Eating More Plant Protein Associated With Lower Risk Of Death

[Travis]

@Travis what do you think of cyproheptadine as a serotonin lowering tool?

I'm not sure. I did notice that it has strong affinity for one of the histamine receptors.

I think the best serotonin antagonist would be specific (unless you want to kill two birds with one stone.) I noticed that some also interact with a dopamine receptor.

And it depends on if you want to hallucinate or not. It was shown in 1984 that hallucinogenic potency correlates very strongly with the binding constant to the serotonin receptor #2 (5-HT₂).

A Pearson correlation coefficient of 1 is perfect. This is close at .924.

But this is not the whole story either, because some very strong ligands like bromo-LSD are not very hallucinogenic. Snyder and Merrill showed in 1965 that hallucinogenic activity also correlates well with the highest occupied molecular orbital (HOMO). This is a quantum mechanical value obtained from the Schrödinger Equation and can be understood as its charge-donating potential.

Thus, despite the crudeness of the theoretical and experimental data discussed here, the close relationship between HOMO energy, an index of electron donation, and the hallucinogenic potency of drugs does favor an electron donation model of drug-receptor interaction. –Snyder

This is different than the redox potential since only one electron, or a fraction (partial transfer), is transferred in a charge-transfer reaction.

Albert Szent-Györgyi started with this line of reasoning before Snyder had.

It would be interesting to see a 3-dimensional graph of 5-HT₂ binding capability, highest occupied molecular orbital, and hallucinogenic potential on mutually perpendicular coordinates. You might expect that a good fit would be produced.

All of these serotonin inhibitors are probably going to be slightly different based on their HOMO and 5-HT₂ binding affinities as well as their interactions with other receptors. I want to try one of the ergot derivatives simply because they are the "classic" serotonin inhibitors and have been used the most historically.

But I don't want to hallucinate, so I need to consider the highest occupied molecular orbital.

I am sort of partial to bromocriptine, mostly because it has a cool name. This and methysergide are probably the two with the most pharmacologic data on.

Glennon, Richard A., Milt Titeler, and J. D. McKenney. "Evidence for 5-HT2 involvement in the mechanism of action of hallucinogenic agents." Life sciences 35.25 (1984): 2505-2511.

Snyder, Solomon H., and Carl R. Merril. "A relationship between the hallucinogenic activity of drugs and their electronic configuration." Proceedings of the National Academy of Sciences 54.1 (1965): 258-266.

 

[jitsmonkey]

risk of death is only 100%

 

[Travis]

"...The intraperitoneal administration of melatonin to rats caused an increase in brain serotonin concentration, especially in the midbrain. This effect could be demonstrated within 20 minutes of melatonin administration and was not associated with changes in norepinephrine concentration."
Melatonin elevates brain serotonin

Abstracts can be misleading.

The authors also noted a decline in cerebral cortex serotonin levels. This is generally considered the area of the brain responsible for higher cognitive functions.

The earliest effect was in the cerebral cortex; 20 minutes after administration of the methoxyindole, serotonin content had declined by 14 percent. After 60 minutes, the cerebral serotonin concentration was still depressed, but the concentration of the amine in the midbrain and the hypothalamus had risen significantly.

This was measured fluorometrically, and he assures the readers that he was actually measuring serotonin and not a melatonin artifact:

Studies in vitro in which various amounts of melatonin were added to brain extracts demonstrated that this rise in brain serotonin concentration was not an artifact caused by fluorescence of melatonin retained in the brain tissue.

It seems as thought melatonin causes a repartitioning of serotonin away from the forebrain, and towards the stem:

The effect of melatonin injections on brain serotonin levels is not the same for all brain regions.

Although the change was smallest in the cerebral cortex, this region makes-up 31% of the rat brain and 77% of the human brain.* The authors make no mention of the change in total brain serotonin. If this value had been determined, it was not reported.

But if you multiply the initial concentrations by the volume ratios and the rat brain mass (2g*), you see that the total apparently "rises" and then "declines" slightly.

t=0m
(.56μg/g)×(6%)×(2g)=.0672μg
(1.67μg/g)×(7%)×(2g)=.2338μg
(.99μg/g)×(31%)×(2g)=.6138μg
Σ=.9148μg

t=60m
(.70μg/g)×(6%)×(2g)=.084μg
(2.35μg/g)×(7%)×(2g)=.329μg
(.84μg/g)×(31%)×(2g)=.5208μg
Σ=.9338μg

t=180m
(.78μg/g)×(6%)×(2g)=.0936μg
(1.41μg/g)×(7%)×(2g)=.1974μg
(.97μg/g)×(31%)×(2g)=.6014μg
Σ=.8924μg


But he didn't measure all brain regions. He only reported the concentrations in brain regions totaling 44% of the total volume.

I'm not sure what to make of this.


Anton-Tay, Fernando, et al. "Brain serotonin concentration: elevation following intraperitoneal administration of melatonin." Science 162.3850 (1968): 277-278.
*Brain Facts and Figures

 

[Amazoniac]

This is what I ate yesterday:
View attachment 6299
View attachment 6300 View attachment 6301
The methionine is low. The tryptophan is a bit high perhaps, but I find that excessive serotonin can be combated with just 1 milligram of natural melatonin.

And Fernstrom proved that the absolute tryptophan intake mattered little, and that the ratio of trytophan over the other large neutral amino acids was actually the best predictor of brain serotonin synthesis.

Pretty interesting.
Do you juice the kale? How do you feel without coffee?

 

[Travis]

I just eat the kale. I'm actually eating arugula this week.

How do you feel without coffee?

I would probably die if I stopped drinking coffee.

Just kidding. I went a few days without coffee a few weeks ago and it's not that hard. There are much more addictive things. I find that dairy products are more addictive, on the same level as tobacco.

It actually feels kinda good to stop drinking coffee for a few days. It's probably not a bad idea to keep Sundays as a coffee-free day.

 

[Mountain]

@Travis are those mature coconut you're eating? The ones with the hard flesh? I tried to eat one the other day and got extreme intestinal pain. I'm not sure if it was due to it abrading my gut or the sudden increase in fibre intake but I might try grating it finely next time. Do you normally eat an entire one in a single sitting? Sorry for all the questions.

 

[Travis]

@Travis are those mature coconut you're eating? The ones with the hard flesh? I tried to eat one the other day and got extreme intestinal pain. I'm not sure if it was due to it abrading my gut or the sudden increase in fibre intake but I might try grating it finely next time. Do you normally eat an entire one in a single sitting? Sorry for all the questions.

I ate half of one today, and they are the mature coconuts I'm eating. They are time consuming, but if you get a new microplane they should go quick enough; my microplane is getting dull but it still only takes a few minutes.

I think I got intestinal pain only once or twice from the dry, pre‐shredded coconut in the bag. This is really coconut‐dependent, as there is no real line between 'young' and 'mature'—as can be said about anything. You'll get a constant thickening of the white part concomitant with a reduction in the sugar content of the coconut water. Some coconuts can be more fibrous, some more fatty, and all of varying thickness; no two coconuts will ever be the same.

 

[stevrd]

Hi Travis,

I just found you on the forum and I am intrigued by your vegan diet. As a very active male, about 180 lbs, I weight lift 3x per week. Over the years my concerns with protein have diminished. After reading Brad Pilon's work, I realized that protein intake is way overblown and the most anybody needs is .8g/lb of lean body mass for muscle gain. There are studies even showing .3g/lb being sufficient for muscle preservation on maintenance calories. If someone is sedentary, their protein needs are much lower. I have dabbled in veganism before and have found some benefit from it. I too, have thought about the low tryptophan and methionine content of plant foods and have thought that this may be one reason why groups like the okinawans live so long and have healthy testosterone levels well into their 90s. Even people like the Kitivans and Tokelauans ate only small amounts of meat, like you have said.

I have no doubt that a sedentary individual can get by on about 50g of protein a day, but someone who is active probably needs at least 80g/day to preserve muscle mass. Do you disagree with this? Do you think that as long as carbohydrate is high then our protein needs are less of a concern?

 

[Travis]

Hi Travis,

I just found you on the forum and I am intrigued by your vegan diet. As a very active male, about 180 lbs, I weight lift 3x per week. Over the years my concerns with protein have diminished. After reading Brad Pilon's work, I realized that protein intake is way overblown and the most anybody needs is .8g/lb of lean body mass for muscle gain. There are studies even showing .3g/lb being sufficient for muscle preservation on maintenance calories. If someone is sedentary, their protein needs are much lower. I have dabbled in veganism before and have found some benefit from it. I too, have thought about the low tryptophan and methionine content of plant foods and have thought that this may be one reason why groups like the okinawans live so long and have healthy testosterone levels well into their 90s. Even people like the Kitivans and Tokelauans ate only small amounts of meat, like you have said.

I have no doubt that a sedentary individual can get by on about 50g of protein a day, but someone who is active probably needs at least 80g/day to preserve muscle mass. Do you disagree with this? Do you think that as long as carbohydrate is high then our protein needs are less of a concern?

You're a heavier guy, and I weigh 155–160 pounds. This is the same weight that I've weighed my entire life despite eating radically different diets; I find that between 30–40‧g/d is fine for me, and even back when I'd been very active.

In attempt to maintain profits at levels they exist currently, the meat industry will promote sales to match; this includes online PR agents who usually pose as just 'normal people'—that is, they don't make it known that they have a paid agenda and often lie about their background. This is nothing peculiar or specific about the meat industry for doing this; you can find online PR agents working in dozens of other areas. To try to counter the increasing awareness of evolutionary, biochemical, and physiological aspects of meat eating they often simply resort to projecting unflattering archetypes and using innuendo against people who don't eat their product—in addition to massively inflating the protein requirements of course, as you've said.

Many protein balance studies show nitrogen balance at .5‧kg/d on average. And even in studies which calculate a higher ~.7‧kg/d intake, for the mean, there were still considerable amounts of test subjects who had done it on .5‧kg/d.

The traditional Okinawans—the ones eating protein in this range—were more active than most Americans.

 

[Ulysses]

It actually feels kinda good to stop drinking coffee for a few days. It's probably not a bad idea to keep Sundays as a coffee-free day.

I was totally dependent on caffeine until I started taking it with plenty of sugar. After a few weeks of drinking my coffee this way, the dependence vanished, and I can now skip a day without any withdrawal symptoms. I've concluded from this that I was actually addicted to the adrenaline rush I was getting from drinking it black, and not the caffeine itself.

 

[Travis]

I was totally dependent on caffeine until I started taking it with plenty of sugar. After a few weeks of drinking my coffee this way, the dependence vanished, and I can now skip a day without any withdrawal symptoms. I've concluded from this that I was actually addicted to the adrenaline rush I was getting from drinking it black, and not the caffeine itself.

Coffee has one thing that radically differentiate it from tea: it has caffeoyl quinide. This molecule is formed upon roasting after the loss of water, turning the carbohydrate ring into a tricylic morphine‐like ring. Thus: caffeoyl quinide binds to μ‐opiate receptors though as an antagonist, where its potency is similar to that of naloxone. I don't think anything can explain the laxative effects of coffee in a better way, as opiate receptors are well‐known to control intestinal motility (sorry about that, but this observation adds weight to the idea that it's physiologically‐active). Opiates decrease cholinergic nerve transmission, and antiopiates such as those found in coffee increase it. It is generally thought that coffee's increased potency over tea was simply the result of 'more caffeine,' but I think the antiopiate effects of caffeoyl quinide better explain this.

So I think the amount of exorphins consumed could also effect a response to coffee, besides those of course coming from sucrose. A person eating pizza everyday might feel a bit more of a 'rush' than a person consuming essentially no exorphins—having only their endogenous enkephalins to displace. I drink coffee all day now just out of habit, as it has lost most of its stimulative activity. I often drink coffee minutes before I go to sleep because the French press is conducive to nearly constant coffee‐drinking (fast and easy to make; even easier to transport in liter‐sized amounts.)

I certainly enjoy black coffee. Free sugar, consumed without protein, will increase brain serotonin synthesis. The leading mechanism proposed to account for this is the induction of insulin followed by the sequential incorporation of amino acids into cells, a process which raises the Fernstrom ratio because tryptophan is the only amino acid bound to albumin (it raises the ratio by decreasing the denominator.) This has actually been proven to occur and could account for some of effects of consuming free sugar. The majority of fruit has a glycemic ratio lower than that of cooked starchy foods like rice, corn, and even wheat.

 

[Ulysses]

I certainly enjoy black coffee. Free sugar, consumed without protein, will increase brain serotonin synthesis. The leading mechanism proposed to account for this is the induction of insulin followed by the sequential incorporation of amino acids into cells, a process which raises the Fernstrom ratio because tryptophan is the only amino acid bound to albumin (it raises the ratio by decreasing the denominator.) This has actually been proven to occur and could account for some of effects of consuming free sugar. The majority of fruit has a glycemic ratio lower than that of cooked starchy foods like rice, corn, and even wheat.

I'm not quite following this - how does albumin come into it?

 

[stevrd]

Many protein balance studies show nitrogen balance at .5‧kg/d on average. And even in studies which calculate a higher ~.7‧kg/d intake, for the mean, there were still considerable amounts of test subjects who had done it on .5‧kg/d.

The traditional Okinawans—the ones eating protein in this range—were more active than most Americans.

What's interesting is that the same people who promote 1g/lb bw fail to realize that many studies show that as the carb to protein ratio decreases, testosterone tends to decrease as well. I have seen research showing that as carb intake goes up, protein requirements go down. This is probably due to the sparing effect of keeping glycogen full (not needing gluconeogenesis). The carbs (especially fructose) also support deiodinase/T4 to T3 conversion when liver glycogen is adequate.

Why then does Ray Peat often suggest that people need at least 80g protein per day to prevent hypothyroidism? I remember him saying that he knew women that increased their protein from 20 to 40g (or something like that) and were able to overcome hypothyroidism.

But to me, I have often noticed that as long as total calorie intake and carb intake is high, protein matters very little. The more I study centenarians and healthy populations on traditional diets, the more I realize that their protein intake is generally low, certainly often less than the 80g/day that Peat mentions.

 

[DaveFoster]

Plant protein is high in glycine IIRC, and low in methionine. Animal protein is just a proxy for muscle meat, normal people don't regularly consume gelatin.

 

[Travis]

What's interesting is that the same people who promote 1g/lb bw fail to realize that many studies show that as the carb to protein ratio decreases, testosterone tends to decrease as well. I have seen research showing that as carb intake goes up, protein requirements go down. This is probably due to the sparing effect of keeping glycogen full (not needing gluconeogenesis). The carbs (especially fructose) also support deiodinase/T4 to T3 conversion when liver glycogen is adequate.

Why then does Ray Peat often suggest that people need at least 80g protein per day to prevent hypothyroidism? I remember him saying that he knew women that increased their protein from 20 to 40g (or something like that) and were able to overcome hypothyroidism.

But to me, I have often noticed that as long as total calorie intake and carb intake is high, protein matters very little. The more I study centenarians and healthy populations on traditional diets, the more I realize that their protein intake is generally low, certainly often less than the 80g/day that Peat mentions.

I have read many of the studies that Ray Peat cites in his articles, and he seems right about most things. He provides a good introduction to eicosanoids, prostaglandins, persorption, lipofuscin, and 'ultraweak fluorescence'—things not known among the general populace. However, when he starts talking about dairy he sounds a bit like an advertisement; I have to agree that dairy has one of the best fatty acid profiles an lots of minerals, but he avoids talking about the exorphins, the androgens, and IGF₁; the latter two cause acne in the exact same way, through the exact same molecular target (SREBP) which increases the sterol and wax ester concentration of sebum at the expense of the more fluid free fatty acids. I read part of a radio show transcript of him where a 'call‐in' inquisitor asked about dairy and acne; his only response had been, more‐or‐less, to 'take high‐dose retinol.' I think goat dairy is much better for its reduced exorphin potential and allergenicity, but nobody would know if people don't talk about it. But there is little you can do about the androstenedione found in dairy, although IGF₁ can be reduced by selecting non‐rBGH milk (there is some debate as to how dairy raises IGF₁, whether it's actually absorbed whole or through some other mechanism.) Most people don't consume enough dairy to get acne, but many teenagers who already have high circulating androgens can 'have their lives wrecked' by acne. These people need to know that the two things most shown to cause acne are IGF₁ and androgens, and they are both increased through dairy consumption. I can induce pimples on by back at will simply by either eating cheese or a few dozen eggs over the course of a week.

Why Ray Peat says to consume 80‧g per day is questionable—especially since he writes about tryptophan, serotonin, growth hormone, methionine, and polyamines. I think there's perhaps a study that he'd read that I haven't, or that he is biased by his dairy consumption. Not many people go into 100% total logic mode when they think about food; I think the reason is because it's internalized. and subconsciously becomes 'part of us.' In my life, I don't know any one person besides myself who had logically and scientifically examined the food that they eat. Most people find every reason, no matter how dubious, to elevate their habitual foods upon the altar; they critically examine information which runs counter to their primitive beliefs while unquestionably accepting the most flaky information which concords with them. In this way, most people that I know suffer heavily from confirmation bias in addition to being uninquisitive in general—nobody can expect to learn much while watching 6 hours of television per day. So although Ray Peat appears to be 90% correct, in my view, this seems to be the limit in constantly changing field of biochemistry. Even Linus Pauling made many embarrassing errors, and Szent‐Györgi was kinda flaky at times; even the more hard‐headed Gilbert Ling created a dubious, though awesome, hypothesis—there is zero evidence, none to this day, that glutamate will actually shift its natural preference from sodium to potassium. Linus Pauling was equally awesome on his wrongness (i.e. his DNA triple helix and his General Theory of Anesthesia)—but he was still wrong, no matter how brilliant it all was.

Nothing can substitute for training; Chinese monks and martial artists show the body type which can be had from a relatively—by Western standards—low‐protein diet. For people wanting to gain muscle rapidly, then more protein with a high tryptophan ratio could be helpful. Brain serotonin is released from the pituitary in response to brain serotonin, which in turn is a function of the plasma Fernstrom ratio (Try/Σ(CAA)). Another signalling amino acid is leucine, which has its own receptor. Both these amino acids can increase muscle synthesis and suppress autophagy through transcriptional—you could perhaps even say hormonal—mechanisms. The anabolic effect of leucine is generally thought to involved in the mTOR pathway, yet at least one serious study has shown that rapamycin does not inhibit these effects.

Mordier, S. "Leucine limitation induces autophagy and activation of lysosome-dependent proteolysis in C2C12 myotubes through a mammalian target of rapamycin-independent signaling pathway." Journal of Biological Chemistry (2000)​

But most people are not trying to rapidly gain in size and might like to know what the range for acceptable protein intake is, and those interested in longevity might know of the Okinawan intake is. There is also plenty of classic studies using rats fed varying degrees of additional tryptophan and methionine, both showing a reduction in longevity (which were probably growth hormone‐ and polyamine‐dependent). I think it would be interesting to see if there had been a rat study comparing leucine vs longevity.. .

 

[Travis]

I'm not quite following this - how does albumin come into it?

Serum albumin has seven tryptophan binding sites. Plasma tryptophan is the precursor for brain serotonin, and it has been shown using in vitro radioactive binding experiments that it matters little whether or not its bound or free. In the brain microcirculatory region, serum albumin is thought to be 'squeezed'—releasing its cargo tryptophan into the brain. Since the Fernstrom ratio and brain serotonin has been shown to increase after 100% carbohydrate intake, it had become necessary to explain this. I think what happens is that insulin creates an amino acid influx out of the plasma and into the cells, a process which more‐or‐less leaves tryptophan bound to albumin. This raises the Fernstrom ratio of the circulation and hence brain serotonin synthesis. This is how Fernstrom himself explains it.

To get confidence in the Fernstrom ratio, you have to see the graphs: a near‐perfect straight line is obtained when plotting brain serotonin synthesis vs the plasma tryptophan over the sum of competing amino acids (Phe + Tyr + Leu + Ile + Val). No other amino acid really competes with serotonin, meaning that these alone six amino acids must pass into the brain in a very similar manner.

 

[stevrd]

Wow Travis. Thank you for the enlightening reply. What do you think about research showing that the IGF-1 in milk has no discernible biological activity in humans? The amount of IGF-1 in milk is said to be about the same amount found in our own saliva and much less than the amount that the liver produces on average.

I'm not saying that milk has no disadvantages. I tend to think that it's just not a satisfying food to consume regularly and can be detrimental for some people due to the high fluid content. But I do think that there are many myths about dairy that persist, one of them being that the IGF-1 content in milk is a pathway that leads to cancer.

Sources:
(1) Collier R.J. & Bauman D.E. (2014) Update on human health concerns of recombinant bovine somatotropin use in dairy cows.
(2) Collier et al. (1991) Factors affecting insulin-like growth factor-I concentration in bovine milk.

 

[Travis]

Wow Travis. Thank you for the enlightening reply. What do you think about research showing that the IGF-1 in milk has no discernible biological activity in humans? The amount of IGF-1 in milk is said to be about the same amount found in our own saliva and much less than the amount that the liver produces on average.

I'm not saying that milk has no disadvantages. I tend to think that it's just not a satisfying food to consume regularly and can be detrimental for some people due to the high fluid content. But I do think that there are many myths about dairy that persist, one of them being that the IGF-1 content in milk is a pathway that leads to cancer.

Sources:
(1) Collier R.J. & Bauman D.E. (2014) Update on human health concerns of recombinant bovine somatotropin use in dairy cows.
(2) Collier et al. (1991) Factors affecting insulin-like growth factor-I concentration in bovine milk.

Dairy doesn't correlate very well with cancer, and I've looked; the risk ratios are about ~1.5 for the highest quartile. It's known that IGF‐1 is absorbed whole in infants, but generally thought to be broken down by humans. However, even skim milk has been shown to raise IGF‐1 and I haven't looked very deeply into the mechanism; the answer is out there somewhere, that I know. A person could perhaps hypothesize that casein forms a 'ball' of protein, as it's thought to do, thereby protecting some proteins from digestion; but even then, IGF‐1 is a rather large protein to be absorbed whole. A radiolabeled study would put all end to the idea of IGF‐1 being absorbed whole, something which seems more logically explained by some other mechanism. It is known that certain protein hormones, such as prolactin, activate phospholipase C on the cell membrane. This causes the cleavage of inositol phosphates from the sn‐3 position of membrane phospholipids—strong calcium chelators. Although inositol hexaphosphate (phytic acid) is best known for this, inositol triphosphate—found on the cell membrane—is nearly just as good. Despite the chelating propensity of IP₃ for calcium being able to explain the calcium influx on a fundamental physico‐chemical level, mainstream explanations seem to invoke a 'membrane pump being 'activated' by inositol triphosphate.' Regardless, it's undeniable that prolactin will cause a sharp and rapid influx of calcium into the cell—exactly why prolactin receptors are found in the greatest density in female breasts (residual prolactin receptors in male breasts can induce gynecomastia in the presence of low dopamine, which increases prolactin release form the pituitary.)

Since calcium balance seems to be under the control of protein hormones such as prolactin—and parathyroid hormone—then perhaps it wouldn't be a stretch to think that Ca²⁺ could influence IGF‐1, either directly or through parathyroid suppression.

'Our study observed a 7% to 8% increase in serum IGF-1 in the protein [whey fraction only] group in comparison with the placebo group after 1 to 2 years of intervention. IGF-1 is a bone growth-promoting factor, and it plays an important role in activating the osteoblast differentiation program and regulating 25-dihydroxyvitamin D₃ hydroxylase activity and the tubular reabsorption of phosphate in the kidney. Growth hormone secretion decreases with aging, and the circulating levels of IGF-1 in more than 30% of elderly people are lower than the young reference, which has implications in age-related osteoporosis. In this study, the increase in serum IGF-1 was not sufficient to result in a beneficial effect on bone mass, which could be due to the fact that the increase of IGF-1 by 7% to 8% observed in this study is rather moderate.' ―Zhu​

Well it seems to involved in calcium influx into the bones, perhaps analogous to prolactin's influence on the breasts. What is interesting about prolactin knockout mice is that they live, proving that prolactin is not required. Prolactin⁻ mice also have less visceral fat.

So I'm starting to think that this IGF-1 spike seen after consuming dairy is a result of the Ca²⁺ ion, and most certainly not in the whey fraction.

'Association of IGF-I levels with dairy products, milk and calcium are consistent with some (Heaney et al, 1999; Ma et al, 2001; Holmes et al, 2002) but not all (Mucci et al, 2001) previous analyses. The strongest evidence of a causal association between higher levels of milk consumption and IGF comes from a randomised trial of dietary milk supplementation, reporting a rise in IGF-I in those supplemented but not the controls (Heaney et al, 1999). While some research suggests that neonates absorb IGF-I from breast milk (Diaz-Gomez et al, 1997), there is no strong evidence that bovine IGF-I in cows milk could be similarly absorbed from the gut (Holmes et al, 2002). Dietary intake of animal protein (essential amino acids) is known to stimulate IGF-I production (Thissen et al, 1994), but we found no evidence of associations with animal protein intake, nor that controlling for animal protein intake attenuated associations with milk (not shown). This contrasts with the findings of Giovannucci et al (2003) and Holmes et al (2002). In Giovannucci et al’s analysis, associations with vegetable protein were, however, of similar magnitude to those for animal protein. Associations of calcium, milk and dairy products with IGF-I suggest a possible pathway linking dietary intake of these factors with prostate cancer (Chan and Giovannucci, 2001).' ―Gunnell​

I haven't been able to find an experimental study on the feeding of just straight calcium, so it's hard to tell for certain. But since bone needs both calcium and protein you might expect IGF‐1 to be created de novo in response to one of those, or both together. It might also be interesting to see where the IGF‐1 receptors are distributed throughout the body; if they are localized towards the bone, then you'd might further suspect calcium ⟶ parathyroid to be behind this IGF-1 increase.

Zhu, K. "The effects of a two‐year randomized, controlled trial of whey protein supplementation on bone structure, IGF‐1, and urinary calcium excretion in older postmenopausal women." Journal of Bone and Mineral Research (2011)
Gunnell, D. "Are diet–prostate cancer associations mediated by the IGF axis? A cross-sectional analysis of diet, IGF-1 and IGFBP-3 in healthy middle-aged men." British Journal of Cancer (2003)​

 

[Obi-wan]

Hi @Travis, as you know I have advanced prostate cancer. It is in my neck, shoulders, etc. I take Firmagon and Extandi and have been following your advise on polyamine restriction. I do consume 2 large glasses of raw milk per day for calcium and other vitamins and minerals. Should I be concerned regarding IGF-1 since prostate cancer is a very hormonal cancer. By the way my PSA just went from 112 to 72. It was as high as 13,000.

 

[G Forrest]

I just eat the kale. I'm actually eating arugula this week.

Hi @Travis. Do you have any issue with digestion and consuming raw leafy greens? Ray has mentioned the issue of raw greens irritating the intestine, since humans don't have the 3 stomachs to process leafy plant matter the way ruminants do. There's also the issue of oxalic in some greens like spinach. Curious to hear your thoughts since you incorporate raw veggies into your diet. Thanks