Month: December 2019

Lots of people talk about how bad eating carbs are and how it makes you fat but not may actually explain how the body handles carbohydrate.

I won’t even come close to explaining it completely and in every situation but I hope to bring you some insight into how it works. This explanation is not meant to be an exact calculation of how much fat someone accumulates per day. It is for example purposes only. I will also not be taking into account any of the inflammation or other potential negatives of eating a high carb diet. This is just to look at how carbs can cause weight gain in context of a high carb diet with moderate fat.

To understand how carbs are dealt with we first need to understand glycogen. Glycogen is the storage form in the body for carbs. We have two major depots for it. Liver and muscle. Glycogen is just very long chains of glucose combined.

Liver is used to provide a steady supply of glucose to the body for things that use alot of it and typically can’t use fat for fuel. Like the brain and red blood cells. There is about 100g of glycogen stored in the liver or about 400 calories. The body can access this glycogen pretty easily and will do so to keep blood glucose levels stable. The glucose derived from glycogen does not typically have much of an affect on blood glucose levels or insulin. It is just metered out as it is needed and will not register on a constant glucose monitoring device other than just very minute up and downs if you zoom in close enough.

Muscles are the other depot. Much larger than the liver stores, the muscles can hold about 400g or 1600 calories worth of glycogen. This glycogen is different. It cannot be readily accessed by the rest of the body. It is reserved for muscles and will only be used there if the level of exercise the body is doing requires glucose. So like running from a bear. In order for it to be returned to the blood it has to undergo a process. One that might be familiar to some. Gluconeogenesis. Most people think this is just where the body creates glucose from protein but it is actually working in other ways and fairly often. So if we have glycogen stored in the muscle and there is an emergency, like low blood glucose, gluconeogenesis could be used to get at the glycogen stored in the muscle. It is a big process though so this is unlikely to happen all that often. In order to get out it has to be converted to various different molecules and then to an amino acid, Alanine, which can then be sent to the liver where it can be converted through multiple reactions back to glucose. It is a process. Just suffice to say this is pretty much off limits to the body except for exercise. If you want to learn how this works here is a very indepth video.

Now that we know the places in which carbs are stored, now we can look at why it is a problem for most people to eat them at recommended levels.

Lets use an example of someone eating a standard diet of 2000 calories per day. We will use the standard recommendations:

• 15% protein = 300 calories/75g
• 35% fat = 700 calories/78g
• 65% carbs = 1300 calories/325g

Let us pretend that this is a brand new human that just appeared on earth and has never eaten anything before. All glycogen is empty. Lets also pretend this new human doesn’t do any exercise. They work from home and don’t workout. They barely move. For simplicity.

Knowing what we know about glycogen we can see that 100g of those carbs will go to the liver that will be used to maintain blood glucose levels. 225g will go to muscles which will be reserved for intense exercise. Like running from a bear. The protein will mostly go to maintaining and repairing lean tissue and making enzymes. A small amount might go to glucose but that will be negligible. For simplicity we will forget about that. The fat will go to adipose tissue for storage and when insulin drops, after about 2 hours in a proper functioning human, the fat will be used for fuel. Some of the byproducts of fat breakdown (glycerol) will contribute to daily glucose needs but like the protein we will forget about that for simplicity.

Lets look at our totals after new human day 1:

• liver 100g of glycogen
• Muscles 225g of glycogen

Since we know the liver will be used to maintain blood glucose that will be fine and will empty out over the course of the day. Cool.

The muscle glycogen doesn’t get used because our new human is sedentary.

Day 2:

Same diet. We will only look at carbs from here on out for simplicity.

325g of carbs consumed. So we know the liver will take the 100g easy. That leaves 225g. Well the muscles still have 225g from yesterday and as we mentioned previously, the capacity is about 400g. So that means only 175g of that glucose from the carbs is going to go to muscles.

Lets look at our situation:

• liver 100g of glycogen
• Muscles 400g of glycogen (MAXED)
• Excess of 50g of glucose

What happens to that glucose? Well it undergoes a process called de novo lipogenesis (creation of new fat). That fat will get taken to fat cells for storage and added to the pool along with the 78g from the daily food intake.

We are probably still in good shape. The 78g of dietary fat plus the 50g made from glucose is still probably not going to contribute to any significant weight gain. The body should be able to use that when not eating.

Day 3:

Same diet.

325g of carbs consumed. So we know the liver will take the 100g easy. That leaves 225g. Well the muscles are maxed out at 400g so that 225g is now excess floating in the blood.

Lets look at our situation:

• liver 100g of glycogen
• Muscles 400g of glycogen (MAXED)
• Excess of 225g of glucose

Like the previous day we know that excess is going to be converted to fat via de novo lipogenesis. Now we have 225g plus 78g of fat. 303g (lets call it 300g for simplictiy) is likely enough to add to net weight gain in a sedentary person. How do I know this?

Lets look at some numbers about fat usage:

At rest a person uses somewhere between 0.06 and 0.10 g of fat per minute for fuel. This is only going to happen when insulin is at baseline. So when you eat you will not be using fat for fuel. Let’s look at how this might play out:

• 3 meals a day
• 2 hours for insulin to return to baseline after each meal
• 8 hours of elevated insulin
• 16 hours of baseline insulin

16 hours of baseline insulin means that there will be 960 minutes of fat burning time. Lets give the upper limit of 0.10g/min of fat oxidation.

That gives is 96g of fat used per day. Lets call it an even 100g.

So if we have 300g of extra fat per day coming from the diet and we only use 100g, that means 200g of fat extra will remain in fat cells per day. Since there is 454g in one pound you can see how fast this might add up. That is 1 pound of fat every 2.25 days.

Now keep in mind that nobody is completely sedentary and not every gram of excess glucose gets converted directly to fat but you can see what happens here in the simplest of terms. There is also the fact that the body will attempt to deal with excess energy by increasing metabolic rate just the same as it adapts to lower calories when you cut calories.

If a person is doing this on a consistent basis they might gain 1 pound every 2.25 days for the first week so you might gain 3lbs. The body will start upregulating metabolism in order to deal with the excess energy. After a few weeks you will likely be gaining marginal amounts of weight. A faster metabolism in the context of a high carb diet usually means more hunger and that person might be likely to start eating more. The higher intake will start the process again.

Now if this brand new human were to exercise this would be a different story. Looking at the chart above you can see that running has a potential oxidation rate of 2g of glucose per minute. Since this hypothetical diet has 225g of glucose going to muscles a day, if the person where to simply run for 112.5 minutes a day they would be in balance. This is where the calories in vs calories in kind of works. Again there will be issues with this. The longer hypothetical human does this running, the more adapted the body will get to this and will be used to running this much and eating this much. If hypothetical human stops running they will gain weight pretty quickly.

Back to the non exercising hypothetical human and their hypothetical diet.

If you don’t use that carbohydrate that is stored as glycogen in the muscles the daily carbohydrate will mostly get converted to fat. This starts quickly building up and filling up fat cells. Once fat cells are full this is when things start going haywire.

First blood triglyceride levels go up as glucose is converted to fat (triglyceride is just fat in the blood). Once those levels are too high that process will be inhibited and the glucose will start to build up in the blood. This increases output of insulin from the pancreas and this reduces the amount of fat you will use per day and increases the need for dietary glucose to supply energy.

This is metabolic syndrome. This is a talk for another day.

Keto ON,

Coach Jack

To continue the trend of going against the grain and being unpopular I am going to be the devils advocate and make a case for insulin and insulin resistance. Say What? I know. I am a sucker for punishment.

While it is true that having chronically high insulin prevents fat from leaving fat cells and the term “Insulin Resistance” or “IR” is all the rage and blamed for all the problems of society, insulin is actually critical and insulin resistance is something that is meant to save our lives. Yes it’s true. Let me explain.

First lets look at insulin and why it is necessary.

The largest bit of evidence of insulin being good is type 1 diabetes. Without insulin we die. Glucagon runs wild and converts muscle and fat to sugar and ketones. This is called ketoacidosis and is deadly. Insulin is necessary to prevent death.

The next reason that insulin is critical is because it is the only thing that can push nutrients into cells. Without insulin we can’t build any tissue and can’t get adequate nutrition.

Without adequate insulin glucose stays in the circulation too long at at too high levels. This is when we start to see higher levels of HbA1c. HbA1c is a measure of how much cells have been glycated or how long they have been soaked in glucose basically. A normal level of HbA1c is 4% to 5.6%. 5.7% to 6.4% is considered pre-diabetic and 6.5% and up is diabetic. These are predictors as to the average blood glucose level and your level of insulin resistance.

When is insulin bad?

Well clearly if you are constantly spiking insulin by eating every 2 hours then you are likely to get fat but not even in all cases. In order to get fat from eating constantly you have to be eating carbs and fat together. if you are eating pure carbohydrate you will not be storing any fat so it is highly unlikely that you will get fat. It is technically possible but I have tried it and it is pretty damn hard. I actually lost weight eating very high carb and very low fat. It was almost impossible to over eat.

It is also bad if you are already “insulin resistant” but more on that later because it is not what you think it is.

Why is Insulin Resistance a good thing?

This comes down to a basic misunderstanding of what is and why it happens.

To get an idea of what it really is lets look at what we all love. Keto. When you are in ketosis you are “Insulin Resistant”. Wha???? How can something that makes us healthy cause something that is associated with obesity?

Well that is because insulin resistance is actually a very diverse function that is actually meant to ensure optimal function and survival. IR in keto is only in certain tissues. Other tissues are perfectly sensitive to inulin.

In keto muscle is insulin resistant but fat cells are not.

By making the muscle cells insulin resistant it prevents them from using glucose. This is necessary to preserve glucose for the cells that absolutely need it. This is critical in ketosis since we have little to no glucose intake and if the muscles continued to be insulin sensitive then the body would make more glucose and that would have to come from lean tissue (muscle) and this would result in a much more rapid death.

If fat cells were also to become insulin resistant then fat would not be able to cycle in and out easily and fat consumed would not leave circulation if not used for energy. It has to constantly flow in and out of cells for proper metabolic health. We would soon suffer from hypertriglyceridemia.

So here we can see not only that IR is critical to survival but it can be active in select cells under different circumstances.

Another example of when IR is positive is when saturated fat, especially stearic acid, is high and unsaturated fats are low. Saturated fats, usually only longer chain fats though, cause mitochondria to release molecules of superoxide that tell the body to do several things. One of them is to make muscle cells more insulin sensitive and fat sells insulin resistant. This allows fat cells to not take anything in at all and muscles to burn more substrate. If glucose is in the diet then they will burn more glucose and none will go into fat. When fat cells become insulin resistant they also start burning more fat internally and start acting like brown adipose rather than white. White adipose is primarily inert and just stores fat. Brown adipose tissue is very metabolically active and is highly involved in body heat. This Browning of white adipose is the reason that when some people eat very high saturated fat their body heat increases dramatically. The fat is burning high rates of fat internally and generating lots of heat. Babies have more brown adipose tissue than white and is why they don’t tend to shiver when cold. Shivering is the muscles trying to increase body heat by shaking and generating friction.

These positive examples are often referred to as peripheral insulin resistance.

So that is how insulin resistance is a good thing. Lets look at what the prevailing theories are about insulin resistance are and why they might be bad.

The negative association of IR comes from obesity/type 2 diabetes characterized by high blood glucose levels and high fasting insulin levels. These are circumstances are referred to as pathological insulin resistance and are signs of dysfunction and a disease state.

My preferred theory is Personal Fat Threshold. This theory states that each person has a level of fat storage and once they reach that capacity the cells just can’t take on any more glucose and glucose builds up in the blood. This would also explain why triglycerides rise as well as glucose. If glucose can’t get in neither can trigs. Insulin then rises as the pancreas increases output which either enlarges or grows new fat cells which again brings glucose under control. This process continues until the pancreas can no longer put out enough insulin to increase fat cell storage capacity. At this point the individual will need exogenous insulin injections. The injections then facilitate the growth/proliferation of fat cells. This study showed that fat cell enlargement was a good predictor and possible contributor to insulin resistance.

The other popular theory is that exposure to insulin itself causes insulin resistance. There is not much supporting evidence for this from what I can tell. It is a chicken egg scenerio. High insulin is present in insulin resistance so it is associated but what makes the insulin high is another story. I point back to the personal fat threshold theory. Proponents of this theory say that just stimulating insulin often causes the body to become “numb” or “deaf” to insulin signals over time. To me, this would indicate that everyone who eats high carb diets would have to be insulin resistant and unfortunately there are billions of high carb eaters that are just stubborn and won’t develop any signs of IR. How dare them.

So I have shown several instances where insulin resistance is saving our lives and presented two theories of why this pathological state occurs. We can maybe see why IR gets a bad rap when it is not at all meant to be the bad guy.

Finally let’s take a look at a case study where the goal was only to get someone off of insulin in an attempt to heal them and why this is a very shortsighted approach.

This is a case study from the Clinic of Dr. Jason Fung.

Over a 4 month period the patient was fasted 24 hours three times a week. Over the 4 months the patient lost 17.8% of his bodyweight and was able to stop taking his insulin despite being on insulin for 10 years. Success right? This was the best possible treatment and the patient was saved right?

Well sadly no.

The part that makes this not the best treatment is that the patients HbA1c was only dropped from 7.7% to 7.2%. He is still very much diabetic and has very poor glucose control. With this level HbA1c he still has a huge risk of disease and mortality. So yes he lost weight and got off insulin but he is still at very high risk.

Why didn’t this work? Remember before when I talked about personal fat threshold and how the pancreas would increase output until it was no longer able to make enough insulin? Well this process burns out the cells in the pancreas so they no longer make enough insulin on their own. This lack of insulin secretion is sometimes referred to as brittle diabetes.

So the patient at the clinic is not taking his insulin anymore but since his pancreas is not making adequate amounts, he is still glycating his cells and keeping his risk high. This is the mistake that is being made by those that think insulin is the bad guy and getting off of it is the solution.

The better solution would be to respect the power of insulin and properly manage the insulin to reduce the HbA1c and reduce mortality risk. Not just to get the person off of insulin.

Thanks for sticking with me on this one. I know it can be a rough read but it is so very important that we properly understand all the underlying players in this game that is insulin resistance.

keto ON,

Coach Jack

I want to start this by saying that I truly love the keto diet. I am a die hard fan and a 15 year veteran with no intention of stopping. I just want to be intellectually honest and play devils advocate.

With that said, we have a problem in the community that makes it rival veganism for its bias and echo chamber like madness.

I am only now realizing this because I was stuck in it hard for over a decade. I had it in my mind that carbs where the devil and insulin was a dangerous drug. It took me doing something crazy to try and prove carbs were the devil to see that I was very wrong and so is the majority of the low carb community. We are too stuck in the echo chamber and it is a detriment to furthering the health of the world.

Again, I am not saying low carb is not the better diet. I am not even saying that low fat is good. I am saying that it isn’t that cut and dry.

Today I am only going to address the reversal of diabetes/insulin resistance. I am not going to address any other issues. Inflammation, overall health, nothing. Just one thing. Reversal of diabetes. The normalizing of glucose control.

The title picture says alot.

Here we have two doctors with opposite advice but both have clinical proof of their reversal of diabetes. We as a low carb community praise one and denounce the other as a quack. Neither one of them are specialists in the field of bariatrics or endocrinology yet people look to them as experts. McDougall is an internist (general physician) with no specialization. Fung is a nephrologist (kidney specialist) with no training in nutrition or endocrinology. Why do we see one as a genius yet the other as a quack?

This is what bias is. We like what one says and we don’t like what the other says. The truth is, they both have results. They both have tons of case studies showing reversal of diabetes with their approaches. The truth is, they are both right in some ways and very wrong in others. We just choose who we think is right based on our preference.

McDougall claims that fat causes insulin resistance and he quotes studies that seem to show this to be true.

Fung claims insulin itself causes insulin resistance and also quotes studies.

Who is right? Well they are both right in some ways and wrong in others. Neither is seeing the whole picture.

McDougall is right that fat does seem to cause insulin resistance. When someone eats a high fat diet, especially with low carb they do become insulin resistant. Absolute fact. He is not lying. The error is that this is not a pathological state. It is a protective measure. The reason we become insulin resistant is so the body will not be trying to use glucose for fuel in tissues that don’t need it and when it is not being supplied at a high rate. If we didn’t become insulin resistant we would run through glucose like crazy and the body would be constantly catabolizing lean tissue to make that glucose. We would waste away and die. So McDougall is right and he is wrong. He is just highlighting what he wants you to see so that he appears to have the truth.

Fung is right in that too much insulin can result in insulin resistance. It is far from accepted in any medical circle that it is caused by exposure to insulin alone. If it was then everyone who eats a high carb diet would have insulin resistance. There are billions of people that eat a high carb diet that are not insulin resistant. There are people eating nearly 95% of their diet as carbs that are not obese, they are not insulin resistant and they will not be. The way it causes insulin resistance is not fully understood but the theory I see the most evidence of is that it is caused by the person fat threshold of the individual. This is why we see some people become insulin resistant at low bodyfat (asians) and some people can become very obese and still not be insulin resistant (caucasians). So Fung is partially right and partially wrong. He does the same thing as McDougall and only shows you the parts that make his theory sound the best.

What was it that lead me to this? Why am I questioning the almighty Gods of the keto community? Or the high carb community for that matter.

The biggest issue of all here is that both sides are comparing to the infamous strawman.

A strawman is a fake opponent. The low fat side compares their ideal diet to the SAD diet (high carb and high fat) and call anything on the other side of that bad. They never look at a true low carb/keto diet.

The low fat side also compare to the same strawman. They look at a SAD diet and say anything on the other side of that bad. Low carb tends to be a little bit more open minded and will admit that low fat whole foods diets are probably better than SAD but they still can’t admit that low fat can see benefit.

I decided last year that I was going to prove once and for all that eating a very high carb diet in and of itself would cause you to get fat.

What happens when a hardcore Ketonian goes high carb raw Vegan for 14 days?

What I found by doing this changed my perspective 100%. Not only did I not have trouble with insulin resistance or glucose control but I lost weight. It was not all positive. There were downsides:

• Healing seemed to be slower
• I spent half my day in the crapper
• I felt gross and bloated half the time

This was probably my most important experiment because it pushed me outside of the echo chamber and forced me to research the other side and see how this was possible. Only when you see the other perspective can you truly get down to the root of things.

I am not the only person to see this. Check out this blog from Denise Minger. She refers to a wonderland at each end of the spectrum and in the middle is swampland. She refers to low carb high fat as carbosis which I think is pretty accurate.

In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)

I think she took alot of flack for this because she never wrote a part 2. I am not scared of the flack. I ain’t afraid of people getting hurt feelings because I threaten the echo chamber. We need to look outside the chamber to get to the truth.

Again, I want to reiterate that I love low carb. I truly think it is the natural way to live. I just want to be clear that it is not the only way to do things and we need to beware of putting people on pedestals just because they agree with our bias.

We really have to look for evidence to the contrary of our bias to see if our theory pans out. This is referred to as the black swan principle in science.

If you see only white swans and you propose a theory that all swans are white then you see a black one. You must admit that your theory is wrong. You can’t just deny that the black swan is not a swan because it is black and all swans are white. You see the issue here?

McDougall – Fat causes insulin resistance and only a high carb low fat diet can be the solution to diabetes and disease.

Millions of people eat very high fat diets and reverse their diabetes. There is your black swan.

Fung – Insulin causes insulin resistance so the only solution is to reduce the amount of insulin secretion we are getting to reverse diabetes and disease.

Billions of people eat very high carb diets and eat multiple times a day and are completely healthy and have no insulin resistance. There is your swan.

Don’t miss the black swans because all you want to see are white ones.

Keto on!

Coach Jack

Is Olive oil healthy?

Olive oil has been touted as something healthy for many years now as a result of the Mediterranean Diet.

The reason they hypothesize this is due to the fatty acid Oleate or Oleic acid.

Like many other things being touted by the mainstream as being healthy I think this has been a mistake.

First we know that the current incarnation of the Mediterranean diet is not how the greeks traditionally ate. The diet was made up. It was based on post war Greece where their food supply was decimated and also when the majority of the food questionaires were gathered it was during lent so they were giving up meat for lent.

What anthropology and history tells us is that the ancient greeks actually ate a lot of meat from lamb, goats, wild pig and seafood. They did have some olive oil but it was not a main component of the meal.

The current idea of the mediterranean diet is actually just the american food pyramid of the 1950s with some olive oil added in. This was an invention of a think tank and not based on the real historical diet of the mediterranean.

Now we seem to drench everything in olive oil because of a misconception.

Humans have an enzyme, the SCD1 enzyme, that converts saturated fat to oleic acid. Clearly it is important to health.

To figure out how much scientists took mice, who have the same gene, and genetically modified the mice to knockout this gene so they could not make any oleate.

They fed them a high fat diet of a mixed ratio of saturated to unsaturated fat. The wild mice on the diet got fat. The knockout mice did not. They had less fat overall, dramatically less dangerous visceral fat and more lean mass. Despite the knockout mice eating 25% more calories than the wild mice.

This was interesting.

They then took mice that were genetically modified to become obese quickly. They also knocked out the SCD1 enzyme. The obese mice became lean.

Very interesting indeed.

They then took the SCD1 knockout mice and fed them a diet of zero oleic acid and only saturated fat. Again the mice were eating ~25% more calories but were staying lean and appeared healthy. When they dug deeper they saw signs of liver damage, inflammation and the start of atherosclerosis. This was troublesome. They then supplemented the smallest amount of oleic acid to the diet and the mice were restored to good health.

Very very interesting.

They then took all the mice and fed them a diet of increasing levels of oleic acid and the further they pushed them toward a oleic heavy diet the fatter the mice got and they started getting fatty liver and diabetes.

Brilliant.

Clearly some oleic acid is needed. This is why we have the enzyme. Then there is also the fact that animal fats are already nearly 50% oleic acid. We should not be adding it in.

If we look at the diet of the french we can see an interesting case here. The French were famously left out of the famous 7 country study that “proved” saturated fat was bad and the cause of heart disease because they didn’t meet the criteria. They ate lots of saturated fat and had very low rates of heart disease.

When we analyze their saturated fat to unsaturated they had a nearly 50/50 ratio. Despite their high carb/high fat and high booze diet, they were lean and realtively free of heart disease. We can see this clearly from the FAO food data from 1970 which I have attached below.

You can see as well that they french rate of obesity has increased. It is slower and less pronounced than the west but it still increases. It also directly correlates with an increase in intentional unsaturated fat increase.
I think this is a pretty strong case that olive oil is not healthy. Stick to animal fats. You can see this in the below image of their food breakdowns. The only real change is the increase in unsaturated fat.

I think this is a pretty strong case that olive oil is not healthy. Stick to animal fats.

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