The FastDay Forum

Lenghty and nerdy stuff, be warned!

One of the good things said about the 5:2 is that it reduces the hormone IGF-1. Both told in the doc and in the book. However, testing that level is not something commonly done because it's expensive, so most of us are in the dark about our IGF-1 levels.
More research connects IGF-1 with increased cancer risk and that 5:2 reduces the hormone is a real great benefit.
But then I started reading about different exercises' impact on weight loss. More and more points to HIT and/or strength training is way better than putting mile after mile behind you jogging or biking. Following that lead I came closer to why: It seems lactic acid promotes weight loss. The harder you train to the max, the more lactic acid you build up, and the more fat you lose. But that was not because of the lactic acid, but because lactic acid in turn makes the liver produce HGH, human growth hormone, which is used (simplified) to build new cells and repair the damaged muscles and tissue (why training makes us stronger)
So far so good, except HGH almost directly triggers IGF-1 (but it must be noted that at the same time it produces a "binder" for IGF-1 so it can't be used by any cancer cells. That's very simplified, but still)

I really want to learn about this and I am looking for answers to:
- What triggers the raised IGF-1 levels in non fasting people that are sedentary?
- Can IGF-1 be produced without HGH?
- Is the raised IGF-1 levels Michael Mosley talks about specific to "wrong diet and too little exercise"?
- Is IGF-1 levels after HIT exercise harmless and in fact needed for the build of muscles and tissue repair to work as intended?
- Or are these levels not raised at all because IGF-1 comes to good use right away?
- I have seen some claims that fasting actually promotes HGH production (leading to more IGF-1). Is it because the cells change "state" and go in repair mode and actually USE the IGF-1 available that makes the IGF-1 levels drop?

I will continue the search but if any of you know something about this or any references I'd love to know.

All good questions that I'd like to know about too. Many thanks.

[carorees]

Hi Running Olsen!

Here are some papers to get you started

http://www.ncbi.nlm.nih.gov/pubmed/22527168
http://www.ncbi.nlm.nih.gov/pubmed/18843793 full text of this paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673798/

It's something I've not been able to get to the bottom of. I think that while HGH and IGF1 are often in tandem, it is not always the case and as you say there is IGF1BP to consider too. However, I think that what is more important is that IGF1 activates the mTOR pathway of cell signalling which controls growth and survival and reduces autophagy. Anything that activates mTOR increases cancer risk and anything that inhibits mTOR reduces cancer risk. High glucose and protein activate MTOR. Fasting, low protein, calorie restriction inhibit it.

Exercise increases autophagy especially if done in the fasted state: http://www.ncbi.nlm.nih.gov/pubmed/23964069#

Thank you @carorees, sleeves up and reading glasses on!

@carorees what does enough low protein look like if you favour a plant based diet with minimal lamb and beef and some fish. Also would chia ramp up protein too much wasting say only on feed days

[carorees]

No-one really knows but we are assuming that keeping to 0.8g/kg body weight would be OK, more if you train hard. However, there is some evidence that plant protein stimulates IGF1 less, whereas milk may stimulate it more. It seeks that certain amino acids are more stimulatory. As with everything, it's v complicated. For now the 0.8g/kg is the best guess.

The problem with most of this research is that it involves very small groups of people (46 in the full text study, for example). As a result the results could easily be skewed by the presence in the group of a few people with unusual response patterns.

More importantly, most such studies are done with people who don't have significant weight problems, which makes it very questionable how well their results would apply to people who do.

I haven't researched this, but I have researched diet studies in middle aged women and people with metabolic disease. In those cases there are fascinating studies (that never get any press) showing that much of what we "know" about exercise doesn't apply to these groups. For example, there is a subgroup of people with slight defects in their mitochondria for whom exercise produces none of the health benefits found in studies of young active, often mostly male college students (who are who get studied in most academic studies.) People with these mitochondrial issues are, not surprisingly, part of the group of obese people prone to develop diabetes. The problems they face aren't caused by their obesity, but the mitochondrial issue which keeps them from burning energy properly and makes them obese over time.

HGH production is something that has a close connection to age, if I recall correctly, so the impact of CR on HGH and other hormones like insulin and IGF which decrease with age may be very different in someone in their 60s than it is in someone in their 40s.

There is far too little understanding of the wide range of individual, genetically-mediated variation in the research done by nutritional researchers. It's not a high status branch of science, and doesn't attract the brightest young scientists. Often the quality of the research is abysmal.

Any study, like the first one linked, that relies on standard nutritional questionnaires and people's memory of what they ate over the past month, is likely to be highly inaccurate, to say nothing of non-reproducible. The questionnaires are designed so that they only are mildly accurate in people eating standard high carb-laden diets and break down entirely when applied to people eating less than 3 meals a day and less than 300 g of carbs a day.

So really, there is no way to answer any of the questions we would all like to know about this or any other diet until very large, long terms studies are run, and even then, the methodological flaws render most such studies barely useful.

Hello All

For what I've found so far I'd like to answer the questions:

- What triggers the raised IGF-1 levels in non fasting people that are sedentary?
Probably a combination of too much sugar and being sedentary.

- Can IGF-1 be produced without HGH?
Probably not, but maybe some food can indirectly act as such

- Is the raised IGF-1 levels Michael Mosley talks about specific to "wrong diet and too little exercise"?
Same as top question really, so probably yes

- Is IGF-1 levels after HIT exercise harmless and in fact needed for the build of muscles and tissue repair to work as intended?
Mostly yes, because when the liver produces IGF-1 after being triggered by Human Growth Hormone, whichc again is triggered by exercise with lactid acid as result (aka HIIT and strength training), the liver also produces "binders" for IGF-1 so the IGF-1 isn't free to create trouble in other places of the body.

- Or are these levels not raised at all because IGF-1 comes to good use right away?
Same as above, so they are raised and used for something good: Muscle repair and growth.

- I have seen some claims that fasting actually promotes HGH production (leading to more IGF-1). Is it because the cells change "state" and go in repair mode and actually USE the IGF-1 available that makes the IGF-1 levels drop?
Probably yes.
My own theory is that there are more cell modes than "gogo mode" and repair mode. For one there is "active mode", which I think is needed to keep the hormone sensory and production system "in tune". It seems intermittent fasting in some ways triggers the same responses as exercise and/or they overlap and have positive effects on one another.

Disclaimer:
These are quite my own non-scientific ideas so far. I find this interesting because I think the real weight loss (or gain) is made by made hormones acting together. I think whatever we do with exercise and nutrition is really to manipulate different hormone levels and interaction. This would explain why "a calorie is not a calorie", some of the differences between men and women, the effects of different types of exercise and the importance of sleep. Maybe this is obvious or stupid, I don't know yet.

[carorees]

I have been keeping my eyes open for papers on this topic since you raised it @RunningOlsen. I found that the effect of HGH depends on the circumstances of its release. In the fed state it promotes IGF-1 production but in the fasting state it does not. This is because the liver becomes resisstant to the effect of GH when fasting. http://www.pnas.org/content/early/2013/ ... 0.full.pdf

Also remember that excess protein intake as well as glucose concentrations stimulate IGF-1.

Finally, having too low IGF-1 may also be detrimental to health,
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820068/
but no-one seems to know what the healthy values of IGF-1 at any particular age should be.

Thanks @carorees, much appreciated!

I thought I'd bump this thread because I found something interesting about protein fasting by a guy called Josh Whiton who suggests that regular protein fasting can introduce a certain type of autophagy without calorie restriction or loss of muscle. So maybe good for those in maintenance. It's another biohack similar to ketone triggered autophagy through low carb dieting, but deals with different types of junk (too complicated for me to get my head around), but obviously gives the body a chance to lower it's IGF-1 and reduce inflammation. However here is more for those who are interested. Don't know if @carorees has seen any research papers on it. http://joshwhiton.com/health/autophagy/, or whether it is just dealing with the same point already in this thread. I'm a tad confused.