32 replies to this topic

[FNC]

Good day to all,

Given that I do not want to interrupt my growth and development,
can someone provide information regarding IGF-1 inhibitors, from supplementation/food or otherwise.

I know of Resveratrol thus far, any others?


Thanks,
Fabien

[woly]

I seem to remember reading somewhere that lycopene lowers IGF-1 levels. I suppose dairy and possibly carbohydrate restriction would help too.

[Blue]

Why should carbohydrate restriction lower it? Protein restriction lower it, at least if you are on CR.

[Blue]

Milk increases IGF-1:
http://informahealth...637480903150114

[Blue]

OBJECTIVE: The aim of this study was to examine the relationship of diet with serum insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 in women. DESIGN: Cross-sectional study. SETTING AND SUBJECTS: The population are 2109 women who were control subjects in a case-control study of breast cancer nested in the European Prospective Investigation into Cancer and Nutrition. Control subjects were randomly chosen among risk sets consisting of female cohort members alive and free of cancer (except non-melanoma skin cancer) at the time of diagnosis of the index case. Matching criteria were age at enrolment, follow-up time, time of the day of blood collection and study centre. Diet was measured through validated questionnaires. Serum hormone concentrations were measured by enzyme-linked immunosorbent assays. The relationship between serum IGF-I, IGFBP-3, and intake of nutrients and foods was explored by linear regression in models adjusted for energy intake, age, body mass index, smoking, physical activity, centre and laboratory batch. RESULTS: Serum IGF-I levels were positively related to protein intake (P(trend)<0.001), but not related to energy, fat or carbohydrate intake. Positive relationships were observed with the intake of milk (P(trend)=0.007), calcium (P(trend)<0.001), magnesium (P(trend)=0.003), phosphorus (P(trend)<0.001), potassium (P(trend)=0.002), vitamin B6 (P(trend)=0.03), vitamin B2 (P(trend)=0.001) and inverse relationships with vegetables (P(trend)=0.02) and beta-carotene (P(trend)=0.02). IGFBP-3 was not related with most of the nutrients and foods in this study. CONCLUSIONS: In this population, circulating IGF-I is modestly related with the intake of protein and minerals, and with milk and cheese, while IGFBP-3 does not appear to be related with diet.
http://www.ncbi.nlm....ubmed/16900085/

The insulin-like growth factor (IGF) axis may play opposing roles in health and disease.The age-related declines in growth hormone and IGF-I may be associated with potentially deleterious changes in body composition and functioning, but recent studies suggest that IGF-I levels may be related to risk of prostate, colorectal, premenopausal breast, and possibly other cancers. Thus, we studied dietary influences on plasma IGF-I and IGF-I:IGF-binding protein-3 ratio in 753 men in the Health Professionals Follow-Up Study who completed a food frequency questionnaire. In this generally well-nourished population of middle-aged to elderly men, plasma IGF-I and IGF-I:IGF-binding protein-3 molar ratio tended to increase with higher intake of protein and minerals, including potassium, zinc, magnesium, calcium, and phosphorus. Men with relatively high intakes of total protein (top quintile) and minerals (top quintile of the five minerals combined) had a 25% higher mean plasma level of IGF-I compared with those in the low quintiles simultaneously. The major sources of animal protein, including milk, fish, and poultry, but not red meat, as well as total vegetable protein, were associated with an increase in IGF-I levels. Energy intake was positively related to plasma IGF-I level but only in men with body mass index <25 kg/m². The age-related decline in plasma IGF-I may be exacerbated by low intakes of protein and minerals. The potential role of these dietary factors on cancer risk through altering IGF-I levels requires study.
http://cebp.aacrjour...2/2/84.abstract

[kismet]

Somatostatin can anyone dig up safety data I'm too lazy right now. However, this drug could be pretty interesting, if low or moderate IGF-1 levels turn out to be benefical.

Edited by kismet, 21 October 2009 - 06:38 PM.

[tunt01]

luteolin has been commented on in other threads and is used by some imminst members as a supplement to lower igf-1.

[nowayout]

Have you guys really thought this through?

How do you plan to recover from daily wear and tear, injuries, and workouts, once you inhibit IGF-1?

[FNC]

Have you guys really thought this through?

How do you plan to recover from daily wear and tear, injuries, and workouts, once you inhibit IGF-1?

Perhaps I did not make my point clear enough,

I want to ensure that I am not consuming supplements or foods which inhibit IGF-1, primarily because I want to allow my body to grow as I'm still 17.

Therefore, I will be consuming moderate amounts of milk and protein to ensure this occurs. I was taking resveratrol until I discovered it was an IGF-1 inhibitor which could interfere with my growth and development. The purpose of this post is to identify other substances which may also act as IGF-1 inhibitors, in order to limit their consumption.

[TheFountain]

I seem to remember reading somewhere that lycopene lowers IGF-1 levels.

Good thing I eat all those tomatoes then.

[FNC]

It's funny that lycopene is an IGF-1 inhibitor, I've practically had tomato sauce with my food for the past 15 years or so, not exactly fantastic, but doesn't phase me either

[FNC]

Are any of the following IGF-1 inhibitors...?

- Green Tea
- Milk Thistle
- Acetyl L Carnitine
- N-Acetyl Cysteine
- R-Alpha Lipoic Acid

Thanks
Fabien

[nowayout]

Are any of the following IGF-1 inhibitors...?

- Green Tea
- Milk Thistle
- Acetyl L Carnitine
- N-Acetyl Cysteine
- R-Alpha Lipoic Acid

Thanks
Fabien

Should a 17 year old really be taking ALCAR and ALA?

Might do more harm than good at your age.

Green tea and milk thistle might, in the quantites found in extracts or supplements, mess with your hormones. For example, green tea does a number on DHT metabolism. You DON't want to mess with DHT or other hormones while you are still growing. If you do, you are asking for long-term trouble.

[FNC]

Should a 17 year old really be taking ALCAR and ALA?

Might do more harm than good at your age.

Green tea and milk thistle might, in the quantites found in extracts or supplements, mess with your hormones. For example, green tea does a number on DHT metabolism. You DON't want to mess with DHT or other hormones while you are still growing. If you do, you are asking for long-term trouble.

Thank you for your concern, is there any further explanation or information which can elaborate upon this in further detail?
At the moment I get the fact that ALCAR and ALA may do harm, but why or how?

Is N-Acetyl-Cysteine acceptable?

Thank you :-)

[TheFountain]

Should a 17 year old really be taking ALCAR and ALA?

Might do more harm than good at your age.

Green tea and milk thistle might, in the quantites found in extracts or supplements, mess with your hormones. For example, green tea does a number on DHT metabolism. You DON't want to mess with DHT or other hormones while you are still growing. If you do, you are asking for long-term trouble.

Thank you for your concern, is there any further explanation or information which can elaborate upon this in further detail?
At the moment I get the fact that ALCAR and ALA may do harm, but why or how?

Is N-Acetyl-Cysteine acceptable?

Thank you :-)

N-acetylecycysteine is a decent lung cleanser and I see no reason why it has to be age dependent.

[nowayout]

Is N-Acetyl-Cysteine acceptable?

N-acetylecycysteine is a decent lung cleanser and I see no reason why it has to be age dependent.

I think you are remembering it wrong.

There is a possibility that NAC might damage the lungs.

http://www.imminst.o...showtopic=17624

This data was sufficient for Zoolander and others here to discontinue this supplement.

[TheFountain]

Is N-Acetyl-Cysteine acceptable?

N-acetylecycysteine is a decent lung cleanser and I see no reason why it has to be age dependent.

I think you are remembering it wrong.

There is a possibility that NAC might damage the lungs.

http://www.imminst.o...showtopic=17624

This data was sufficient for Zoolander and others here to discontinue this supplement.

Interesting, since when I started a thread about lung cleansers NAC was the one everyone seemed to agree on. And don't forget there are more studies indicating that it IS beneficial for the lungs as opposed to the opposite. Why trust one study?

N-Acetyl Cysteine Slows Lung Decline in Pulmonary Fibrosis

The Idiopathic Pulmonary Fibrosis International Group Exploring N-Acetyl Cysteine I Annual (IFIGENIA) trial reported that N-acetyl cysteine, a precursor of the antioxidant glutathione, slows the deterioration of lung function in patients being treated for idiopathic pulmonary fibrosis. Idiopathic pulmonary fibrosis is a chronic progressive interstitial pneumonia whose cause is unknown, although an oxidant-antioxidant imbalance may contribute to the disease process. The findings were reported in the November 24 2005 issue of the New England Journal of Medicine.

In a double-blind placebo controlled trial, 182 pulmonary fibrosis patients were randomized to receive 600 milligrams N-acetylcysteine or a placebo three times per day for one year. Participants were also given prednisone and azathioprine, which are standard drugs prescribed for the disease. Vital capacity and and single-breath carbon monoxide diffusing capacity, which are measures of lung function, were measured at the beginning of the study, and at six and twelve months.

One hundred eight of the original participants completed the one-year study. Subjects who received N-acetyl cysteine experienced a slower loss of vital capacity and single-breath carbon monoxide diffusing capacity than did those who received the placebo, and had greater values for both measurements at twelve months. Mortality was slightly lower among those who received N-acetyl cysteine.

The authors concluded that adding 600 milligrams acetyl cysteine three times daily to a regimen of prednisone and azathioprine helps preserve lung function in idiopathic pulmonary fibrosis patients better than drug therapy alone. "High-dose acetylcysteine in addition to standard therapy is," they write, "therefore, a rational treatment option for patients with idiopathic pulmonary fibrosis."

Edited by TheFountain, 23 October 2009 - 08:35 PM.

[nowayout]

N-Acetyl Cysteine Slows Lung Decline in Pulmonary Fibrosis

Those are very ill patients. This means nothing for healthy people.

[TheFountain]

N-Acetyl Cysteine Slows Lung Decline in Pulmonary Fibrosis

Those are very ill patients. This means nothing for healthy people.

Well I could say of the other study that they were mice, which means nothing for humans. Where do you draw the line with this form of reasoning? And how do you explain this study which states that NAC has a protective effect against PH?


Arfsten D, Johnson E, Thitoff A et al., Impact of 30-day oral dosing with N-acetyl-L-cysteine on Sprague-Dawley rat physiology. Int J Toxicol. 2004 Jul-Aug; 23(4): 239-47.] The doses used were huge; by weight they were 50 times greater than that recommended as a human dietary supplement. In fact, NAC was found to protect rats from hypoxia-induced PH [Hoshikawa Y, Ono S, Suzuki S, et al., Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia. J Appl Physiol. 2001 Apr;90(4):1299-306.] This protectective effect in PH was confirmed by another group [Lachmanova V, Hnilickova O, Povysilova V, et al., N-acetylcysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia. Life Sci. 2005 May 27;77(2): 175-82.] Also, NAC is used extensively by athletes for long periods; there are no reports of PH. As shortness of breath on exercise is an early symptom of PH this disease should be readily apparent in athletes. Indeed, NAC is a very commonly used supplement, and there have never been any reports of PH. Further, NAC has been used as a sputum thinner for long periods in persons with cystic fibrosis and chronic bronchitis, again without any reports of PH. It was used for 6 months in a group of persons with Chronic Obstructive Pulmonary Disease with apparent benefit. [Pela R, Calcagni AM, Subiaco S, et al., N-acetylcysteine reduces the exacerbation rate in patients with moderate to severe COPD. Respiration.

So why trust the one study instead of the dozens and dozens of other's? I want reasoning not sensationalism and fear mongering.

[niner]

N-Acetyl Cysteine Slows Lung Decline in Pulmonary Fibrosis

Those are very ill patients. This means nothing for healthy people.

Well I could say of the other study that they were mice, which means nothing for humans. Where do you draw the line with this form of reasoning? And how do you explain this study which states that NAC has a protective effect against PH?

Arfsten D, Johnson E, Thitoff A et al., Impact of 30-day oral dosing with N-acetyl-L-cysteine on Sprague-Dawley rat physiology. Int J Toxicol. 2004 Jul-Aug; 23(4): 239-47.] The doses used were huge; by weight they were 50 times greater than that recommended as a human dietary supplement. In fact, NAC was found to protect rats from hypoxia-induced PH [Hoshikawa Y, Ono S, Suzuki S, et al., Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia. J Appl Physiol. 2001 Apr;90(4):1299-306.] This protectective effect in PH was confirmed by another group [Lachmanova V, Hnilickova O, Povysilova V, et al., N-acetylcysteine inhibits hypoxic pulmonary hypertension most effectively in the initial phase of chronic hypoxia. Life Sci. 2005 May 27;77(2): 175-82.] Also, NAC is used extensively by athletes for long periods; there are no reports of PH. As shortness of breath on exercise is an early symptom of PH this disease should be readily apparent in athletes. Indeed, NAC is a very commonly used supplement, and there have never been any reports of PH. Further, NAC has been used as a sputum thinner for long periods in persons with cystic fibrosis and chronic bronchitis, again without any reports of PH. It was used for 6 months in a group of persons with Chronic Obstructive Pulmonary Disease with apparent benefit. [Pela R, Calcagni AM, Subiaco S, et al., N-acetylcysteine reduces the exacerbation rate in patients with moderate to severe COPD. Respiration.

So why trust the one study instead of the dozens and dozens of other's? I want reasoning not sensationalism and fear mongering.

Everything you're citing here is in people or animals who are sick or injured (hypoxia is an injury). If there isn't any evidence that NAC helps healthy humans, then I would hesitate to use it. That's neither sensationalism nor fear mongering; just looking for evidence of benefit in someone like myself. The important thing to bear in mind is that correcting a disease state is not evidence that a substance will help a healthy person, otherwise we would all be taking antibiotics.

[TheFountain]

Everything you're citing here is in people or animals who are sick or injured (hypoxia is an injury).

If there isn't any evidence that NAC helps healthy humans, then I would hesitate to use it. That's neither sensationalism nor fear mongering; just looking for evidence of benefit in someone like myself. The important thing to bear in mind is that correcting a disease state is not evidence that a substance will help a healthy person, otherwise we would all be taking antibiotics.

Did the rats in that study have induced Hypoxia or is it just stating that in cases of oxygenation some rats appeared to have a decrease in hypoxic related PH onset? I don't see where it says specifically that all the rats had Hypoxia induced in them but I could be missing something. In any event this is an animal study, the mouse study showing enzyme/oxygen PH correlation is also an animal study. The question is why trust the mouse study over the rat study or any other study?

[FNC]

After reviewing some articles, I believe that the good outweighs the bad. Given the hypoxia in rats, who were given huge doses anyway, the best thing to do is to take it in a lower dose than usual; and see how I feel as I go along.

Is there anything to suggest ALCAR and ALA will 'harm me'? Apart from the fact that ALCAR is an IGF-1 inhibitor, thus I probably shouldn't be taking it just yet.

http://bloodjournal..../full/99/5/1552

Edit: Added Link

Edited by Fabien, 24 October 2009 - 02:17 AM.

[niner]

Everything you're citing here is in people or animals who are sick or injured (hypoxia is an injury).

If there isn't any evidence that NAC helps healthy humans, then I would hesitate to use it. That's neither sensationalism nor fear mongering; just looking for evidence of benefit in someone like myself. The important thing to bear in mind is that correcting a disease state is not evidence that a substance will help a healthy person, otherwise we would all be taking antibiotics.

Did the rats in that study have induced Hypoxia or is it just stating that in cases of oxygenation some rats appeared to have a decrease in hypoxic related PH onset? I don't see where it says specifically that all the rats had Hypoxia induced in them but I could be missing something. In any event this is an animal study, the mouse study showing enzyme/oxygen PH correlation is also an animal study. The question is why trust the mouse study over the rat study or any other study?

The hypoxia would have to be induced unless the animals were very sick. Either way, I don't think it's very relevant to healthy humans. It's easier to do harm than to do good by ingesting chemicals, so I would want to see some evidence that it will help me and not hurt me. The best evidence would be an experiment in healthy humans that shows some sort of believable improved outcome. If the only human use was in sick people, then you would have to think more about it. (Drugs that are good for diabetics are often good for healthy people as well, given that glycation is prevalent in diabetics and is also something that contributes to aging. Whether or not the benefits of such a drug outweigh the risks is still something that requires human experiments to determine. Other diseases are a different story.) Animal data is a significant step down the ladder, with sick animals on a distinctly lower rung than healthy animals. Cell data is only slightly off the floor, and acellular in vitro data is in the basement.

Edited by niner, 24 October 2009 - 02:49 AM.

[niner]

After reviewing some articles, I believe that the good outweighs the bad. Given the hypoxia in rats, who were given huge doses anyway, the best thing to do is to take it in a lower dose than usual; and see how I feel as I go along.

Is there anything to suggest ALCAR and ALA will 'harm me'? Apart from the fact that ALCAR is an IGF-1 inhibitor, thus I probably shouldn't be taking it just yet.

http://bloodjournal..../full/99/5/1552

I doubt that your hypoxic ventilatory response and EPO production need any help. I don't know if ALCAR will harm you, but your mitochondria probably don't need it either. There are a lot of people on this forum who have stopped taking ALA, all of them significantly older than you, thus presumably "needing it" more. Their reasoning has been various combinations of a disturbing result from a rodent experiment, a concern over antioxidants having a negative impact on exercise response, and in my case, ALA causing hypotension. The main rule should be "Do no harm." Absent a compelling case to take something, don't take it.

[FNC]

I doubt that your hypoxic ventilatory response and EPO production need any help. I don't know if ALCAR will harm you, but your mitochondria probably don't need it either. There are a lot of people on this forum who have stopped taking ALA, all of them significantly older than you, thus presumably "needing it" more. Their reasoning has been various combinations of a disturbing result from a rodent experiment, a concern over antioxidants having a negative impact on exercise response, and in my case, ALA causing hypotension. The main rule should be "Do no harm." Absent a compelling case to take something, don't take it.

Speaking of compelling cases, you make a compelling case. Thanks Niner :-)

[steampoweredgod]

Bumping to see if anyone's gotten any more info on inhibitors

I heard somewhere that egcg from green tea is an inhibitor, should verify to make sure.(it also appears to have little or no conflict or adverse interaction with meds, iirc)

So we have resveratrol, egcg, lycopene, and low protein diets(has anyone tried protein cycling, how would that affect it?).

Have you guys really thought this through?

How do you plan to recover from daily wear and tear, injuries, and workouts, once you inhibit IGF-1?

Laron dwarf humans have levels so low as to likely be unattainable for all their lives, and they seem to be able to reach old ages. There are claims of what appears as substantial cancer and diabetes resistance(though I've heard conflicting reports regarding diabetes.).

We know CR can put blood parameters within peak human ideal states, likely doing away with cardiovascular disease risk, if you can knock cancer risk too, probability of long lifespan likely drastically goes up.

IF IIRC the methuselah record was achieved by growth hormone knockout with CR combination achieving 100% lifespan increase, again iirc.

The finding that in human centenarians it seem slightly defective igf-1 receptors are present, and laron dwarf humans with even more extreme deficits along the igf-1 axis manage to survive with seeming high resistance to cancer, is promising.

Edited by steampoweredgod, 08 December 2011 - 04:33 AM.

[hivemind]

Low IGF-1 bad idea at least for men:

http://onlinelibrary...05.00148.x/full

However, reduced GH/IGF-1 signalling may also have adverse effects, especially in old age, as increased induction of apoptosis is associated with growth factor withdrawal. Throughout adulthood, serum GH concentration and pulsatile GH secretion rates fall steadily, with an estimated 14% per decade in men, a phenomenon known as somatopause (Iranmanesh et al., 1991). The reduced GH secretion is believed to contribute to many age-related diseases, such as loss of muscle mass, increased adiposity, reduced bone mineral density and a decline in cognition(reviewed in Bartke et al., 2003). In these parameters too, sex differences have been found. Premenopausal women are significantly better protected than men from the negative impact of increasing age on GH levels (reviewed in Giustina & Veldhuis, 1998). Our results suggest that in females but not in males the beneficial effects of reduced cumulative exposure to GH/IGF-1 outweigh the possible detrimental effects of lower GH/IGF-1 levels at old age.

Edited by hivemind, 08 December 2011 - 04:38 AM.

[scottknl]

IGF-1 levels start lower in CR followers, but in the end they remain higher than ad-lib eaters. The slope of the degradation curve over time is flatter for CR followers and steeper for ad-lib eaters.

[hivemind]

IGF-1 levels start lower in CR followers, but in the end they remain higher than ad-lib eaters. The slope of the degradation curve over time is flatter for CR followers and steeper for ad-lib eaters.

CR followers = old people already in their youth, be old longer!

Edited by hivemind, 08 December 2011 - 05:10 AM.

[steampoweredgod]

The reduced GH secretion is believed to contribute to many age-related diseases, such as loss of muscle mass, increased adiposity, reduced bone mineral density and a decline in cognition

we would have to see a direct link, in centenarians cognitive performance is commonly preserved, despite supposedly more common igf1 less functional receptors, in laron dwarf I've not heard of systematic cognitive deficits despite lifelong severe igf-1 deficits. In animals igf1 deficits preserve cognitive function.

Low Igf-1, iirc, boost autophagocitosis rates likely protecting from alzheimers, parkinsons and other neurodegenerative diseases.

loss of muscle mass, increased adiposity, reduced bone mineral density and a decline in cognition

Vegetarian lifestyle which is known to have lower igf-1 is associated with improved healthspan in men, providing when combined with other factors nearly 10 years added lifespan.

Five simple health behaviors promoted by the Seventh-day Adventist Church for more than 100 years (not smoking, eating a plant based diet, eating nuts several times per week, regular exercise and maintaining normal body weight) increase life span up to 10 years...

Researchers discovered that the life expectancy of a 30-year-old vegetarian
Adventist woman was 85.7 years, and 83.3 years for a vegetarian Adventist man.
This exceeds the life expectancies of other Californians by 6.1 years for women
and 9.5 years for men. Non-vegetarian Adventist women in the group had a life
expectancy of 84 years, and non-vegetarian men, 81 years.