body to be in for fat loss to take place.

How do you affect the most fat loss then? Well, that’s easy. Spend more time in the Fasted State than what you do in the Fed State right?

This is the principle and theory behind the rise, and also a reasonable amount of success, in the popularity of fasting diets. Or variations of, such as with intermittent fasting. These diets seek to prolong this fasting state, so you can stay in a fat burning mode longer.

Another benefit of Fasting is it also improves your insulin sensitivity and glucose tolerance. Even though the fasted state has been studied, it has literally only been the last couple of years that researchers are again looking at the benefits of prolonged and intermittent fasting as a treatment modality of obesity. Not only can you control peoples energy intake this way, you also serve to improve their glucose tolerance, which helps a great deal in Type II diabetes management.

But. The fasting state is not without consequence. If blood glucose levels remain low over an extended period, your body will literally start cannibalising itself in order to get what it needs to make more. So you will be at a greater risk losing muscle. Remember, your body can’t convert fat in to glucose, but it can convert amino acids in to glucose. If you don’t have enough ingested orally through the foods you eat, your body will have no choice but to eat in to its own flesh to unlock some.

If only the was a way to mimic this fasting state without eating in to your hard earned gym gains…

Also remember, this is only looking at a small piece of an overall puzzle. There are other factors that influence the flux of a fat cell beyond what happens after a meal and what happens between meals.

Key Points 

1) Fasting State = releasing mode = ideal for fat burning

2) Fasting State by scientific definition is several hours after a meal and is characterised by Glucagon

*I’m not condoning nor condemning fasted diets. Only giving you the background and principle on which they are founded and the science of why they work. It is up to you whether you believe this is the best method to decrease body fat. I wouldn’t necessarily be making that conclusion half way through the series though…

Things you should be asking yourself at this stage:

Is there is a way to manipulate the Fed and Fasting states by changing the composition of your meals and by also changing the timing of your meals?

Could you somehow mimic the fasting state, but offset the potential muscle loss?

Could you somehow manipulate your carbohydrate intake to prolong the fasting state, but still have enough to recover and fuel your training sessions?

Can you think of some ways of doing this before we continue with Part 5.1??

Calories Don't CountBen 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 iBooksAmazon 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 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.

The Fed State 1

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.

The Fed State 2

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

Calories Don't CountBen 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 iBooksAmazon 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?

Calories Don't CountBen 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 iBooksAmazon 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

Calories Don't CountBen 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 iBooksAmazon 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

LipolysisHow 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)

Calories Don't CountBen 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 iBooksAmazon 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

How You Store Fat

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

Calories Don't CountBen 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 iBooksAmazon 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.