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.
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:
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.
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.
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.
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.
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.
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".
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