Intermittent Fasting for Strength Training and Fat Loss

[gjohnson5]

When you say "detox' what are you referring to
Fasting is used with clensing processes such liver flush and some colon clensese do as well
These type things you'd have to initiate yourself

or are you talking about chaperone induction where damaged proteins are removed from cells?

[RU4A69]

Does anyone know approx how many hours after fasting detox begins? I read somewhere that it's 24 but I thought that seemed a little high

Excess sodium will start flushing out of your system fairly early on. Everything I've read says the real detox doesn't occur till days 3-10; but that is neither here nor there, because the "deep physiological rest" occurs early on and really starts kicking in after 24+ hrs. What I mean here is the break from digestion. To give you an idea, take your pulse a bit after waking, and then take it after a meal to give you an idea of "stress from digestion" that is daily imposed on your body. You can note the difference by checking your blood pressure, blood sugar, and insulin levels in fasted state vs. post-meal to get an idea of what I'm talking about.

[RU4A69]

Sry this is long, but thought not a few would find it interesting

Intermittent fasting.

In regular fasting one goes entirely without food, which is caloric restriction carried to the extreme. Going entirely without food in the short term leads to improvement in health, but also leads to an extremely short life unless the fast is aborted.

Intermittent fasting (IF) is just as its name implies: a period of fasting alternated with a period of eating.

But isn't that what we do anyway? We eat breakfast, then fast until lunch. Then, after lunch, we fast until supper. Then we fast all night. Uh, not exactly.

In research settings animals that are intermittently fasted are fed every other day, so they eat whatever they want for a day, then they are denied food for a day. Interestingly, on feeding days most of the animals eat a almost double the amount that their ad lib fed mates do. Thus the IF animals eat about the same number of calories overall that the ad lib fed animals eat, but, and this is a huge 'but,' the IF animals enjoy all the health advantages that the CR animals do, and, in fact, are even healthier than the CR animals.

Like caloric restriction, intermittent fasting reduces oxidative stress, makes the animals more resistant to acute stress in general, reduces blood pressure, reduces blood sugar, improves insulin sensitivity, reduces the incidence of cancer, diabetes, and heart disease, and improves cognitive ability. But IF does even more. Animals that are intermittently fasted greatly increase the amount of brain-derived neurotrophic factor (BDNF) relative to CR animals. CR animals don't produce much more BDNF than do ad libitum fed animals.

What's BDNF? (The Wikipedia definition is actually pretty good)

BDNF, as its name implies, is a substance that increases the growth of new nerve cells in the brain, but it does much more than that. BDNF is neuroprotective against stress and toxic insults to the brain and is somehow--no one yet knows how, exactly--involved in the insulin sensitivity/glucose regulating mechanism. Infusing BDNF into animals increases their insulin sensitivity and makes them lose weight. Humans with greater levels of BDNF have lower levels of depression. BDNF given to depressed humans reduces their depression. And Increased levels of BDNF improves cognitive ability. In short, you want as much BDNF as you can get., and with IF you can get a lot.

But, who wants to go all day every other day without food?

Well, you don't have to. MD and I, using ourselves (selflessly, I might add) as subjects have worked it out.

Most rodents feed throughout the day and night, so restricting them for 24 hours does just that: it restricts them for 24 hours. In humans, however, the situation is different. We humans, for the most part, eat only during our waking hours. So if we fast for a day, we end up fasting for about 34 hours and eating for 14, which isn't the same as 24 on, 24 off.

Let me show you what I mean.

Let's say you pick a day to start. You eat all day, then go to bed, wake up in the morning and fast all day, then go to bed. You wake up the next morning and eat all day, then go to bed and start again. So, assuming you eat until 10 PM on your eat day, once you quit eating you don't eat again until 8 AM 34 hours later. If you eat from 8 AM that day until 10 PM, you've eaten for 14 hours. so, you're on (eating) for 14 hours and off (fasting) for 34. MD and I spent a couple of weeks doing it that way, and I'm here to tell you, it's no fun. At least not on the fast days. The eating days were a different story; they were great, but we would spend the entire day dreading the fast day coming up.

We fooled around with a number of different eat-fast-eat regimens and came up with something that works pretty well. We set up our cutoff time as 6 PM. On the day we started, we ate until 6 PM, then fasted until 6 PM the next day. On the next day we ate supper right after 6 PM and ate breakfast and lunch (and a few snacks) the next day until 6 PM when we started fasting again.

The advantage of this regimen is that we were able to eat every day. One day we would get supper--the next day we would get breakfast and lunch. On no days would we go entirely without food. This schedule worked the best for us.

On the times during the day that we ate, we didn't stick with our normal low-carb fare; we ate pretty much whatever we wanted, including a fare amount of higher carb stuff. We stuck with the regimen for a few weeks just to see if we could tolerated it, which we did just fine. We ultimately drifted back to our normal low-carb diet, however, just because it seemed to work better with our schedules. We could have been happy on the intermittent fasting regimen for the long term.

I would think that the optimal way to go would be to follow an intermittent fast using low-carb foods during the eating periods. One would get the best of all worlds healthwise this way.

...

[RU4A69]

Over the period that we followed the various IF regimens we lost a little weight because, unlike the rodents, we couldn't eat twice as much during the eating days as we would have eaten were we not fasting. We didn't check any lab work to see if any values had changed. We weren't doing a hard core study; we were simply evaluating IF as a practical means for humans to use to improve their health.

In thinking about the process I came to the conclusion that IF was probably the way Paleolithic man ate. We modern humans have become acculturated to the three square meals per day regimen. Animals in the wild, particularly carnivorous animals, don't eat thrice per day; they eat when they make a kill. I would imagine that Paleolithic man did the same. If I had to make an intelligent guess, I would say that Paleolithic man probably ate once per day or maybe even twice every three days. In data gathered from humans still living in non-Westernized cultures in the last century, it appears that they would gorge after a kill and sleep and lay around doing not much of anything for the next day or so. When these folks got hungry, they went out and hunted and started the cycle again.

If you buy into the idea that the Paleolithic diet is the optimal diet for us today because it is the diet we were molded by the forces of natural selection to perform best on, then you should probably also buy into the idea that a meal timing schedule more like that of Paleolithic mean would provide benefit as well.

One of the things MD and I took away from our IF experience is the idea that we don't have to eat three meals per day. We now often skip lunch and don't seem any the worse for it. Sometimes we get up and get going with all our projects and don't eat breakfast. We try to skip a meal here and there because figure it's probably good for us. When you get used to it, you don't really even think about it. And it's good for you. Don't take my word for it--look at the medical literature.

There have been a few human studies on IF, and all have shown a marked improvement in virtually every parameter tested. None of the subjects in any of these studies has done the full 24 on-24 off that MD and I did. Most fasted until 5 or 6 PM on the fast days, then ate, then ate regularly on the eat days. Even with this wimpy IF schedule the subjects did better.

One of the recent papers published on the less rigid IF schedules caught my eye because one of the authors was Don Laub, who used to be the chairman of the plastic surgery department at Stanford. When I was in medical school I thought I wanted to be a plastic surgeon so I went to Stanford during a part of my senior year and worked with Dr. Laub as my mentor.

In this study, published in the journal Medical Hypothesis in March of this year, Dr. Laub along with two other physicians (neither of whom I know) underwent their version of and intermittent fast. The three of them have since May 2003 been on a version of the IF in which they consume about 20-50 percent of their estimated daily energy requirements on the fast day and eat whatever they want on the non-fast days.

Since starting their regimen they have

observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes.

In their paper these researchers discuss a 1957 paper from the Spanish medical literature.

...the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.

...

[crazymutha]

...

Good article.

I wish they would have commented about body composition, but then again, these were old people and probably did not exercise.

Makes me feel guilty for eating breakfast.

Since I cannot handle morning workouts any more (losing sleep), I may try some fasting again...lower carb for sure

[Annaerobic]

Some people can tolerate low carb beautifully and some cannot. The thing to consider is this: BEFORE you workout you aren't necessarily depleted of anything (glycogen), it is only AFTER that you would be depleted. So if you're going to include carbs in your diet, sometime after your workout would be appropriate.

Hmm... I could try that. Maybe a little bit of caffeine beforehand would do the trick.

If you stick to low intensity cardio, like walking preferably, you won't have this problem.

I've worked out a regular program since I last posted; my plan is a 3-day workout split (3x12-15 upper body, 3x12-15 lower, 5x6 upper), 3-day HIIT cardio since I've found it to be tremendously more effective for me than steady state, and one day completely off.

This past week- and possibly next- I'm alternating IF and regular feedings. My body gets reallt finnicky when it comes to digestion. But eventually when I switch to every day, I plan to eat "around" my workouts and HIIT. And as a college student in the city, I get plenty of low intensity cardio walking back and forth to classes and generally avoiding expensive public transportation.

You'd be absolutely astonished at how much water just a tiny bit of exogenous salt in your diet can make you retain. I cut salt from my already very very low salt keto diet and dropped about 6lbs in a couple days.

Just something to consider, I realize most people cannot bear life without salting their food.

I already don't use salt in anything and eat low-sodium versions of everything, but that's an interesting point. I've never really tracked my sodium intake like I should, maybe I'll start doing that.

Thank you so much for the advice!

[RU4A69]

low-sodium versions of everything, !

Like I said, just a DASH of inorganic sodium will cause some water retention. The organic sodium in food is plenty enough for your body.

Best of luck to you

[Ultrablack]

I had my first all-day water fast on tuesday and went to bed dreaming about food. Woke up on wednesday morning totally not hungry and had more energy than usual especially since I only slept for 6-7 hours. Pretty weird. I guess its my appetite resetting or something.

[scoot557]

Great study on one mechanism behind why fasting is muscle sparing, vs the intuitive thought that muscle protein would break down.

The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown.
N?rrelund H, Nair KS, J?rgensen JO, Christiansen JS, M?ller N.

Medical Department M, Aarhus Kommunehospital, Denmark. helenenorrelund@dadlnet.dk

The metabolic response to fasting involves a series of hormonal and metabolic adaptations leading to protein conservation. An increase in the serum level of growth hormone (GH) during fasting has been well substantiated. The present study was designed to test the hypothesis that GH may be a principal mediator of protein conservation during fasting and to assess the underlying mechanisms. Eight normal subjects were examined on four occasions: 1) in the basal postabsorptive state (basal), 2) after 40 h of fasting (fast), 3) after 40 h of fasting with ****tostatin suppression of GH (fast-GH), and 4) after 40 h of fasting with suppression of GH and exogenous GH replacement (fast+GH). The two ****tostatin experiments were identical in terms of hormone replacement (except for GH), meaning that ****tostatin, insulin, glucagon and GH were administered for 28 h; during the last 4 h, substrate metabolism was investigated. Compared with the GH administration protocol, IGF-I and free IGF-I decreased 35 and 70%, respectively, during fasting without GH. Urinary urea excretion and serum urea increased when participants fasted without GH (urea excretion: basal 392 +/- 44, fast 440 +/- 32, fast-GH 609 +/- 76, and fast+GH 408 +/- 36 mmol/24 h, P < 0.05; serum urea: basal 4.6 +/- 0.1, fast 6.2 +/- 0.1, fast-GH 7.0 +/- 0.2, and fast+GH 4.3 +/- 0.2 mmol/1, P < 0.01). There was a net release of phenylalanine across the forearm, and the negative phenylalanine balance was higher during fasting with GH suppression (balance: basal 9 +/- 3, fast 15 +/- 6, fast-GH 17 +/- 4, and fast+GH 11 +/- 5 nmol/min, P < 0.05). Muscle-protein breakdown was increased among participants who fasted without GH (phenylalanine rate of appearance: basal 17 +/- 4, fast 26 +/- 9, fast-GH 33 +/- 7, fast+GH 25 +/- 6 nmol/min, P < 0.05). Levels of free fatty acids and oxidation of lipid decreased during fasting without GH (P < 0.01). In summary, we find that suppression of GH during fasting leads to a 50% increase in urea-nitrogen excretion, together with an increased net release and appearance rate of phenylalanine across the forearm. These results demonstrate that GH-possibly by maintenance of circulating concentrations of free IGF-I--is a decisive component of protein conservation during fasting and provide evidence that the underlying mechanism involves a decrease in muscle protein breakdown.

linky: http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

[gjohnson5]

Great study on one mechanism behind why fasting is muscle sparing, vs the intuitive thought that muscle protein would break down.



linky: http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

The study is common knowledge...
We know that IGF is anabolic

What the study doesn't say is if lean body tissue remained the same during the 40 hours in the fasted subjects [without the ****tostatin which is a negative feedback to HGH]

[gjohnson5]

But the study does give me an idea about my question about increased rate of adrenal hormone release during fasting. Probably the adrenal glands (well the endocrine system in it's entirety) are trying to secrete enough epinephrine / norepinephrine to maintain bodily functions since IGF is clearly going to decrease while fasting. But in order to do this , muscle (smooth or skeletal) is metabolized and proteins broken down for thier phenylalanine in order to increase adrenal hormone levels + chemicals in the brain which control bodily functions

[scoot557]

The study is common knowledge...
We know that IGF is anabolic

What the study doesn't say is if lean body tissue remained the same during the 40 hours in the fasted subjects [without the ****tostatin which is a negative feedback to HGH]

I was posting it for those who may not know about elevated GH levels during fasting. At any rate, I agree - FFM lost would've been good to know. My intuition would say that some fat free mass would be lost...the ratio of fat free mass to fat mass lost would be an even more important piece of information.

Even more applicable for the audience in this thread would be a study that combined it with resistance training...and studied the role of nutrition before the fast. Also - the optimal length of the fast is yet to be determined...so many variables could lead to a breakthrough in nutrition. Or to a disappointing conclusion. I'm leaning towards the former, however.

The timing of weight training, eating, and prolonged fasting could all determine whether or not there are any beneficial or harmful effects. I say prolonged because I think there could be some benefit for fasting an entire day or even longer...


More on this topic to come, I'm working on an 'outside the box' type of training/diet schedule and implementing it on myself and one of my roommates (i love free guinea pigs). Hopefully my results will be worthy of making it public.

[gjohnson5]

I was posting it for those who may not know about elevated GH levels during fasting. At any rate, I agree - FFM lost would've been good to know. My intuition would say that some fat free mass would be lost...the ratio of fat free mass to fat mass lost would be an even more important piece of information.

Even more applicable for the audience in this thread would be a study that combined it with resistance training...and studied the role of nutrition before the fast. Also - the optimal length of the fast is yet to be determined...so many variables could lead to a breakthrough in nutrition. Or to a disappointing conclusion. I'm leaning towards the former, however.

The timing of weight training, eating, and prolonged fasting could all determine whether or not there are any beneficial or harmful effects. I say prolonged because I think there could be some benefit for fasting an entire day or even longer...


More on this topic to come, I'm working on an 'outside the box' type of training/diet schedule and implementing it on myself and one of my roommates (i love free guinea pigs). Hopefully my results will be worthy of making it public.

What you didn't get in that study was that HGH stimulates IGF release. It's the IGF that is actually muscle sparing...
If they did the same study and did a 40 hour fast with ****tostatin as well as IGF infusion , I bet you'd see the same if not less phenylalanine release then the fasted folks with no infusion at all...

The problem with using HGH as a means of anti catabolism while on a fast is clearly stated in the study. ****tostatin is a negative feedback to HGH. ****tostatin release also increases with age. So someone around my age would have much less serum growth hormone then someone who's 21. I guess what I'm trying to say is that fasted training is only a good idea if you're 21....

[scoot557]

What you didn't get in that study was that HGH stimulates IGF release. It's the IGF that is actually muscle sparing...
If they did the same study and did a 40 hour fast with ****tostatin as well as IGF infusion , I bet you'd see the same if not less phenylalanine release then the fasted folks with no infusion at all...

The problem with using HGH as a means of anti catabolism while on a fast is clearly stated in the study. ****tostatin is a negative feedback to HGH. ****tostatin release also increases with age. So someone around my age would have much less serum growth hormone then someone who's 21. I guess what I'm trying to say is that fasted training is only a good idea if you're 21....

GH's anabolic effects are not limited to IGF-1 production stimulation, and I'll try to illustrate why I think the other benefits of GH is the driving force behind the muscle sparing.

Points we agree on(these are facts...so there really isn't much debate):
HGH increases during fast
HGH stimulates IGF Production

You make the claim that the IGF is responsible for the muscle sparing, but you followed it up by saying IGF Levels decrease during fasting. Those two statements disagree with eachother, as well as disagreeing with HGH stimulating IGF production. I was hoping you could elaborate.

If you're referring to Free IGF decreasing during a fast, then we agree. But that's not what you said. IGFBP-1 has been shown to steadily increases during fasting, binding to IGF-1 and lowering Free IGF serum levels, which would limit the ability of IGF-1 to bind to other receptors and provide that anabolic goodness. That also implies that the muscle sparing effects are, in part, due to another mechanism. I'd have to see the timeline on IBFP1 increase vs amino acid breakdown to accurately say that IGF-1 is the only muscle sparing factor at play here.

As to your last point - your GH production being lower at old age would reduce the benefit slightly, but hear me out. Your baseline 24h mean GH levels would be adversely affected by the elevated ****tostatin levels, but a two-fold increase over baseline 24h mean growth hormone levels is still beneficial.

I'm curious as to your thoughts on those points?

[gjohnson5]

GH's anabolic effects are not limited to IGF-1 production stimulation, and I'll try to illustrate why I think the other benefits of GH is the driving force behind the muscle sparing.

Points we agree on(these are facts...so there really isn't much debate):
HGH increases during fast
HGH stimulates IGF Production

HGH increases on a fast at what expense to skeletal muscle?

You make the claim that the IGF is responsible for the muscle sparing, but you followed it up by saying IGF Levels decrease during fasting. Those two statements disagree with eachother, as well as disagreeing with HGH stimulating IGF production. I was hoping you could elaborate.

You're reaching bro. IGF release is stimulated by tons of mechanisms. Many of them revolve around insulin release. Estrogen release can cause IGF-1 secretion... it's a typical situation when one gets gyno, estrogen causes the gyno and IGF causes the gyno to grow... common knowledge

If you're referring to Free IGF decreasing during a fast, then we agree. But that's not what you said. IGFBP-1 has been shown to steadily increases during fasting, binding to IGF-1 and lowering Free IGF serum levels, which would limit the ability of IGF-1 to bind to other receptors and provide that anabolic goodness. That also implies that the muscle sparing effects are, in part, due to another mechanism. I'd have to see the timeline on IBFP1 increase vs amino acid breakdown to accurately say that IGF-1 is the only muscle sparing factor at play here.

I'm saying that Free AND total IGF will decrease. Insulin and estrogen play a bigger role in IGF release then HGH....

As to your last point - your GH production being lower at old age would reduce the benefit slightly, but hear me out. Your baseline 24h mean GH levels would be adversely affected by the elevated ****tostatin levels, but a two-fold increase over baseline 24h mean growth hormone levels is still beneficial.

I'm curious as to your thoughts on those points?

How would a man create a 2x mean HGH release, especially an older man?

[RU4A69]

There is every reason to assume that nitrogen retention in a weight trained individual would be better during a fast than in an untrained individual.

[Rugger7]

Wow, sorry to just jump in this thread after reading the first page, I'm sure my answer is within the 100+ pages but... if someone could tell me, what is the estimated maintence cals per lb/bw (not including workout expenditures) when doing intermittent fasting? For a 24, M, 5'10"...

Approximately how many calories can I eat in that 8 hour window and lose 1 lb of fat a week is what I am after.

[gjohnson5]

IGF is the whole reason I advocate 6+ meals a day.
The insulin release and the cascade of hromone secretions that follow (testosterone , IGF) would spare muscle. Aromatization of testosterone would cause estrogen release (hence more IGF-1)

Keeping the calories in check + cardio can do the fat burning (cardio can stimulate HGH which would lead to even more IGF)

This is the initial question I posted like 60 pages ago
How is this any better then eating smaller meals 6x a day while keeping a caloric deficit

If I'm training intensely , the last thing you'd want to do is fast due to the above

[RU4A69]

Wow, sorry to just jump in this thread after reading the first page, I'm sure my answer is within the 100+ pages but... if someone could tell me, what is the estimated maintence cals per lb/bw (not including workout expenditures) when doing intermittent fasting? For a 24, M, 5'10"...

Approximately how many calories can I eat in that 8 hour window and lose 1 lb of fat a week is what I am after.

??????????

You have to find that out yourself.

[scoot557]

HGH increases on a fast at what expense to skeletal muscle?
You're reaching bro. IGF release is stimulated by tons of mechanisms. Many of them revolve around insulin release. Estrogen release can cause IGF-1 secretion... it's a typical situation when one gets gyno, estrogen causes the gyno and IGF causes the gyno to grow... common knowledge

I'm saying that Free AND total IGF will decrease. Insulin and estrogen play a bigger role in IGF release then HGH....

How would a man create a 2x mean HGH release, especially an older man?

Let's take it to PM...

[scoot557]

Let's take it to PM...

This is getting nowhere, he has a fundamental misunderstanding of simple hormonal function.

I never read your initial question, as I pop in and out of this thread. I'm studying IF as a means of manipulating hormones via eating patterns.

Improved insulin sensitivity at the very least is a benefit. Like anything else, your body can develop a tolerance to constant levels of insulin. Most diets are give and take - give up some benefits to reap others.

I had great results with 6 meals/day...I just like to try extreme things in hopes of finding something better.

In re to the IGF debate - estrogen upregulates IGF via an increase in GH. It's not a direct relationship, IGF production is a direct relationship to circulating GH levels.

Steroid hormones basics
aromatization of testosterone (E2) causes the liver to produce IGF without respect to growth hormone...

He is dead serious. This is ridiculous. Just so no one here reads this nonsense and gets confused - Go read a book on the human reproductive system. Seriously. The mechanism for increased IGF is via increased GH. Testosterone aromatizing to estradiol upregulates GH, which in turn upregulates IGF.

http://books.google.com/books?id=DK-...esult#PPA33,M1
Read page 33 on ****tic growth.
Can't spell it out any more than that. Aromatizing testosterone into estradiol produces a rise in GH which triggers a rise in IGF.

Anyway there is no evidence of a Loww glycaemic load diet increasing insulin resistance especially since insulin resistance itself if genetic....
The insulin sensitivity card is also majorly overplayed since r+ala can be used to increase uptake of glucose

In the absence of insulin, your sensitivity to it will go up. Like anything else. Excess downregulates sensitivity and depravity upregulates it. Improved insulin sensitivity is very real and has been demonstrated in every study featuring fasting and refeeding. That being said, there are many different ways to improve insulin sensitivity. Fasting is by no means the only way - but it certainly is one way.

As to your last point,
Low glycemic != fasting. It's apples to oranges because plenty of food combinations, regardless of glycemix index, result in insulin release.

I'm done here. You know nothing about the body's response to hormones or nutrition and are clearly a troll. You are so sure of yourself, yet you lack a fundamental understanding of the most rudimentary hormonal responses. Can we get this guy either banned, or prevented from ****ting up this thread any further? He is spreading misinformation with every post.



I can't wait for him to tell me that the IGF increase is not a result of the increase of growth hormone...again. Instead of arguing with me - go argue with the authors of every book on the human body.

[crazymutha]

This is getting nowhere, he has a fundamental misunderstanding of simple hormonal function.


He is dead serious. This is ridiculous. Just so no one here reads this nonsense and gets confused - Go read a book on the human reproductive system. Seriously. The mechanism for increased IGF is via increased GH. Testosterone aromatizing to estradiol upregulates GH, which in turn upregulates IGF.

http://books.google.com/books?id=DK-...esult#PPA33,M1
Read page 33 on ****tic growth.
Can't spell it out any more than that. Aromatizing testosterone into estradiol produces a rise in GH which triggers a rise in IGF.





In the absence of insulin, your sensitivity to it will go up. Like anything else. Excess downregulates sensitivity and depravity upregulates it. Improved insulin sensitivity is very real and has been demonstrated in every study featuring fasting and refeeding. That being said, there are many different ways to improve insulin sensitivity. Fasting is by no means the only way - but it certainly is one way.

As to your last point,
Low glycemic != fasting. It's apples to oranges because plenty of food combinations, regardless of glycemix index, result in insulin release.

I'm done here. You know nothing about the body's response to hormones or nutrition and are clearly a troll. You are so sure of yourself, yet you lack a fundamental understanding of the most rudimentary hormonal responses. Can we get this guy either banned, or prevented from ****ting up this thread any further? He is spreading misinformation with every post.



I can't wait for him to tell me that the IGF increase is not a result of the increase of growth hormone...again. Instead of arguing with me - go argue with the authors of every book on the human body.

Relax, man.

If you are right, then tell him peacibly.

He is not a troll, for sure.

This very thread is controversial in nature and most people, especially on this board, reject this whole thread.


The truth stands on its own, once called out. No need to bash him.


It is good that you post accurate information, though.


Anyway, do you post on dragondoor? Your screen name looks familiar...

[gjohnson5]

Relax, man.

If you are right, then tell him peacibly.

He is not a troll, for sure.

This very thread is controversial in nature and most people, especially on this board, reject this whole thread.


The truth stands on its own, once called out. No need to bash him.


It is good that you post accurate information, though.


Anyway, do you post on dragondoor? Your screen name looks familiar...

I got getter things to do then live on this thread
A response to hit nonsense is coming

[gjohnson5]

Interesting that he says let's take it to PM , and then he posts my PM publically
Is that even abiding by the rules of the forum????

[Ultrablack]

Approx how many hours after doing a water fast does your metabolism slow down to the point where your body starts burning muscle? I posted this a while back but never got a response. I'm going to do a water fast for this weekend btw if anyone was wondering.

[gjohnson5]

Well Sorry I had to do this , but dude clearly needs to be corrected....

GH and IGF have clear and separate functions in the

http://www.ncbi.nlm.nih.gov/pubmed/15701568

Are the metabolic effects of GH and IGF-I separable?
Mauras N, Haymond MW.

Division of Endocrinology, The Department of Pediatrics at the Nemours Children's Clinic, 807 Children's Way, Jacksonville, FL 32207, USA. nmauras@nemours.org

IGF-I mediates some, but not all of the metabolic actions of GH and it has both GH-like and insulin-like actions in vivo. GH and IGF-I both have a net anabolic effect in man enhancing whole body protein synthesis over a period of weeks and perhaps months. Both hormones favorably improve body composition in GH deficient subjects with an increase in lean body mass and decreased adiposity. This is also observed when IGF-I is given to patients with GH-receptor mutations. These compounds, however, have divergent effects on carbohydrate metabolism. A potent glucose lowering effect is typically observed after IGF-I administration, with improved insulin sensitivity with marked lowering of circulating insulin concentrations, whereas GH therapy is associated with mild compensatory hyperinsulinemia, a reflection of relative insulin resistance. The latter observation makes IGF-I a potentially more convenient anabolic agent to use in conditions where carbohydrate metabolism is more likely to be impaired. GH increases lipolysis as a direct effect of GH on the adipocyte, as well as lipid oxidation by increasing substrate availability. However IGF-I increases lipid oxidation only when given chronically, most likely as a result of chronic insulinopenia. These compounds have been tried in a variety of catabolic conditions in man and both hormones have been effective in reducing the protein wasting effects of glucocorticosteroids and mitigate some of the catabolic effects of severe hypogonadism in males. A comparison of these and other effects of these hormones is provided in this brief review. Subsequent studies are still needed to fully elucidate the safety and efficacy of IGF-I for use in humans.

PMID: 15701568 [PubMed - indexed for MEDLINE]

IGF-1 growth stimulation is independant of GH

Insulin-like growth factor 1 (IGF-1): a growth hormone.
Laron Z.

Endocrinology and Diabetes Research Unit, WHO Collaborating Center for the Study of Diabetes in Youth, Schneider Children's Medical Center, Tel Aviv University, 14 Kaplan Street, Petah Tikva 49202, Tel Aviv, Israel. laronz@clalit.org.il

AIM: To contribute to the debate about whether growth hormone (GH) and insulin-like growth factor 1 (IGF-1) act independently on the growth process. METHODS: To describe growth in human and animal models of isolated IGF-1 deficiency (IGHD), such as in Laron syndrome (LS; primary IGF-1 deficiency and GH resistance) and IGF-1 gene or GH receptor gene knockout (KO) mice. RESULTS: Since the description of LS in 1966, 51 patients were followed, many since infancy. Newborns with LS are shorter (42-47 cm) than healthy babies (49-52 cm), suggesting that IGF-1 has some influence on intrauterine growth. Newborn mice with IGF-1 gene KO are 30% smaller. The postnatal growth rate of patients with LS is very slow, the distance from the lowest normal centile increasing progressively. If untreated, the final height is 100-136 cm for female and 109-138 cm for male patients. They have acromicia, organomicria including the brain, heart, gonads, genitalia, and retardation of skeletal maturation. The availability of biosynthetic IGF-1 since 1988 has enabled it to be administered to children with LS. It accelerated linear growth rates to 8-9 cm in the first year of treatment, compared with 10-12 cm/year during GH treatment of IGHD. The growth rate in following years was 5-6.5 cm/year. CONCLUSION: IGF-1 is an important growth hormone, mediating the protein anabolic and linear growth promoting effect of pituitary GH. It has a GH independent growth stimulating effect, which with respect to cartilage cells is possibly optimised by the synergistic action with GH.

PMID: 11577173 [PubMed - indexed for MEDLINE]


Insulin decreases IGFBP thus increases free IGF-1

Insulin: the other anabolic hormone of puberty.
Caprio S.

Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut, USA. sonia.caprio@yale.edu

To determine the effect of puberty on insulin action, we used the euglycaemic-hyperinsulinaemic clamp technique in combination with stable isotopes and indirect calorimetry in lean pre-adolescents, adolescents and adults. These studies indicated that the insulin resistance induced by normal puberty alters glucose metabolism but is insufficient to adversely affect insulin-stimulated protein metabolism or to inhibit lipolysis. Using the hyperglycaemic clamp technique, we evaluated the impact of the insulin resistance on insulin secretion in pre-adolescents, adolescents and young adults. These studies revealed that the insulin and C-peptide responses to a standardized intravenous hyperglycaemic stimulus were two- to threefold greater in adolescents than in pre-adolescent children and adults. As growth hormone (GH), insulin-like growth factor I (IGF-I) and insulin levels normally peak during puberty, we examined the influence of insulin on IGF-I regulation by measuring basal GH, total and free IGF-I, and IGF binding protein (IGFBP) levels in lean adolescents and young adults. During the clamp studies, the adolescents exhibited low levels of IGFBP-1 and -2 as well as a reduced insulin-induced suppression of IGFBP-1, compared with lean adults. Thus, we postulate that the insulin resistance of puberty induces compensatory hyperinsulinaemia, which in turn suppresses circulating levels of IGFBP-1, which in turn leads to increased levels of free IGF-1.

Testosterone initiates release of IGF without regards to HGH

Identification of Androgen Response Elements in the IGF-1 Upstream Promotor
Yong Wu, Weidong Zhao, Jingbo Zhao, Jiangping Pan, Qiaqia Wu, Yuanfei Zhang, William A. Bauman, and Christopher P. Cardozo*

Department of Veterans Affairs, Center of Excellence for the Medical Consequences of Spinal Cord Injury, James J. Peters Medical Center, Bronx NY, and Department of Medicine, Mount Sinai School of Medicine, 1 Gustave Levy Place, New York, NY 10029

* To whom correspondence should be addressed. E-mail: Chris.Cardozo{at}mssm.edu.

Testosterone stimulates the expression of insulin-like growth factor-1 (IGF-1) in cells and tissues that include prostate, muscle and muscle satellite cells, and the uterus. Here, the molecular mechanisms of this effect of testosterone were explored. Testosterone increased IGF-1 mRNA levels in HepG2 and LNCaP cells and stimulated the activity of reporter genes controlled by 1.6 kb of the upstream promotor of the human IGF-1 gene. An androgen-responsive region that was located between -1320 and -1420 bases upstream of the first codon was identified by truncation studies. The androgen-responsive region was found to contain two sequences resembling known AR binding sites from the Pem1 gene. Reporter genes incorporating these sequences were strongly stimulated by androgens. Each of the androgen-responsive elements bound recombinant AR-DNA binding domain in gel-shift experiments; binding was greatly enhanced by sequences flanking the apparent AR-binding half-sites. Testosterone induced recruitment of AR to sequences of genomic DNA containing these AREs. The two AREs were activated 5-fold more by AR than GR. Collectively, these findings indicate the presence of two AREs within the IGF-1 upstream promotor that act in cis to activate IGF-1 expression. These AREs seem likely to contribute to the upregulation of the IGF-1 gene in prostate tissues, HepG2 cells, and potentially other tissues.

http://endo.endojournals.org/cgi/rap...006-1653v1.pdf

DHT stimulates IGF release in prostate cells

http://carcin.oxfordjournals.org/cgi...tract/bgn011v1

Lycopene inhibits IGF-I signal transduction and growth in normal prostate epithelial cells by decreasing DHT-modulated IGF-I production in cocultured reactive stromal cells
Xunxian Liu, Jeffrey D. Allen, Julia T. Arnold and Marc R. Blackman*

Endocrine Section, Laboratory of Clinical Investigation, Division of Intramural Research, National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892

* To whom correspondence should be addressed. Tel: 202-745-8478; Fax: 202-518-4645; Email: Marc.Blackman@va.gov

Prostate stromal and epithelial cell communication is important in prostate functioning and cancer development. Primary human stromal cells from normal prostate (PRSC) maintain a smooth muscle phenotype, whereas those from prostate cancer (6S) display reactive and fibroblastic characteristics. DHT stimulates IGF-I production by 6S but not PSRC cells. Effects of reactive versus normal stroma on normal human prostate epithelial (NPE or PREC) cells are poorly understood. We cocultured NPE plus 6S or PRSC cells to compare influences of different stromal cells on normal epithelium. Because NPE and PREC cells lose AR expression in culture, DHT effects must be modulated by associated stromal cells. When treated with camptothecin (CM), NPE cells, alone and in stromal cocultures, displayed a dose dependent increase in DNA fragmentation. NPE/6S cocultures exhibited reduced CM-induced cell-death with exposure to DHT, whereas NPE/PRSC cocultures exhibited CM-induced cell-death regardless of DHT treatment. DHT blocked CM-induced, IGF-I mediated, NPE death in cocultured NPE/6S cells without, but not with, added anti-IGF-I and anti-IGF-R antibodies. Lycopene consumption is inversely related to human prostate cancer risk and inhibits IGF-I and androgen signaling in rat prostate cancer. In this study, lycopene, in dietary concentrations, reversed DHT effects of 6S cells on NPE cell-death; decreased 6S cell IGF-I production by reducing AR and β-catenin nuclear localization; and inhibited IGF-I stimulated NPE and PREC growth, perhaps by attenuating IGF-I's effects on serine phosphorylation of Akt and GSK3β, and tyrosine phosphorylation of GSK3. This study expands the understanding of the preventive mechanisms of lycopene in prostate cancer.

Received September 11, 2007; revised January 3, 2008; accepted January 3, 2008.


Hell even breast tissue stimulates IGF-1 without regard for HGH

Increase of free insulin-like growth factor-1 in normal human breast in vivo late in the menstrual cycle.
Dabrosin C.

Division of Gynecologic Oncology, University Hospital, Faculty of Health Sciences, Link?ping, Sweden. lotda@imk.liu.se

Prolonged exposure to endogenous and exogenous sex steroids increases the risk of breast cancer but the mechanisms are poorly understood. Increased levels of circulating insulin-like growth factor-1 (IGF-1) and low levels of IGF binding protein are associated with increased risk of breast cancer suggesting that IGF-1 has to be in its free form to be biologically active. Little is known about sex steroid regulation of IGF-1 locally in the breast. In this study microdialysis was used to determine the local levels of free IGF-1 in normal human breast tissue in healthy female volunteers during the menstrual cycle. The results showed that the extracellular levels of free IGF-1 locally in the breast were doubled in the luteal phase, when estradiol and progesterone levels were elevated, compared with the follicular phase. In plasma, free IGF-1 levels also exhibited a cyclic variation but to a less extent. The increased local levels of the free form of IGF-1 may promote proliferation in the breast epithelium. This could be important in sex steroid dependent breast cancer development.
http://www.ncbi.nlm.nih.gov/pubmed/12908822

[gjohnson5]

Also:



Well last but not least , there would be much fewer incidences of cancer if IGF-1 was solely dependant on growth hormone levels. This study which I will not cite clearly states several hypothesis why IGF-1 is elevated in cancer patients without assocated GH increase.

http://www.sciencedirect.com/science...59eaa0fa61cdc2


But you might wanna read more before posting my PM's....

[gjohnson5]

In the absence of insulin, your sensitivity to it will go up. Like anything else. Excess downregulates sensitivity and depravity upregulates it. Improved insulin sensitivity is very real and has been demonstrated in every study featuring fasting and refeeding. That being said, there are many different ways to improve insulin sensitivity. Fasting is by no means the only way - but it certainly is one way.

LOL @ this mess
You went on a rampage and are clearly wrong on all points...
But I'm glad you showed your true colors and you were just trying to have an argument
Now that you're clearly wrong, what's next

For you , atleast start reading science instead of books.google.com


Insulin resistance is genetic. These scientists believe they have identified genes which cause insulin resistance...

http://www.sciencedaily.com/releases...1027095416.htm

Which means clearly that not everyone is going to become insulin resistant in the first place.
So for those folks , there may be no reason to fast at all because insulin resistance may not be a problem for them genetically

[scoot557]

Well Sorry I had to do this , but dude clearly needs to be corrected....

Nothing is corrected.

GH and IGF have clear and separate functions in the

No ****.

Are the metabolic effects of GH and IGF-I separable?
Mauras N, Haymond MW.

This study further proves my point that IGF is upregulated by circulating GH. They were administering IGF-1 to GH deficient humans for a reason. GH deficiency would also lead to IGF-1 deficiency and they were attempting to see if IGF-1 administration would be effective.

IGF-1 growth stimulation is independant of GH

Insulin-like growth factor 1 (IGF-1): a growth hormone.

So the mechanism that IGF-1 spurs growth is independent of the mechanism that GH spurs growth. Also true, however does not unlink IGF production from a rise in GH levels.

Insulin decreases IGFBP thus increases free IGF-1

Insulin: the other anabolic hormone of puberty.

Increasing Free-IGF via a decrease in IGFBP is not increasing IGF-1. It improves the ratio of available IGF-1 to bind to other cells. Same thing applies to Testosterone vs Free Testosterone. Anything that inhibits SHBG will bring up Free Testosterone levels, not necessarily total test levels. This is severely crude, but I am dumbing it down in hopes that you will understand: If you have X amount IGF-1 and Y amount IGFBP, your Free-IGF1 would be X - Y. IGFBP(there are several of these) binds to IGF-1 and inhibits its effect to bind to IGF Receptors on other cells. Hence why it is no longer Free-IGF.

Testosterone initiates release of IGF without regards to HGH

Identification of Androgen Response Elements in the IGF-1 Upstream Promotor
Yong Wu, Weidong Zhao, Jingbo Zhao, Jiangping Pan, Qiaqia Wu, Yuanfei Zhang, William A. Bauman, and Christopher P. Cardozo*

Your first study that *might* be applicable, but inconclusive at best. Read the last sentence. These AREs seem likely to contribute to the IGF-1 prodcution. Hardly sounds like a definitive statement. I tried to read the full study but the link didn't work. If you could attach the study I'd love to read it.

DHT stimulates IGF release in prostate cells

http://carcin.oxfordjournals.org/cgi...tract/bgn011v1

Lycopene inhibits IGF-I signal transduction and growth in normal prostate epithelial cells by decreasing DHT-modulated IGF-I production in cocultured reactive stromal cells
Xunxian Liu, Jeffrey D. Allen, Julia T. Arnold and Marc R. Blackman*

Endocrine Section, Laboratory of Clinical Investigation, Division of Intramural Research, National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland 20892

* To whom correspondence should be addressed. Tel: 202-745-8478; Fax: 202-518-4645; Email: Marc.Blackman@va.gov

Prostate stromal and epithelial cell communication is important in prostate functioning and cancer development. Primary human stromal cells from normal prostate (PRSC) maintain a smooth muscle phenotype, whereas those from prostate cancer (6S) display reactive and fibroblastic characteristics. DHT stimulates IGF-I production by 6S but not PSRC cells.

That's great, since I don't have prostate cancer this doesn't apply.

Increase of free insulin-like growth factor-1 in normal human breast in vivo late in the menstrual cycle.
Dabrosin C.
...
The results showed that the extracellular levels of free IGF-1 locally in the breast were doubled in the luteal phase, when estradiol and progesterone levels were elevated,
...

I already went over why this elevates IGF-1. Estradiol upregulates HGH. Thanks for hammering my point home.

What do you think Google books is, by the way? The link I sent you was to a science book. Jesus you are dumb

[gjohnson5]

I see you're too dumb to understand that some cells work differently then others in your post above
The point of the cancer cells was to point that out

The same is true with breast tissue. It's a benign growth which posseses the ability to generate IGF-1 locally. No growth hormone elevation is needed in those cases...

I believe the same is true for the liver, but didn't have time to find a study on that