Achieving Leptin
Knowledge in the area of leptin is still sadly limited. Heck, what can you expect. The hormone was only discovered in 1995. Scientific knowledge builds, but you still can't go from zero knowledge to complete mastery in a little over a decade.
Science doesn't have my answer yet.
Health sciences, likewise, don't have my answer because science itself is still scrambling and tripping and stumbling around the basics of this little but quite important hormone.
What science does know:
In fat people, leptin is abundant but nonetheless does not tamp down appetite either because leptin resistance is at play or because the high triglycerides in the average obese person's bloodstream prevent leptin from successfully passing the blood-brain barrier to tell the receptors there that--Hey! We're FULL OF FAT, STOP EATING! (Dr Eades explored this in a post if I recall correctly.)
I suspect it's a combo of both.
What is unclear is whether leptin resistance, once created in an obese body, eases over time in the body of someone following a low-carb diet at a healthy body weight. I've been unable to find reference to any study--casual of clinical--that looked at this.
So I could remain leptin resistant even if I had a healthy level of leptin in my body. Shrug. We'll cross that bridge if we encounter it.
What else does science know: people with massive weight loss can sometimes end up with suppressed leptin level probably because in the very obese fat cells actually multiply and when huge amounts of weight are lost, those fat cells don't disappear--they wither. Instead of having a normal level of normal-sized fat cells, a formerly obese person attaining a healthful weight will have a far greater number of tiny, shrunken fat cells. If the size of the fat cell (puny versus plump) is what causes the release of leptin, clearly this would make for low low low levels of leptin.
Again, what do you do? Liposuction? More surgery to reduce areas of sagging skin with accompanying subQ fat? Possibly. Science has neither studied nor answered this.
What more does science know?
Leptin powerfully regulates reproductive hormones and metabolic ones too--estrogen, GnRH, LH, FSH, T3. All of these seem to be throttled back when leptin is low. This is logical. The body thinks it's experiencing famine times. It's not a good time to reproduce, nor is it a good time to play fast and loose with the energy stores the body still possesses. (Remember, the body thinks it's starving.)
So women with low leptin? They can develop hypothalamic amenorrhea rendering them infertile and stealing the monthly cycle of hormones that give life color, spark, meaning, happiness... (headaches, water retention, depression, fury, carb-cravings)
Whoops, we've encountered a tangent. Stop immediately!
Back to science and what it knows about leptin:
Exercise that does not induce weight loss does not reduce leptin levels. Exercise decreases leptin resistance.
Sleep increases leptin--or at least, lack of sleep decreases leptin. Same coin, different side.
It also appears that estrogen may increase leptin.
Science also knows that "white fat" cells produce leptin whereas "brown fat" cells apparently do not. Human babies have brown fat on their backs. Most adults lose the extra capillaries in this "brown fat" and it becomes more akin to white fat, but may retain some brown fat in the upper chest and neck.
And now, the most pertinent factor for me at present: higher insulin means higher leptin. Insulin "regulates" leptin. Now how precisely this is achieved, I cannot say. I've been unable to find a description of the mechanism and it's possible science does not know the how, merely the fact itself.
The fact itself, however, is sufficient for me to consider a "leptin refeed" carb day despite being warned against it by one of the wisest and most hormonally insightful minds I've encountered online.
It's not clear whether it is the highest level of insulin, or the quantity, or the act of a spike that regulates the leptin level--I dearly wish that I knew. All that is clear is that "insulin is reported to directly stimulate leptin" per this text. Shrug.
It is known that increases in dietary fat and protein do not lead to increases in leptin even if the caloric intake is increased.
So: carbs increase insulin and increase leptin.
Leptin is necessary for normal fertility.
Insulin may also play a key regulatory part in fertility via pulsative LH.
So a girl with lowwww leptin on a lowwww carb diet and maintaining her size two hips and her bony wrists and getting nowwwwhere with fertility and going insane with low estrogen and low T3 and getting hungry and moody...
Well, that girl should probably look at the meager facts science has amassed and do her best to go forward. While that girl does believe in and understand the merits of low carb dieting--especially for someone with insulin resistance and a high risk for DMII and probably history of PCOS--that girl also wants to achieve fertilty.
The question is: if that girl consumes carbs in order to raise leptin and increase fertility, will her probable underlying PCOS rise up and negate the effort?
Shrug.
Science doesn't have the answer yet.
We know that leptin follows insulin. We know that insulin is not increased by fructose and that, in fact, fructose consumption decreases the chance of a leptin increase. We want straight glucose or chained glucose. So we want: rice, potatoes, rice syrup.
It also looks like Fish Oil increases leptin whereas beef fat decreases it.
So. If a girl were to devise a leptin-maximizing diet, she would do the following:
Take in carbs that are glucose-based.
To prevent the health hits of a carb and fat heavy diet, reduce fat intake drastically. 20-30g (whimper!)
Take in only the amount of protein needed to maintain lean body mass.
What does that diet look like?
For carbs: rice, rice cereal, potatoes, rice syrup, maybe some milk
For protein: fish, in particular tuna and salmon
On my first day (and perhaps last), I'm shooting for 10% above maintenance calories. Maintenance is between 1680 and 1750, so let us say 1750 plus 175 for a total of 1925. Per Jenny's calculator I need 43 grams of protein. That's 178 calories worth. Let us just shoot for around 25 - a max or 40g of fat. That leaves us with about 340g carb?
Good lordy, I don't know how I'm going to attain that. But I'll get crackin'.
The icon says it all.
I know that this is not the healthiest thing for my own body, but it might also be the only accessible means of achieving fertility.
And I will work for a baby.
~L
Science doesn't have my answer yet.
Health sciences, likewise, don't have my answer because science itself is still scrambling and tripping and stumbling around the basics of this little but quite important hormone.
What science does know:
In fat people, leptin is abundant but nonetheless does not tamp down appetite either because leptin resistance is at play or because the high triglycerides in the average obese person's bloodstream prevent leptin from successfully passing the blood-brain barrier to tell the receptors there that--Hey! We're FULL OF FAT, STOP EATING! (Dr Eades explored this in a post if I recall correctly.)
I suspect it's a combo of both.
What is unclear is whether leptin resistance, once created in an obese body, eases over time in the body of someone following a low-carb diet at a healthy body weight. I've been unable to find reference to any study--casual of clinical--that looked at this.
So I could remain leptin resistant even if I had a healthy level of leptin in my body. Shrug. We'll cross that bridge if we encounter it.
What else does science know: people with massive weight loss can sometimes end up with suppressed leptin level probably because in the very obese fat cells actually multiply and when huge amounts of weight are lost, those fat cells don't disappear--they wither. Instead of having a normal level of normal-sized fat cells, a formerly obese person attaining a healthful weight will have a far greater number of tiny, shrunken fat cells. If the size of the fat cell (puny versus plump) is what causes the release of leptin, clearly this would make for low low low levels of leptin.
Again, what do you do? Liposuction? More surgery to reduce areas of sagging skin with accompanying subQ fat? Possibly. Science has neither studied nor answered this.
What more does science know?
Leptin powerfully regulates reproductive hormones and metabolic ones too--estrogen, GnRH, LH, FSH, T3. All of these seem to be throttled back when leptin is low. This is logical. The body thinks it's experiencing famine times. It's not a good time to reproduce, nor is it a good time to play fast and loose with the energy stores the body still possesses. (Remember, the body thinks it's starving.)
So women with low leptin? They can develop hypothalamic amenorrhea rendering them infertile and stealing the monthly cycle of hormones that give life color, spark, meaning, happiness... (headaches, water retention, depression, fury, carb-cravings)
Whoops, we've encountered a tangent. Stop immediately!
Back to science and what it knows about leptin:
Exercise that does not induce weight loss does not reduce leptin levels. Exercise decreases leptin resistance.
Sleep increases leptin--or at least, lack of sleep decreases leptin. Same coin, different side.
It also appears that estrogen may increase leptin.
Science also knows that "white fat" cells produce leptin whereas "brown fat" cells apparently do not. Human babies have brown fat on their backs. Most adults lose the extra capillaries in this "brown fat" and it becomes more akin to white fat, but may retain some brown fat in the upper chest and neck.
And now, the most pertinent factor for me at present: higher insulin means higher leptin. Insulin "regulates" leptin. Now how precisely this is achieved, I cannot say. I've been unable to find a description of the mechanism and it's possible science does not know the how, merely the fact itself.
The fact itself, however, is sufficient for me to consider a "leptin refeed" carb day despite being warned against it by one of the wisest and most hormonally insightful minds I've encountered online.
It's not clear whether it is the highest level of insulin, or the quantity, or the act of a spike that regulates the leptin level--I dearly wish that I knew. All that is clear is that "insulin is reported to directly stimulate leptin" per this text. Shrug.
It is known that increases in dietary fat and protein do not lead to increases in leptin even if the caloric intake is increased.
So: carbs increase insulin and increase leptin.
Leptin is necessary for normal fertility.
Insulin may also play a key regulatory part in fertility via pulsative LH.
So a girl with lowwww leptin on a lowwww carb diet and maintaining her size two hips and her bony wrists and getting nowwwwhere with fertility and going insane with low estrogen and low T3 and getting hungry and moody...
Well, that girl should probably look at the meager facts science has amassed and do her best to go forward. While that girl does believe in and understand the merits of low carb dieting--especially for someone with insulin resistance and a high risk for DMII and probably history of PCOS--that girl also wants to achieve fertilty.
The question is: if that girl consumes carbs in order to raise leptin and increase fertility, will her probable underlying PCOS rise up and negate the effort?
Shrug.
Science doesn't have the answer yet.
We know that leptin follows insulin. We know that insulin is not increased by fructose and that, in fact, fructose consumption decreases the chance of a leptin increase. We want straight glucose or chained glucose. So we want: rice, potatoes, rice syrup.
It also looks like Fish Oil increases leptin whereas beef fat decreases it.
So. If a girl were to devise a leptin-maximizing diet, she would do the following:
Take in carbs that are glucose-based.
To prevent the health hits of a carb and fat heavy diet, reduce fat intake drastically. 20-30g (whimper!)
Take in only the amount of protein needed to maintain lean body mass.
What does that diet look like?
For carbs: rice, rice cereal, potatoes, rice syrup, maybe some milk
For protein: fish, in particular tuna and salmon
On my first day (and perhaps last), I'm shooting for 10% above maintenance calories. Maintenance is between 1680 and 1750, so let us say 1750 plus 175 for a total of 1925. Per Jenny's calculator I need 43 grams of protein. That's 178 calories worth. Let us just shoot for around 25 - a max or 40g of fat. That leaves us with about 340g carb?
Good lordy, I don't know how I'm going to attain that. But I'll get crackin'.
The icon says it all.
I know that this is not the healthiest thing for my own body, but it might also be the only accessible means of achieving fertility.
And I will work for a baby.
~L