Leptin and insulin????

healthy491

''People with higher leptin and insulin sensitivity are generally going to have an easier time losing weight and maintaing a healthy weight. Other hormones like thyroid, testosterone, and estrogen also play a role.''
Someone shared this article and I am curious to what that means. Does it mean its not all about CI<CO

ogmomma2012

Maybe you should link the article, so other people can read it.

kommodevaran

I'm not especially fond of fearmongering. I also think it's important to focus on the large bits that have a real impact, before worrying about the minor details, and control what you can control. Calorie counting works if you make it work, and calorie intake is in the control of healthy, functioning adults. And for most people, hunger/satiety/appetite is controlled by habits, environment and attitudes. Many of us are used to constantly eating and have no idea what "hungry" means.

Maxematics

No it doesn't because all of that is a part of CI<CO which is what some people don't understand.

"I ate what x app told me to and didn't lose weight!" That usually comes down to errors in food logging, but if someone truly isn't losing while at a deficit, they need to find out if they have any medical conditions that affect their CO. It's up to the individual to tweak their CI if they're being as accurate as humanly possible and still not yielding results based on their estimated CO.

rainbowbow

healthy491 wrote: »

''People with higher leptin and insulin sensitivity are generally going to have an easier time losing weight and maintaing a healthy weight. Other hormones like thyroid, testosterone, and estrogen also play a role.''
Someone shared this article and I am curious to what that means. Does it mean its not all about CI<CO

No, it doesn't mean that. I dont feel like re-typing this, but here's some good information to know. I am copy and pasting it from another thread:




This is an interesting idea, unfortunately, our hunger is fueled by the hormones leptin and ghrelin not necessarily the calories we intake.

"Leptin and ghrelin are two hormones that have been recognized to have a major influence on energy balance. Leptin is a mediator of long-term regulation of energy balance, suppressing food intake and thereby inducing weight loss. Ghrelin on the other hand is a fast-acting hormone, seemingly playing a role in meal initiation. As a growing number of people suffer from obesity, understanding the mechanisms by which various hormones and neurotransmitters have influence on energy balance has been a subject of intensive research. "

http://www.ncbi.nlm.nih.gov/pubmed/17212793

"Levels of leptin -- the appetite suppressor -- are lower when you're thin and higher when you're fat. But many obese people have built up a resistance to the appetite-suppressing effects of leptin, says obesity expert Mary Dallman, PhD, from University of California at San Francisco."

"Ghrelin, the appetite increaser, is released primarily in the stomach and is thought to signal hunger to the brain. You'd expect the body to increase ghrelin if a person is undereating and decrease it if he or she is overeating. Sure enough, ghrelin levels have been found to increase in children with anorexia nervosa and decrease in children who are obese."

http://www.webmd.com/diet/your-hunger-hormones

Appetite suppression:
So while these two hormones are mainly responsible for our feelings of hunger, the mechanisms by which they work are complex and entirely different. Leptin which is produced by fat cells SHOULD theoretically keep your appetite lower the more body fat you have to produce it. As stated above, some people may experience a resistance to this (especially if they are overweight for an extended period of time).

Hunger:
Ghrelin on the other hand is produced in the gut when it's empty and is lowered significantly when food has been eaten (specifically when the stomach is stretched). After eating it takes about 3 hours for ghrelin levels to shoot back up enough to increase appetite.

So, unfortunately, no. It doesn't have anything to do with the specific number of calories you are eating, but more to do with the volume of food in your stomach, when/how often you eat, the rate of digestion of the foods you eat, etc. This is why you commonly see people recommending a higher volume of low calorie veggies, increased fats, increased water intake, increased meal frequency, and increased fiber to help satiate their hunger.

You can also see a bunch of dumb products being made like "full bar" which use this mechanism to their advantage. Hell, there's even surgery like the lap band, stomach stapling, etc. to trigger the stomach being stretched and decreasing ghrelin levels.

It's important to note, that you absolutely CAN push past and just "deal" with being hungry while being on a deficit. But for most people this makes them more likely to binge or go off on a tangent eating all the things.

They've developed a hunger chart and have certain recommendations to help people who are gaining or losing stay on track. It's ideal for the average person to stay within the 4-6 range at all times.




Anecdotally, I find that after eating a certain amount of food (in a deficit OR surplus) I generally level out after a few weeks. When losing the hunger goes away and becomes normal, and when gaining, I go from being sickly full to a bottomless pit.

so, as stated above... it still comes down to what you eat, when you eat, what types of foods you eat, the overall calories consumed, etc. But isn't it easier to say "but it's harder for me!"

RoxieDawn

.

abatonfan

The high levels of insulin promoting weight loss is most likely false. Insulin is a hormone that directs cabohydrate metabolism at the cellular level. The most basic physiology is that when carbs are consumed, insulin that is released by the pancreas will "tell" the glucose (because all carbs will be digested into glucose) to first go to the cells to be used to produce ATP (through glycolysis), any excess carbs after that to the liver (and muscles to an extent) to be stored as glycogen (a very long chain of glucose molecules that is an intermediate-duration energy source for the body. When we fast, the body will break down the glycogen into glucose that can then be used to fuel the body), and then any excess carbs after that to the adipose cells to be stored as fat.

One of the big components of diabetes pathology is insulin levels. Type 1 diabetes is the result of an autoimmune attack on the pancreatic beta cells that causes very little to zero insulin to be naturally produced. Because no insulin is present within the body, carbs cannot be used as fuel, and the glucose has nowhere to go but to build up within the blood. This often results in very rapid unintentional weight loss (I lost 70-80lbs in three months due to undiagnosed type 1 diabetes) and a lot of other life-threatening complications. The body will turn to ketosis, and the combination of very large ketone production (MUCH larger than someone who is on keto), dehydration (because the kidneys are trying to filter out excess glucose through the urine, and lots of water is lost that way), hyperglycemia, and electrolyte imbalances causes the pH of the blood to shift to dangerously acidic levels (diabetic ketoacidosis).

Type 2 diabetes, on the other hand, initially starts out with large amounts of insulin being produced. The hallmark of type 2 diabetes is insulin resistance, so the pancreas first compensates for that by producing more insulin. If you remember that insulin is a "fat-storing" hormone, this is where things start to get pretty ugly in someone with type 2 diabetes. Excess insulin is produced in response to hyperglycemia (and because of the hyperglycemia one might feel super hungry and eat above maintenance kcals), which might lead to more fat being stored, which then leads to weight gain and more insulin resistance. This process is one of the reasons why some people with type 2 diabetes treat with a low carb diet (fewer carbs consumed, less insulin is needed to "cover" the carbs) and why weight loss is one of the crucial components of type 2 diabetes treatment (weight loss reduces insulin resistance).

rainbowbow

abatonfan wrote: »

The high levels of insulin promoting weight loss is most likely false. Insulin is a hormone that directs cabohydrate metabolism at the cellular level. The most basic physiology is that when carbs are consumed, insulin that is released by the pancreas will "tell" the glucose (because all carbs will be digested into glucose) to first go to the cells to be used to produce ATP (through glycolysis), any excess carbs after that to the liver (and muscles to an extent) to be stored as glycogen (a very long chain of glucose molecules that is an intermediate-duration energy source for the body. When we fast, the body will break down the glycogen into glucose that can then be used to fuel the body), and then any excess carbs after that to the adipose cells to be stored as fat.

One of the big components of diabetes pathology is insulin levels. Type 1 diabetes is the result of an autoimmune attack on the pancreatic beta cells that causes very little to zero insulin to be naturally produced. Because no insulin is present within the body, carbs cannot be used as fuel, and the glucose has nowhere to go but to build up within the blood. This often results in very rapid unintentional weight loss (I lost 70-80lbs in three months due to undiagnosed type 1 diabetes) and a lot of other life-threatening complications. The body will turn to ketosis, and the combination of very large ketone production (MUCH larger than someone who is on keto), dehydration (because the kidneys are trying to filter out excess glucose through the urine, and lots of water is lost that way), hyperglycemia, and electrolyte imbalances causes the pH of the blood to shift to dangerously acidic levels (diabetic ketoacidosis).

Type 2 diabetes, on the other hand, initially starts out with large amounts of insulin being produced. The hallmark of type 2 diabetes is insulin resistance, so the pancreas first compensates for that by producing more insulin. If you remember that insulin is a "fat-storing" hormone, this is where things start to get pretty ugly in someone with type 2 diabetes. Excess insulin is produced in response to hyperglycemia (and because of the hyperglycemia one might feel super hungry and eat above maintenance kcals), which might lead to more fat being stored, which then leads to weight gain and more insulin resistance. This process is one of the reasons why some people with type 2 diabetes treat with a low carb diet (fewer carbs consumed, less insulin is needed to "cover" the carbs) and why weight loss is one of the crucial components of type 2 diabetes treatment (weight loss reduces insulin resistance).

This is very true!


I've always wondered though, what is the threshold for de novo lipogenesis to occur as a result of carbohydrates? I've read a few studies that show that the ratio of carbohydrates that were stored as fat is very low and instead the excess fat gain was a result of inhibition of oxidation of dietary fat consumed. I.E. When someone was overeating total calories from carbohydrates the body will inhibit dietary fat oxidation and use the excess carbs as energy first.

I'm sure this probably works differently in someone who is insulin resistant or diabetic though.