Six common beliefs addressed, Part 58

1. There are no fasting myths.

There is only one extended fasting myth - that it's a viable treatment for obesity. Everything else negative that is said about extended fasting are not myths, they are facts.

An intermittent fasting myth is that these negative effects of extended fasting apply to it as well. Intermittent fasting does not cause the negative effects extended fasting does.

2. It's sugar and carbohydrates that cause heart disease, not cholesterol.

There are many reasons for the development of cardiovascular disease (CVD), as it’s a multifactorial disease. It’s considered a "disease of civilization", because many of the factors involved, in the development of CVD, are directly the result of modernity, such as living longer, being more sedentary and having higher body fat. All of these affect metabolism. Certain metabolic states put you at risk for the development of CVD.

Diet quality is one determiner of your metabolic state. But, sugar and other carbohydrates are not the only culprits in a bad quality diet. Fat is as well. The difference in the fat intake of hunter/gatherers, who have none to low levels of CVD, and Westernized humans, who have high levels of CVD, is primarily in the type of fat and how it's eaten.

• Hunter/gatherers eat the saturated animal fat that comes along with protein. They do not consume isolated and/or refined plant fats, such as "oils".
• Hunter/gatherers do not add fat to their food. They do not cook with fat, nor add fatty sauces or other condiments to their meals. Food is cooked over an open fire or pit, so no isolated cooking fats are required.

Cholesterols involvement in CVD is exclusively related to damaged lipoproteins and abnormalities in apolipoproteins. These cannot be detected through a total cholesterol panel. They are also not solely diet related. They are actually more genetically determined than anything else. Diet can only exacerbate and contribute to the disease process, these damaging genetic lipid profiles can cause, through direct effects on the arterial lining. But, diet alone is not enough to produce these negative effects if the lipid profile did not have a genetic abnormality to begin with.

The bottom line is that there is no one "cause" for CVD. There are only causes. Be leery of anyone making claims that any one thing is the culprit for such a complex disease, such as CVD. If there was only one cause for CVD, across the board, it would have been eradicated a long time ago, just like smallpox. But, CVD is more of a "syndrome" than a disease, as it manifests differently in different people and has multiple contributing causes.

3. Carbohydrates are not fat, so they don't contribute to body fat.

Carbohydrate is turned into palmitoleic acid, through denovo lipogenesis. This has been found to be true irrespective of caloric amounts, in high carbohydrate diets, particularly in people who have insulin resistance. Some people make more of this fat than others, so there is a genetic component to fatty acid management that also comes into play.

Palmitoleic acid is the main fatty acid that contributes to cardiovascular disease (CVD) and predicts metabolic syndrome. The production of this fatty acid is most responsive to carbohydrate consumption and tends to drop significantly when carbohydrates are reduced to less than 50 grams a day. This is why a typical low fat/high carb diet is not necessarily "low fat" at all. The saturated fat is being produced endogenously, instead of being consumed as fat in the diet.

As long as the fat being consumed is not being stored, this is not the case for low carb diets.

4. Are retinopathy and neuropathy the consequences of high blood glucose?

Chronically high blood glucose damages tissues vascularly. In other words, the excess glucose molecules are like shards of glass, which begin shredding the microvascular system and eventually this leads to organ malfunction, as tissues are unable to supply themselves with sufficient oxygen due to impaired blood flow. Though this occurs peripherally, the damage spreads and eventually the entire organ fails. This can be described as a result of glucose toxicity and why some doctors believe diabetes is primarily a vascular disease.

But, conditions like retinopathy, neuropathy and kidney damage are oftentimes detected long before glucose reaches very high levels. In fact, most diabetics experience these pathologies while maintaining "controlled" blood glucose. While this supposedly "controlled" blood glucose range is not considered normal or low, it is also not high enough to cause such extensive damage to tissues. There are people with certain genetic conditions, which cause them to always run blood glucose in a hyperglycemic range, but yet they never experience these "diabetic" pathologies. This means that something else is causing this damage to Type II diabetics besides high blood glucose. Usually this is where insulin toxicity comes in.

Insulin toxicity is described as chronic insulin action on tissues, producing damaging inflammation. Even though this is a fact of hyperinsulinemia, it is still not the exact cause of damage, as there are certain genetic conditions that cause chronically, higher than normal, insulin levels and no damage to organs and/or tissues occurs. So, what's really going on? What makes diabetes different? Why is there damage with diabetes and not with isolated high insulin or high blood glucose?

Retinas, nerve cells and kidney cells all have one thing in common - they are dependent on glucose. Red blood cells do not even contain mitochondria, so they cannot use fat for fuel, at all. People who have had chronic high insulin, for years, due to abnormalities in blood glucose regulation, develop insulin resistance in various tissues, in order to slow down the cells glucose uptake. This protective mechanism is actually detrimental for cells that primarily use glucose. Insulin resistance technically starves them, causing them to malfunction. So, all of this damage is not the result of high glucose or high insulin, they are the result of insulin malfunction caused by high glucose and high insulin. In other words, pathological insulin resistance of glucose dependent cells.

Lowering your glucose and insulin oftentimes results in glucose dependent cells to suffer further. This is why nasal insulin sprays have been shown to improve cognitive function in patients with certain dementias. The extra insulin is facilitating better glucose entry into glucose dependent cells, which have become diseased. This is why I always say that lowering glucose and insulin will not necessarily resolve the problem. There are certain effects caused by hormones, like insulin, that aren't necessarily reversed by its absence. This is because insulin is a type of hormone that causes long term effects in tissues, even when it's absent.

5. Are low carb diets very easy?

Obesity advice should prepare people for facing the Herculean effort of a complete lifestyle change, instead of trying to create soft cushions for them in excuses and concessions. That's where all the fake food and psycho babble comes in. These are just ways to placate the person into continuing their obesogenic habits, in a new way, but we all know that will not work.

If you ever go to the bookstore, pick up any low carb diet book, and you will see what I mean. Page after page of mock Standard American Diet (SAD) foods, to try and "help you stick to the diet". This isn't going to work. Getting "motivated" with recipes is not enough. Motivation is always fleeting, especially on such a long and difficult road as obtaining normal blood glucose regulation can be. Instead, you need discipline, not motivation. Discipline is when you commit to do something, even if it's difficult, and even when it fails before it works.

On this blog, change is not optional. It's a requirement. I don't make any bones about how difficult obesity is to reverse or how complicated diabetes really is. I want to make sure that everyone is aware of what this journey requires, in order for it to be successful. Excuses don't make you thin, neither do lies. Dedication does. We don't believe in "fat shaming", but we also don't believe in "fat blaming", that's when you blame a million things besides your own actions, on the inability to adhere to your protocol.

You are solely responsible for adhering to your protocol and I am here to explain what causes the ups and downs, along the way, even with strict adherence. What we don't deal with here, is inability to adhere, because that's just a waste of time. We already know what the result of non adherence is - it's not working because your aren't doing it. There really is no new information to provide there.

You will come across the "it's easy" advice many times. Well, it's not easy. If it was, no one would be on this blog. Read through the content in here to get a more realistic view of this lifestyle and what to expect from it.

6. Insulin is a "slimming hormone" because it builds leans muscle mass.

First, insulin is an anabolic hormone. Though anabolic describes growth, you can still consider insulin a "slimming hormone" depending on the context it's being discussed in. For example, the term anabolic used in the context of muscle building, describes a slimming process. Muscle is fat's nemesis. So, if your insulin is growing muscle and not fat, then insulin is very slimming.

The metabolism of the obese is not primed for growing muscle, their insulin only grows fat. So, insulin, in this context, is not a slimming hormone, but it's also not an obesity hormone, as the low carb crowd would like you to think. It's simply a hormone required for both fat growth and muscle growth. Your metabolic state decides which one it's growing more of.

Six common beliefs addressed, Part 36

1. Are calories the same as energy?

The calorie is a unit of energy. There are actually two units with that name. The small calorie or gram calorie (cal) is the amount of heat energy needed to raise the temperature of one gram of water by one degree Celsius (or one kelvin). The large calorie, food calorie, or kilocalorie (Cal or kcal) is the amount of heat needed to cause the same increase on one kilogram of water. All of this is great to know when using a calorimeter, but not so good when it comes to the human body.

For this reason, though the term calorie can be used interchangeably with energy, it is a bit of a misnomer. If you are speaking about the human body, it's best to use the actual macronutrients you are referring to, since the energy contained in each is used very differently by the body and can give context. The body does not have a linear relationship with energy availability and energy usage like a calorimeter. It compartmentalizes and partitions energy for different tasks.

• Protein energy is used to build lean body mass.
• Carbohydrate energy is used to build fat mass and short term energy stores.
• Fat energy is used to build fat mass and long term energy stores.

This is why referencing a calorie, as far as the human body's metabolic process is concerned, is pretty much useless. It is much more useful to speak in terms of grams of specific macronutrients. That will better help you decide when and what to eat. 

Calories are a simple metric that can be applied for simple goals, such as the loss of vanity weight or alongside an existing macronutrient recommendation, but should never be used alone or as primary intervention, since it does not provide enough information and is very imprecise.

2. Can ketogenic diets correct leptin resistance?

Leptin resistance does not respond to a ketogenic diet and ketosis will not correct leptin deficiency/poor expression. That should not be surprising to anyone, since ketone presence is a signal of starvation, to the body, and leptin is a starvation hormone. If you are starving, leptin will hold onto stored fat more strongly. If there is plenty of energy coming in, then leptin will signal for fat cells to release and burn fat, as storage is not necessary. This is why starvation makes leptin resistance worse.

In order for a ketogenic intervention to have benefits, the person must have adequate and in tact leptin expression. Otherwise, they will not achieve appetite suppression and adequate burning of fat. This is why some people might not see benefits on a ketogenic diet. A subset of people will actually gain weight, following a ketogenic diet, rather than lose.

Obesity is much more complicated than just "carbs". There is no "one size fits all" diet for addressing metabolic dysfunction, because it is not a syndrome of only one thing. Obesity is the result of many different things.

3. There is no difference between the metabolism of an obese person and a healthy person's. Their only difference is weight.

Obese people are lean resistant and their bodies actively defend body fat and easily acquire more of it, with any chance it gets. There are many factors that play into this. Important ones are hormones, the brain, body composition and the fat mass itself. But, there is one thing that is a main contributing factor - poor blood glucose regulation. 

The metabolism of the obese is not driven towards anything, not burning fat. A vicious feedback loop has been set into motion to where the fatter the person is, the fatter they become, as the fat mass is driving more fat storage and refusing to be accessed. You are now insulin resistant. When you are insulin resistant you can't:

• Regulate your blood glucose. This means that the body will not produce its own glucose, when needed, nor halt production when it's not. This mechanism causes chronic hyper/hypoglycemia.
• Regulate your body's catabolism. The body will not tightly regulate its glucose production and will release excessive amounts of glucose through the over activation of counter regulatory systems, particularly glucagon. This keeps insulin chronically stimulated.
• Regulate your body's fat burning. This means that the body does not have proper leptin/adiponectin signaling, at the fat mass, and the brain is not receiving adequate information of how much is stored and how much is being burned. Now you store fat but don't burn enough of it.

So, obesity is not just simple weight gain. It is a complex metabolic state that cannot be addressed the same way simple weight gain can.

4. Ceramides are the root cause of metabolic syndrome/diabetes.

Ceramides are a family of waxy lipids. They play a very important role in cell health, since they are part of the sphingomyelin lipid system, which is the predominant lipid found in many cell membranes.

Ceramides are being coined as "toxic fat", since they play a role in lipotoxicity, when found in excess. In other words, they are known to cause dysfunction in how other lipids work. Fat cells not only store triglycerides, but they also help the body sense its nutritional status by secreting compounds that communicate with other cells. Among those signaling compounds are ceramides. Abnormal alterations to this cellular nutritional status signaling is believed to be at "the root" of metabolic dysfunction.

Since ceramides decrease metabolic activity of fat tissue, when they are blocked, fat cells can burn more energy. In the laboratory, mice that produced fewer ceramides were protected from diabetes and fatty liver disease. Blocking ceramides also helps increase the number of beige or brown fat cells. Beige and brown fat cells are full of mitochondria. These cells are more metabolically active than white fat cells because they burn more energy, rather than store it.

Because of all of this, you might start believing that ceramides are bad news, but remember what I wrote in the beginning. These abnormalities only occur when ceramides are in excess. So, I beg to differ about ceramides being "toxic fat". That claim might make great clickbait, but it's a lie. Ceramides are not, in of themselves, "toxic". They just behave that way under the context of metabolic dysfunction, which increases their numbers dramatically.

This ceramide abnormality is just one more manifestation, in a long laundry list of abnormalities, present in metabolic dysfunction. Ceramides do not spontaneously become abnormal, something causes them to become that way. Why do people with metabolic dysfunction have excess ceramides? Some of the stimuli that increase the production of ceramides are apoptosis and cytokines.

• Apoptosis is a form of cell death. It is a normal and controlled part of an organism's growth, but certain conditions cause for it to occur more frequently than it should. Apoptosis is a common occurrence in the fat cells of the obese, because they are abnormal, and this attracts cytokines. 
• Cytokines are a number of substances secreted by certain cells of the immune system. Cytokines are found in abundance in the fat tissue of people with excess body fat. This gives us a clue, as to one of the reasons behind this excess in ceramides found in the obese and metabolically abnormal.

What can reduce ceramides? If you don't have time to wait for Big Pharma to make yet another pill, for you to add to your metformin, Victoza and insulin, then you can lower ceramides the old fashioned way, for free, with - exercise.

Exercise of moderate intensity results in a reduction of both ceramide and sphingomyelin fatty acids, with an overall higher reduction of total ceramide fatty acids. Exercise also reduces the activity of ceramides on the fat cells. This means that there is a sphingomyelin signaling pathway, present in skeletal muscle and it is affected by prolonged contractile activity.

Well, it seems like "the root" cause of excess ceramides, is sitting on your behind all day. Who would have guessed.....

5. Low carb/"keto" diets will improve neuropathy and retinopathy.

There has been some studies that have shown that certain diabetic complications, like neuropathy and retinopathy, can become worse on low carbohydrate/ketogenic diets, in some individuals. The exact mechanism of how this occurs is not well understood, but it seems to be related to lower insulin levels and insulin resistance.

Low carbohydrate/ketogenic diets lower insulin levels. But, a lowered insulin level does not automatically cause an increase in insulin sensitivity. At least not in the short term. That is an effect that occurs in the long term, but it's not guaranteed, as insulin resistance effects different tissues of the body in multiple ways. 

Nervous system cells and retina cells could suffer if they are still experiencing persistent insulin resistance, since both of these cell types are completely dependent on glucose. They require for insulin to facilitate their glucose uptake. Lower insulin levels means they will have a harder time up taking glucose. These cells cannot compensate with fat. They do not use fat. If glucose cannot be delivered to them, effectively, they will eventually die.

If you are experiencing a worsening of these conditions, you must reevaluate your protocol and analyze your metabolic markers more closely.

6. Is diabetes "carbohydrate intolerance"?

No. 

Diabetes is the inability to sustain proper blood glucose regulation. At the stage of diabetes, multiple glucoregulatory feed back loops become dysfunctional, amongst other systems which all help perpetuate the condition further. This is why diabetes is a disease that is chronic and progressive. 

There is no such thing as "carbohydrate intolerance". There is only blood glucose effects from carbohydrate. These effects can deteriorate blood glucose regulation over time. The amount of carbohydrate intake for this deterioration to occur, varies in individuals. The ability to retain proper blood glucose regulation, irrespective of carbohydrate intake, also varies in individuals. But there is no "intolerance".