I was having a discussion about epilepsy. That led to high ketones which led to how you get high ketones and when.
This led me to the paper below.
Oxaloacetate Deficiency in Mct-Induced Ketogenesis
This is a study on why MCT causes increased ketones but it tells us so much more. Let’s start with how ketones are made:
Ketones are made when insulin is very low and all stored glucose in the liver has been depleted. That is the basic part of it. Lets get a little deeper. First we have to look at the Krebs cycle or also known as the citric acid cycle. The Krebs cycle is the first major step in ATP creation.
It all starts with AcetylCoA at the top but the other major player we are going to talk about today is just to the left, Oxaloacetate. When insulin is very low there will be lots of fat being released from adipose tissue. When glucose is broken down for use in the krebs cycle it only results in one AcetylCoA but when fat is used it breaks down to two. When you have lots of AcetylCoA like when insulin is low then you end up having a limiter in the amount of cycles the krebs cycle can turn due to the limit of Oxaloacetate. Oxaloacetate is also needed to run another process we know about, gluconeogenesis or GNG for short. Since GNG is critical to the maintenance of blood sugar level it gets priority over the amount of oxaloacetate that is supplied to the Krebs cycle so there is a limit to the amount of AcetylCoA that can be turned to ATP. When you have lots of fat converted to twice as much AcetylCoA and the krebs cycle is limited in how fast it can process it, you get a build up of AcetylCoA waiting at the krebs cycle door. This results in ketogenesis.
So now we understand that when we have ketones we already have more AcetylCoA than the krebs cycle can use to create energy so it gets diverted to ketones. Now lets look at MCT oil and what it does.
MCT oil cannot be stored as fat. It must be oxidized in the liver to AcetylCoA. When we have ketones in the blood this means we already have too much AcetylCoA so adding MCT oil at this time is not going to do anything other than make more ketones. It can’t go through the Krebs cycle any more than any of the other fats at this point. All it is doing is keeping the AcetylCoA pool full and generating ketones. We only need so many ketones. More ketones does not equal more energy. ketones are not energy. They are potential energy. Just like glucose and just like fats. They are just a potential energy source. They still have to be metabolized like any other fuel and having more of it does not mean we are going to use it. Ketones will really only be used in certain tissues like brain and red blood cells and they can only use so much. Having super high levels is not a benefit. Especially when it is MCT oil supplied. You are better off to leave it out.
Now why won’t it help you lose weight and might actually keep you from losing weight.
Because it goes right to the liver while other fats go to adipose first before they get into circulation, MCT oil is going to take precedence over other fats in the AcetylCoA pool. It has to be utilized first because it cannot be sent back to storage and it can’t circulate in the blood. It must be used first. If it is taking precedence then it will leave fat that has come from adipose tissue, like your own bodyfat, in circulation where it could eventually make it back into storage if and when insulin levels rise.
Writing this article led me to discover an answer to why people tend to make less ketones the longer they are on keto but that will be an article for another day. 🙂
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:
Levels of fat Oxidation at rest/walking/running
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.
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 tissueis 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.
Babies don’t shiver when cold
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.
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.
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.
Keto bias leads to false idols
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 wasit 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 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.
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.
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.
One of my clients sent this picture to me. This is the kind of ridiculous nonsense that infuriates me about most people pushing keto without regard for how the body works or to your health and longevity.
Besides the fact that this is starvations level caloric restriction, which will tear into soon, lets look at the glaring problems.
Many of the veggies here are full of anti-nutrients like lectins and oxalates. Spinach, for example, is a potent goitrogen which blocks iodine uptake and causes thyroid dysfunction.
Many of the the fat sources are also high in carbs. If you start with your carbs and build 10g then add 30g of fat from the fats column you will be going higher in the carbs. You will likely end up with 15-20g of carbs per meal.
Some of the correct things.
Protein is right. 20g for women and 25-30g for men. Perfect.
In small print it says if you are hungry eat more fat. Correct. Way more than 30g per meal though. More like 55g minimum.
Thats it for good.
100% absolutely not acceptable. This is 1170 calories per day. This is severe caloric restriction and will destroy your metabolism and thyroid function. You will lose lean muscle mass and bone mass. You will break you body in long lasting ways.
When does starvation ever work? How many of you have ever sustained for life on 1200 calories? You can’t. Your body won’t let you and unless you continue eating 1200 cals for life you will gain the weight back and fast. Keto is not different in this respect.
The recommended caloric intake for a 2 year old is 1600 calories. The average 2 year old weighs 27lbs. How on earth does anyone think that someone that weighs 5 or more times this weight can survive on 400 calories less.
Your brain takes 500-600 calories per day to function. Your liver takes about the same. So that leaves nothing for your heart, lungs, intestines, muscles etc to function.
If you eat this little calories per day your forcing your body to adapt to survive. Primary goal is to keep the brain alive. If the brain dies the body dies. It gets its calories. Next is the heart, liver and lungs. Everything else is pretty much up for digestion.
Your metabolism will lower as fast as it can by reducing metabolic rate to reduce catabolism. It does this by dropping thyroid output and increasing reverse T3 thyroid hormone which blocks additional active thyroid hormones. This will shut down metabolism as much as it can but you can’t starve the brain or the heart, liver or lungs so you can’t really get a metabolism less than 1200 calories.
At this point the body has to give up certain functions to preserve important body tissue.
The first thing to go is typically hair and fingernails. Hair falls out and fingernails get brittle. These are non essentials. They don’t keep you alive. They can go.
Body heat reduces to save energy. You are always cold. You can live if you are cold.
Next is muscle. Muscle is very calorie intensive and not generally important for survival. You can live with very little lean muscle mass.
Next is bone. None density will reduce as you don’t need all that bone to support the reduced muscle.
Before you get past this point the hunger sets in. You start getting hungry and craving anything you can to get energy.
This is the point where most people break and cheat.
If you manage to keep going this is where eating disorders come in. The not eating is more important than the hunger.
Lean mass continues to go. You may start to look skeletal.
At the end stages your body will start to consume your diaphragm and other organs.
The diaphragm is typically first to go which results in fluid building in the lungs and you drown. Some see their kidneys or liver shut down first but typically it is the diaphragm.
This is the only pathway for this level of calories. Wether it is keto or low fat or Weight Watchers or Slim fast 1170 calories will do the exact same thing.
If you want to eat 1170 calories you could 1170 calories of cake and lose weight for a short term. It will work the same exact way. You can eat anything you want at 1170 calories per day and lose the exact same amount of weight and it will end the same way.
Bottomed out metabolism
Tanked thyroid function
Hair loss and brittle nails
Hunger
Quitting or eating disorder
You cannot win this battle. The thing that infuriates me the most is that keto does not require starving to death. People knew this in 1953.
“There appears, however, to be an even greater advantage to this method of treatment, in contrast to general restriction of the whole dietary pattern; for, when carbohydrate, alone, is restricted, there is no decline in the basal caloric expenditure. When, however, the total caloric intake is restricted, a decline in basal caloric expenditure is to be expected.” – Pennington, 1953
You don’t have to restrict calories. You just have to restrict carbs. Pennington found that people could consume 3,000 cals a day so long as carbs were restricted and still lose weight and not see a drop in metabolic rate.
Here is an indepth article I wrote awhile ago about this.
There are many people out there that seem to think that the body seeks protein and will overeat to try and fulfill the protein need. They use data which shows that when people eat higher protein they tend to eat less over the course of a day. Like this is actually a good thing. Here is an alternate view point to that theory and why the protein leverage theory is likely wrong.
This graph is from data collected from MyFitnessPal. It shows percentage of calories to target consumed vs percentage of protein in the diet. The insinuation is made that the more protein you eat the less you will eat and this is good.
There are a few issues with this graph and what is trying to be said about it.
The target calories are often set far too low. It is not uncommon to see calorie targets in these apps as low as 1100 cals. This is starvation level caloric restriction and is not healthy long term. Just for reference, 150lb men where given 1500 calories a day during the famous Minnesota Starvation experiment to see how they would react to a dramatically reduced caloric intake due to food scarcity after the war. These men suffered from various issues such as extreme weight loss, muscle atrophy, food obsession, and mental illness. Many of them had to be committed and one of them even mutilated himself with an ax.
Is eating that much less than these targets beneficial? It is pretty well established that we can lose weight with caloric restriction. This we know and it has been done by millions year after year. What we also know is that only 2% of those people actually keep it off. The reason for this is actually very simple. You lower caloric intake and your metabolic rate drops to compensate. The bodies primary goal is to not lose weight as this means you are at risk of death. This was the case for all of our evolution and only in the last 50 years or so has it not been an issue because of the massive food availability and the composition of our diets. If you restrict for too long you only make your metabolism lower and if you restrict too much you can do long term damage to this metabolic rate. This was seen in the Biggest loser study. In this study they followed the biggest loser contestants for 6 years and saw that their metabolic rate had dropped an average of 600 calories due to their over exercise and under eating. This caused them all to gain back considerable amounts of weight regardless of maintaining their diet and exercise. If you restrict and exercise you drop your metabolic rate so low that any increase in calories or slight decrease in exercise means inevitable weight gain. This is why calories in vs calories out in these simple terms does not work.
Are the people eating less because they are satisfied or is this something else all together? This is the beef of the issue and I will get into it in depth.
Is this graph showing satiety or something else?
Those that use this type of data to propose more protein being great are looking at it from the wrong perspective. If reducing calories and increasing protein was the solution and you were only eating less because you are hitting some magical protein number that fulfilled all your needs then why do we see these issues with calorie restriction? Even with huge protein amounts:
hair loss – This is one of the most common issues I see from people following this low fat, low carb, low calorie and high protein method. Hair falling out by the handfull. Only when they eat more calories does it stop. Protein alone is not enough.
Bruising – There is one well known proponent of this method that was seen commenting in a group that he was bruising when working out on his low fat/low carb/high protein diet. This is due to excess protein without adequate fat. This is referred to as Rabbit Starvation and it has many other symptoms such as diarrhea, fatigue, headache, low blood pressure, slow heart rate, and vague discomfort that can only be satisfied by eating fat.
Lowered thyroid function – With all calorie restriction, even with higher protein, you get lowered thyroid function and this is only a protective mechanism to keep you from losing weight. If you resume eating adequate calories thryoid function resumes. It may be possible to do long term damage if caloric restriction is maintained long term.
These are just a few issues with maintain a caloric deficit. What about the opposite side of the coin? The Fat leverage Theory.
Looking at this graph all we see is protein vs calories. It is not comparing a very low carb/high fat diet to a low fat/low carb/high protein diet. The people eating above 100% of their goal are more likely to be eating foods that are highly palatable and those foods are foods that are high in fat and carbs. We are designed to go after those foods because those foods are the foods that will maximize fat storage and fat storage meant safety for pretty much all of our evolutionary history. This is an interesting article about how our ability to get fat allowed us to evolve. This is the problem with just looking at high level data like this. We are making correlations that don’t take into account all factors. Shark attacks are much higher when icecream sales are also higher. Should we avoid icecream to prevent shark attacks? No. Just linking one intake of one macronutrient to overall caloric intake is only 1/100th of the story. This is what is referred to as cherry picking at the highest level.
So these folks like to say that eating higher protein makes you satisfied so you eat less. Well then why do people that go very high fat/low carb/moderate protein also lose almost all hunger? I often see folks eating less than 1,000 cals a day on keto and constantly say they just aren’t hungry. These are always the people that are stalled and can’t lose weight despite eating 1,000 cals a day. Why is this if protein is the magical satiety factor that leads to reduced caloric intake and the magical wonderland of sustained weight loss? That is because reduced hunger is not always a good thing. People that fast often report they feel no hunger as do people that are actually starving. Why is that?
The reason people that fast/starve/caloric restrict seem to lose hunger is a survival mechanism like many others. If a starving hunter gather was plagued by hunger would they be an effective hunter? No. They would be too distracted and likely die. People that fast/caloric restrict/starve also report that they have more energy. Is this a magical effect of ketosis or more protein or less calories? No. It is called epinephrine. Epinephrine is an adrenal hormone and when you are in too much of a negative energy balance your body is pumping this stuff out like crazy in order to keep you upright and alert enough to hunt. Epinephrine is a potent stimulant and like all other stimulants, it reduces hunger and gives you energy. Ask a meth user if they are hungry after they use. They won’t be. They are also usually pretty damn skinny. No I am not comparing caloric restriction to using meth directly. Just the fact that they are both stimulants and they both reduce hunger.
So what about the fat leverage theory being the reason we eat less with more protein intake?
Perhaps the reason people eat less when they consume more protein is because of a negative feedback loop. In nature protein and fat typically came hand and hand. Usually in at least a 50/50 ratio. There are theories that say when you seek out too much lean protein and avoid fat the body actually down regulates hunger to avoid getting too much protein rather than just down regulating hunger because you are getting what you need. Since in nature fat rarely comes without protein, if you were continue to eat you would reach a level of protein that is dangerous such as Rabbit Starvation. There is no such level of fat consumption that is dangerous that we know.
As previously mentioned, fat is needed for the body to function properly and when inadequate amounts are consumed we can suffer the consequences of Rabbit Starvation. I propose that the reason we stop eating when we consume lots of protein is to protect us against protein poisoning. it is not a satiety signal at all. Just a protective mechanism like many others I have spoken about already.
Just to finish off, here is some interesting data on how humans have always strived and worked incredibly hard to get fat. Much harder than anyone ever did to seek out protein.
There are several well known advocates of low carb eating that also claim that protein is of no concern when it comes to weight loss or insulin response. They almost always use the same study to fluff up their point of view. You will always see this graph.
glucose/insulin/glucagon response to IV injected protein (Alanine)
This shows that an injection of the amino acid (protein) Alanine has no significant insulin response while it does have a glucagon response and a blood glucose response. The glucose response is to be expected by anyone who understands the physiology here. No insulin response but a glucagon response means a net rise in glucose levels as there is no insulin to push the glucose into the cells. There are a few problems with using this study as proof that protein does not have an insulin response.
This is a study on dogs and normally I don’t consider studies done on animals as evidence of something in humans this is probably still going to be the same effect in humans. That is not the real issue. The real issue is that the protein is being injected intravenously and that bypasses one of the most crucial factors of the insulin response. The Incretin Response.
The Incretin Response takes place in the gut and is responsible for the bulk of the insulin secretion. If something does not pass through the gut then we do not get the majority of the insulin response.
Insulin response to IV glucose vs oral glucose
You can see in the chart above there is a dramatic difference in the insulin response to IV glucose vs oral. That is because the incretin response in the gut is responsible for most of the effect. This makes perfect sense. You would not want endogenously created glucose to stimulate a large insulin response. The whole reason for endogenous glucose creation is to bring up blood glucose levels. If this glucose had an insulin response it would just be shunted away into the cells again and this would result in unstable glucose levels.
Now that we know that IV injected glucose does not have the same insulin response as oral glucose, due to the incretin affect in the gut, why would we assume that protein injected isn’t the same situation? Are these people purposely misleading us into thinking protein is not insulinagenic? I doubt it. It just goes to show that just because someone is well known or even that they are a “real” scientist that they can miss very crucial points.
I have yet to be able to find a study showing the incretin affect on protein but we have already seen the effect on glucose. Now we can see one on fat as well. If a clear difference in insulin response can be seen between oral and IV glucose can be seen and a clear difference in insulin response can be seen between oral and IV fat can be seen then why on earth would protein be any different? It isn’t.
So yes, protein has an insulin response as does everything. Even fat has a small insulin response. Insulin is largely responsible for shuttling nutrients into cells so if there was no response to protein then we would not be able to absorb it. Why this is so complicated I have no idea. Using a dog study with injected amino acids does not prove in any way that protein is not insulinagenic.
In closing, I want you to look at those people that claim that protein is not a problem in weight loss. Have they ever had a weight problem? It is easy to claim something is not a problem when you have never had to experience this problem in the first place. Just because they can eat protein by the pound and don’t have a problem with weight does not mean someone that has been dieting for 20 years and has difficulty losing weight will not have a problem with it. I can eat all the protein I want as well and not gain weight but I am not you. I also workout 2 hours a day and have 12% bodyfat. If that is you then you likely don’t have a problem with unlimited protein either.
Keto ON Friends,
Coach Jack
If you want to get your Ketogenic Diet back to a place of Common Sense and learn how to heal your metabolism you can get personalized coaching from Coach Jack.
As anyone that has every read anything I’ve posted likely knows, I think fasting is stupid and Fung is a flake. He has the right idea about insulin lowering and weight loss but has this fasting thing totally blown out of proportion. The problem is that he sounds credible and people hoping for a miracle will jump into the fasting pool hoping to swim but will only end up drowning. Here is an example of how anyone can make anything sound logical if they don’t compare apples to apples.
In this article Fung claims that fasting not only doesn’t slow metabolism but speeds it up! Wait, what? This is where you have to use a tiny bit of common sense.
If metabolism speeds up during fasting would Ghandi have survived his many fasts including one for 21 days. If you’ve ever seen Ghandi he didn’t have a bunch of weight to lose.
What would happen if Ghandi’s metabolism where to speed up as Fung suggests? He didn’t have much fat to get him through so he would have quickly died. This just doesn’t hit very high on the old common sense meter does it? We have evolved a brilliant system over the years to deal with a lack of food. It was never intended to be used as a weight loss tool but as a survival mechanism for a harsh environment where food availability was not always a certainty. The metabolism must slow in order to preserve ourselves and if it did not then anyone lean, like most where for almost all of our evolution, would not make it long. This is just the first place where Fung’g logic falls flat. This can be seen easily by measuring the thyroid levels in someone who has fasted for any substancial amount of time. Thyroid is what controls metabolism for the most part and thyroid levels tank when fasting. Here is a measure from Peter Attia when he fasted. Look at the drop in Free T3 during the fast. His metabolism is in the shitter.
Now lets look at his major failure. Comparing data. He starts by talking about the metabolic adaptation of the contestants of the biggest loser in a 6 year follow up.
This study shows that the caloric restriction and intense exercise caused a dramatic decrease in metabolic rate that persisted for 6 years after the contest ended. Great. He then tries to say that this is because they were calorie restricted and that if they had of fasted they would not have seen this happen. He uses some interesting logic about insulin being high or low to explain it but he does not support this with any actual science. He actually states that after 4 days of fasting the metabolism increases by 13% but conveniently does not site any literature to support this. I did find an article that shows a similar result.
The explanation of this is pretty much what I would expect. The increase is due to an increase in the adrenal hormone norepinephrine. As this adrenal hormone increased so did metabolic rate. This rise only continued for 4 days and reduced there after despite the continued rise in epinephrine.
“We cannot explain the decline in energy expenditure on day 4 of our study, even though norepinephrine was still rising. Although not studied by us, it has been suggested that energy deprivation has suppressive effects on the hypothalamus-pituitary-thyroid axis that diminish the metabolic rate.”
What do we think would happen if one continued this fast past 4 days? That is right, metabolism would drop. Another important thing to note is that apparently Fung has never heard of adrenal fatigue. This is real and there are millions of people that can attest to that. Chronic fatigue is rampant and the direct cause is adrenal fatigue. What do we think years of forcing massive increases in adrenal hormones is going to result in? Funny enough caloric restriction also results in increased adrenal output. Unfortunately I have not been able to find any studies showing the result of 4 days of caloric restriction on metabolic rate but I would predict you would see similar results as far as energy expenditure and norepinephrine concentration.
He goes on to talk about a study that showed metabolism didn’t drop after 22 days of alternate day fasting. He again fails to site the study because god forbid anyone be able to actually read the study and see if what he is saying is true. I was able to find it though.
Well this is hardly a bolster to his hypothesis. The results showed that after 22 days of alternate day fasting the metabolic rate in fact did drop. From 1594 cals to 1512 cals. While that sounds like very little it is still a drop and this is only after 22 days of alternate day fasting. So only 11 days of fasting. that is 82 calories in 22 days or about a 3.72 calorie a day decrease. The biggest loser study was after 30 weeks of caloric restriction and showed an average drop of 610 cals after 210 days. That is a drop in metabolic rate of 2.9 cals per day……Less than fasting. Imagine that. Lets see a study of alternate day fasters after 210 days. Now that would be interesting wouldn’t it.
Here is the reality of all of this. Fasting is caloric restriction. It is just broken up differently. Essentially the results will be the same long term depending on what the average calories are. The metabolism will slow the same and the weight loss will be the same.
Person A eats 3 meals a day every day and eats 1800 cals a day. Their metabolic rate is 2800 cals per day. That is a 1,000 calorie per day or 7,000 calorie per week deficit. They will likely lose about 2 lbs a week until their metabolism slows. The weight loss will slow as the metabolism slows and will eventually stop.
Person B does alternate day fasting and eats 3600 calories on eating day and no calories on fasting days. Their metabolic rate is 2800 cals. This results in an average caloric intake of 1800 cals per day which is a 1,000 calorie per day deficit or a 7,000 calorie per week deficit. They will likely lose about 2lbs per week until their metabolism slows. The weight loss will slow as the metabolism slows and will eventually stop.
They are exactly the same. They will have the same long term result and this is why all of these long term fasters like Jimmy Moore and Carl Franklin can no longer lose weight.
This study comparing Alternate day fasting (ADF) to straight caloric restriction (CR) shows this directly.
“At 8 weeks, ADF achieved a 376 kcal/day greater energy deficit; however, there were no significant between‐group differences in change in weight (mean ± SE; ADF −8.2 ± 0.9 kg, CR −7.1 ± 1.0 kg), body composition, lipids, or Si.”
The only benefit this study might have shown was that in the 24 weeks after the initial 8 weeks the ADF group seemed to gain more lean mass and less fat mass back. The difference was minimal and could be confounded by measurement techniques. The test used only measures fat and not fat so depending on hydration levels this could swing wildly. Water will show up as lean mass making the fat mass % seem larger. Overall weight regain in the followup was again, the same.
So to close, Fung compares apples to nothing. He looks at a 4 day result in metabolic increase from fasting, which was actually related to an increase in adrenal output and not to lowered insulin, and compares it to a 6 year long study of caloric restriction. He also tries to compare a 22 day study on alternate day fasting with a 3.72 calorie per day drop in metabolism to a 210 day diet contest TV show that resulted in a 2.9 calorie per day drop in metabolism. Fung needs a small lesson in statistics here. I fail to see how any of this proves his point.
Remember, friends don’t let friends do stupid things like fasting and listening to people that say fasting is a good idea.
Keto ON Friends,
Coach Jack
If you want to get your Ketogenic Diet back to a place of Common Sense and learn how to heal your metabolism you can get personalized coaching from Coach Jack.
Melatonin is a hormone that helps regulate our wake and sleep cycles. It is released at greater and greater amounts the later in the day it gets. What does a sleep hormone have to do with insulin? Let me explain. It’s fascinating. At least to me. 🙂
We have been told for years that it is a bad idea to eat at night. Nobody was ever really sure why but it was just one of those bits of advice that has always floated around. Sometimes these bits of wisdom passed down are exactly right and what we should be listening to. Here is some science to back up this particular gem.
The study below looked at the effect of melatonin on insulin secretion. It was found that melatonin binds to receptors on the insulin producing beta cells in the pancreas and limit the amount of insulin they can secrete. In addition to this, about 30% of the population have a mutation of these receptors that cause an increased sensitivity to melatonin and will secrete even less insulin in response to melatonin.
What is the relevance to this and eating at night? Isn’t less insulin a good thing? That depends. It isn’t a good thing to a type 1. It also isn’t a good thing if you are eating food that may raise blood glucose. You need insulin to put away that glucose where it is supposed to be and not left in the blood. Lets look at what happens when you eat at night. We will use a carb meal as an example to start then we will discuss a low carb and protein rich meal.
food is consumed and digested
blood glucose rises
Insulin should come in now and push glucose out of blood and where it should be like the liver and muscles. Since insulin is suppressed by melatonin, the glucose levels in the blood rise.
High blood glucose is a negative situation for the body. It is damaging to blood vessels and needs to be dealt with. To deal with this the body up-regulates utilization in order to get rid of the glucose. When glucose is being preferentially oxidized then fat cannot be used.
Since usually energy expenditure at night is low blood glucose stays elevated.
So if you consume anything that will elevate blood glucose at night when melatonin is elevated you will have high blood glucose throughout the night and you will be preferentially using glucose for fuel due to the bodies need to get rid of the glucose in the blood. This means less fat being used at night.
Now lets look at what happens when you consume protein.
food is consumed and digested
insulin normally comes along to help shunt amino acids into cells where they are needed. Since insulin is suppressed we will not have the amino acids being sent to where it needs to go and we cannot effectively use these building blocks for what they are intended for. The body will use them as fuel at this point as having free floating amino acids is also a negative situation. Since protein does not contain glucose there will not be a rise in glucose directly so that is not an issue so far. But……
In addition to the above, with protein consumption you also have a glucagon response. Glucagon is a counter regulatory hormone to insulin. Where insulin puts energy away for storage, glucagon brings it out for use. The reason we get a glucagon response with protein is because it has an insulin response and an insulin response in a food that contains no carbohydrate would result in low blood glucose and that is a negative as well. To combat that the body is smart and releases glucagon simultaneously to raise glucose levels in the blood to counter the drop from the insulin response.
The glucagon response starts looking for glucose to raise blood sugar. If you are in a glycogen depleted state, like a low carb/ketogenic diet, your body will start making glucose from amino acids. This is a problem because without the insulin to counter act the glucagon response you end up with high blood sugar.
You now have elevated blood glucose, despite not having any carbohydrate, and also a mass of free floating amino acids. These two things are both problematic and will compete for space in fuel utilization.
I hope this throws some light on why it is a bad idea to eat and night and how complex our body is. It is still not completely understood as to why melatonin suppresses insulin but it is hypothesized that it is a protective mechanism to prevent against night time hypoglycaemia (low blood sugar). In the evening it was more typical that food intake was low in most of our evolution so this inhibition of insulin secretion would allow for more fuel available in the blood for longer. What we do know is that having high glucose levels in the evening is not a great idea. Eat early and stop early.
Keto ON,
Coach Jack
If you want to get your Ketogenic Diet back to a place of Common Sense and learn how to heal your metabolism you can get personalized coaching from Coach Jack.
