The science has shown inconsistent results in incretin hormone release, and their stimulation of insulin, when it comes to the taste and/or smell of food.
But, what has been very consistent is that the taste of sweet affects the brain. It causes dopamine abnormalities and dopamine is a metabolic regulator. Dopamine abnormalities will affect fat storage and burning. Leptin influences the dopamine system and vice versa.
This is why the taste of sweet should be avoided, as we never evolved to taste sweet 365 days a year.
2. You do not have to be so strict with your diet.
The people who make these suggestion are usually obese themselves. But, you will not get that type of advice here. In here, you are encouraged to be very strict with your diet. After all, if you're serious about tackling a very complicated disease, like metabolic disease is, that's how it should be. You will most likely not see results with anything less than very strict adherence.
The person with obesity/metabolic have several issues that are working against them on their path to better health:
3. Fat intake from a previous meal can set your metabolic table.
(Fall asleep here.) This statement pertains to a very complex biochemical mechanism, which has been known for a very long time, of how fat consumption from a previous meal, will displace glucose oxidation of the next meal, decreasing fat storage due to a complex interplay between insulin, enterocytes, chylomicrons, blah, blah, blah. (Start snoring here.)
I see a lot of this stuff going around the internet. People get caught up on individual metabolic mechanisms, as they occur biochemically, and then run with them, proposing all kinds of diets, hacks and protocols based on completely useless nonsense. Detailed metabolic mechanisms are very interesting, but cannot win the battle against obesity. This is because it doesn't really matter what occurs at the micro level, on any one isolated aspect of a complex system, because what we truly care about is what occurs at the macro level to the entire system.
(Wake up here.) Obesity is not responsive to what occurs in the short term from individual meals. For this reason, the obese can follow a diet consistently, for a month or six months, and see no significant changes with their weight. It may appear to be a "long time" for them, but six months is a drop in the bucket when it comes to reversing the metabolic adaptation of the obese. For this reason, it doesn't matter what biochemical effects supposedly occur from one macronutrient in a meal, since what ultimately dictates where your next meal goes is your blood glucose. People get caught up on what's on their plate, but ignore how it affects their blood glucose. But, it's blood glucose that ultimately decides where the macronutrients on their plate go. The more disruption in blood glucose, the more you store food as fat, whether it's carbohydrate or fat based. If it's energy, the obese will store it.
So, this statement is fun research for first year biochemistry students with insomnia, who are also lean and want to experiment with "The Croissant Diet", but it is completely useless for the treatment of the overweight/obese.
4. Alanine aminotransaminase activity (ALT) should always be kept low.
ALT is a biomarker that is generally used to detect hepatic disease. It is expected to be low if the liver is healthy, but recent new research has associated this biomarker with overall health. Low levels seem to be correlated with frailty, cardiovascular disease amongst other issues. ALT is influenced by many things, including viruses, medications, etc. (basically anything that affects the liver) and it has recently been linked to metabolic abnormalities as well, so the "normal ranges" for ALT have been updated.
ALT is just another part of metabolic function. It's part of the alanine cycle. The problem seems to generate from the ALT enzyme, which is found mainly in the liver, but also in various other tissues, including kidney, skeletal muscle and myocardium. Interestingly those are all the organs that seem to be most susceptible to metabolic dysfunction.
This is a complex part of metabolic function, at the biochemical level, so the only thing thing a person can actually do is follow a proper diet and exercise protocol to decrease their risk, but risk is never eliminated.
5. You cannot prioritize protein if you eat a lot of vegetables.
The vegetable content of the diet does not displace protein. You can eat a large amount of vegetables, as long as you also eat plenty of meat. The problem only occurs when meat is reduced or replaced with vegetables, but eating plenty of both is not an issue.
6. There aren't any "low carb doctors" who promote a proper diet.
Most are charlatans, but both Dr. Naiman and Dr. Bernstein's dietary protocols are the most metabolically and scientifically correct regimens, I have seen, from the low carb community. These are the only two doctors I would recommend following.
This is why the taste of sweet should be avoided, as we never evolved to taste sweet 365 days a year.
2. You do not have to be so strict with your diet.
The people who make these suggestion are usually obese themselves. But, you will not get that type of advice here. In here, you are encouraged to be very strict with your diet. After all, if you're serious about tackling a very complicated disease, like metabolic disease is, that's how it should be. You will most likely not see results with anything less than very strict adherence.
The person with obesity/metabolic have several issues that are working against them on their path to better health:
- No satiety signaling - Most people who are overweight/obese, have no satiety signaling, so they cannot trust their bodies to prevent them from overeating or eating too often. This is why many people must track macros and have a daily intermittent fasting protocol in order to control the onslaught. Others must include calorie tracking to avoid excess. You cannot stabilize blood glucose eating constantly.
- No hunger signaling - It sounds ludicrous, but many obese people do not have proper hunger signaling, either. They can go a long time without eating, pushing themselves into extended fasting territory. This is detrimental for the obese, because it's only causing their metabolism to double down its thrift response, encouraging their fat cells to store even more fat, once they do eat. You cannot stabilize blood glucose through starvation.
- Dopamine abnormalities - Ah, the never ending search for the dragon of sweet. This constant hit of dopamine, from the sweetener pipe, dysregulates the body's metabolic circadian rhythm, pushing it into more fat storage.
- Behavioral issues - Years of biological drives, as a result of metabolic dysfunction, cause for many obese people to develop habits and beliefs, around food, that further perpetuate obesity. They must constantly struggle with these habits, so they can take control of their relationship with food. Ironically, one of these beliefs is that "you shouldn't be strict with your diet", since being half-assed and lazy has worked so well so far.
- Excess body fat - The battle of the bulge is real. Excess fat mass is a driver for becoming more fat. Everything that is eaten, is allocated to these hungry fat cells, before it can reach any other cell. This means that food quality is of utmost importance, because the obese are simply better at storing more fat. You will continue storing fat until you stabilize blood glucose.
- Exaggerated response to conditions of fat mass growth - Caloric restriction, extended fasting, low protein with high carbs and fat, sedentary lifestyles, sex hormone status and heck, even pregnancy are all conditions that spare fat mass and grow more of it. The obese are exceptionally sensitive to any condition that will grow more fat.
- Exaggerated metabolic thrift response - The metabolism of the obese is honed and prepared to react to any inkling of starvation, so that it can store more fat and not release any of it for fuel.
3. Fat intake from a previous meal can set your metabolic table.
(Fall asleep here.) This statement pertains to a very complex biochemical mechanism, which has been known for a very long time, of how fat consumption from a previous meal, will displace glucose oxidation of the next meal, decreasing fat storage due to a complex interplay between insulin, enterocytes, chylomicrons, blah, blah, blah. (Start snoring here.)
I see a lot of this stuff going around the internet. People get caught up on individual metabolic mechanisms, as they occur biochemically, and then run with them, proposing all kinds of diets, hacks and protocols based on completely useless nonsense. Detailed metabolic mechanisms are very interesting, but cannot win the battle against obesity. This is because it doesn't really matter what occurs at the micro level, on any one isolated aspect of a complex system, because what we truly care about is what occurs at the macro level to the entire system.
(Wake up here.) Obesity is not responsive to what occurs in the short term from individual meals. For this reason, the obese can follow a diet consistently, for a month or six months, and see no significant changes with their weight. It may appear to be a "long time" for them, but six months is a drop in the bucket when it comes to reversing the metabolic adaptation of the obese. For this reason, it doesn't matter what biochemical effects supposedly occur from one macronutrient in a meal, since what ultimately dictates where your next meal goes is your blood glucose. People get caught up on what's on their plate, but ignore how it affects their blood glucose. But, it's blood glucose that ultimately decides where the macronutrients on their plate go. The more disruption in blood glucose, the more you store food as fat, whether it's carbohydrate or fat based. If it's energy, the obese will store it.
So, this statement is fun research for first year biochemistry students with insomnia, who are also lean and want to experiment with "The Croissant Diet", but it is completely useless for the treatment of the overweight/obese.
4. Alanine aminotransaminase activity (ALT) should always be kept low.
ALT is a biomarker that is generally used to detect hepatic disease. It is expected to be low if the liver is healthy, but recent new research has associated this biomarker with overall health. Low levels seem to be correlated with frailty, cardiovascular disease amongst other issues. ALT is influenced by many things, including viruses, medications, etc. (basically anything that affects the liver) and it has recently been linked to metabolic abnormalities as well, so the "normal ranges" for ALT have been updated.
ALT is just another part of metabolic function. It's part of the alanine cycle. The problem seems to generate from the ALT enzyme, which is found mainly in the liver, but also in various other tissues, including kidney, skeletal muscle and myocardium. Interestingly those are all the organs that seem to be most susceptible to metabolic dysfunction.
This is a complex part of metabolic function, at the biochemical level, so the only thing thing a person can actually do is follow a proper diet and exercise protocol to decrease their risk, but risk is never eliminated.
5. You cannot prioritize protein if you eat a lot of vegetables.
The vegetable content of the diet does not displace protein. You can eat a large amount of vegetables, as long as you also eat plenty of meat. The problem only occurs when meat is reduced or replaced with vegetables, but eating plenty of both is not an issue.
6. There aren't any "low carb doctors" who promote a proper diet.
Most are charlatans, but both Dr. Naiman and Dr. Bernstein's dietary protocols are the most metabolically and scientifically correct regimens, I have seen, from the low carb community. These are the only two doctors I would recommend following.
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