Eating More Plant Protein Associated With Lower Risk Of Death

Wagner83

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@Travis, given the effects of carbs and insulin on serotonin, isn't it enough to suggest that someone who eats more glucose as in starch would have a higher need for proteins ?
 

Travis

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@Travis, given the effects of carbs and insulin on serotonin, isn't it enough to suggest that someone who eats more glucose as in starch would have a higher need for proteins ?
Not necessarily. This is primarily an effect from eating 100% sugar, like soda‐drinking. Not even candy bars would do this since they often have enough protein to replace that pulled into the cells. Fernstrom had found this phenomenon to occur only with pure carbohydrate, although very low protein fruit juice could do the same.

Although fruit is seen as 'low protein' on charts, the water content can give a false impression. Also, most fruits have a low glycemic index which prevents the insulin spike which is actually the primary cause (it's not sugar per se). Even potatoes and rice, with their higher glycemic index, have enough protein to prevent this from happening; it's really only a practical hazard in those who bolt soda and/or refined fruit juice all day (or honey + coffee).

This phenomenon is only the result of an insulin spike and only when the subject had consumed a negligible amount of protein.
 

Travis

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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
No problems, and there are plenty of monogastric animals which consume leaves. And what is not commonly known is that humans actually digest over 90% of the cellulose they consume, and also over 80% of the hemicellulose.*

[*] Holloway, W. D. "Digestion of certain fractions of dietary fiber in humans." The American journal of clinical nutrition (1978)
 

ratstrain

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I have some B₁₂ in the cabinet that I take every month or so. I am not entirely convinced that I "need to". You know that I think the science is questionable on that, with it being produced by bacteria in the intestines. I still cannot believe that you need intrinsic factor—a molecule about 33 times heavier than B₁₂—to absorb it. Why would the body totally exclude a 1.3 kilodalton molecule yet permit said molecule attached to a 50 kDa molecule? Cobalamin only slightly bigger than heme.

And yes, I just read about the trytophan–niacin (you need an en-dash for that one Dante, not a hyphen) pathway a bit after reading about raised kyneurine levels in people given tryptophan. Is this what causes the sleepiness?

It's like a filter system, reducing the absorption of inactive (and counteractive) analogues as haptocorrin presents both active B12 and inactive analogues from the digestive tract and from the circulation to the B12-selective intrinsic factor. It also limits cobalt and B12 absorption.

B12 produced by bacteria in the ileum could bind with remaining intrinsic factor to the cubam receptor.

There is passive diffusion, but doses have to be high for this route to be effective.

Bovine transcobalamin, found in cow milk, seems to be better absorbed than other forms.

Haptocorrin, which carries B12 in human milk, binds (at least) in infants to proteins in brush border membranes, (at least) when the intrinsic factor system is still maturing.

Bacteria may not make enough (at the right place and everywhere), may take too much for themselves, and may produce too much analogues, depending on the diet and the genes of the host.

Regarding B12, just a hunch but I think it's the Cobalt ion(the way it's complexed and the valency maybe) is what makes b12 special. No other vitamin has got metal in it . You still need to have small amount of Cobalt in the diet if you believe we can absorb the bacterial Cobalt complex.
A doc once told me that SIBO (inhibiting the absorption) and poor liver health (major storage site) is what causes most people difficulty in holding on to B12 even after adequate intake.

Legumes are good sources of cobalt and prebiotics, and most are low in PUFAs.

Regarding SIBO, there are confounding factors. Bacteria can increase the level of methylmalonic acid by producing propionic acid, independantly of vitamin B12 status, so antibiotics can lower the level of methylmalonic acid without correcting the B12 deficiency when there is a deficiency. Also, inflammation as well as oxidative and nitrosative stress associated with bacterial overgrowth can reduce B12 absorption and inactivate B12. It's not necessarily that the bacteria steal all the dietary B12 and flood the host with analogues. The main site of B12 absorption is in the ileum, so (especially) when relying on bacteria for B12, a small intestinal bacterial (over)growth is not necessarily undesirable.

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.

Methylxanthines increase cyclic AMP, this can explain the diarrhea.
 

Travis

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Methylxanthines increase cyclic AMP, this can explain the diarrhea.
Perhaps, but can it explain it better than a powerful opiate antagonist?

Does tea do likewise in any amount? or Coca~Cola™?
 

Travis

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@Travis I have seen you mention many times for people to try switch to goat milk and see how it affects them. Do you also think people should switch to things like goat butter too?
Shouldn't matter as much as other dairy fractions. Of course their are differences in vitamin D, vitamin A, and saturated fatty acid content between animal species, but butter has negligible amount of casein. This makes butter a perfectly safe food, although it could perhaps deliver too much retinol if one were to eat unusual amounts.
 

ratstrain

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Perhaps, but can it explain it better than a powerful opiate antagonist?

Does tea do likewise in any amount? or Coca~Cola™?

Diarrhea is an adverse effect of theophylline as a pharmaceutical drug.

Indeed, tea, and Coca~Cola™, contain less caffeine than coffee, typically, in a cup.

Furthermore, tannins in tea may have an anti-diarrheal effect. Carbon dioxide in Coke too.

There are sulfur compounds including 2-furfurylthiol in coffee that may also play a role in its laxative effect.

Still, the laxative effect of coffee is moderate.

Opioids like morphine have paradoxical effects not to be confused with effects of withdrawal. Aside from opioid-induced hyperalgesia and narcotic bowel syndrome, there are reports of opioid-induced diarrhea.

If the antagonistic effect of caffeoyl quinide was strong enough to cause diarrhea, I suppose drinking coffee wouldn't be rewarding.

Another thing is that coffee, like tea and chocolate, can cause stimulant-induced psychosis and skin picking, which points towards a stimulatory effect on endorphin and prolactin. But a rebound effect is also a possible explanation.
 
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Travis

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If the antagonistic effect of caffeoyl quinide was strong enough to cause diarrhea, I suppose drinking coffee wouldn't be rewarding.
Likewise: If methylxanthines were strong enough to cause diarrhea, than coffee‐drinking wouldn't be rewarding. If you accept your own logic, than you must accept this.

Methylxanthines are found in chocolate and tea, yet only coffee has an anti‐opiate. Also: only coffee appears to have a laxative effect in the non‐habituated.

 
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ratstrain

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Likewise: If methylxanthines were strong enough to cause diarrhea than coffee‐drinking wouldn't be rewarding.

Methylxanthines are found in chocolate and tea, yet only coffee has the anti‐opiate. Also, only coffee appears to have a laxative effect in nonusers.

I'm not saying this in the sense that diarrhea is annoying, but in the sense that diarrhea as a symptom would then reflect a significant inhibition on the endogenous rewarding opioid system overall. Unless the effect is local only. And caffeoyl quinide would have to counteract both methylxanthines and basal opioids.

Interestingly, cyclic AMP stimulates beta-endorphin.
 

Travis

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ratstrain

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Likewise: If methylxanthines were strong enough to cause diarrhea, than coffee‐drinking wouldn't be rewarding. If you accept your own logic, than you must accept this.

Methylxanthines are found in chocolate and tea, yet only coffee has an anti‐opiate. Also: only coffee appears to have a laxative effect in the non‐habituated.


My understanding is that blocking endogenous opioids prevents reward.

That said, methylxanthines, even though they increase beta-endorphin, appear to have some anti-opioid effects themselves (Simón Brailowsky et al., 1981).

Chocolate contains predominantly theobromine, which has less of an effect. Tea as a beverage contains less caffeine than coffee, is rather astringent and contains theanine.

There are compounds in coffee that inhibit cyclic AMP phosphodiesterases more than caffeine (Montoya GA et al., 2014; Teresa Röhrig et al., 2017).

And compounds that seem to act as muscarinic agonists (Argirova MD et al., 2013).

Caffeoyl quinide is not one of them according to the descriptions.

It does so in what organ?

It's a hypothalamo-pituitary response, and levels increase in the plasma (Furuki Y., 1983; J. L. Meyerhoff et al., 1988; Kapcala LP, Weng CF, 1992). Immune cells also have the ability to synthesize beta-endorphin.
 

EIRE24

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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.
I read a similar comment from Matt Stone (I know he isnt the best example) but it was how when he had a low metabolism and was not eating enough food he relied heavily on coffee and caffeine but when he began to eat more food and carbs in general he had no interest in coffee. I can vouch and say I am the exact same.
 

Travis

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That said, methylxanthines, even though they increase beta-endorphin, appear to have some anti-opioid effects themselves (Simón Brailowsky et al., 1981). [...]

It's a hypothalamo-pituitary response, and levels increase in the plasma (Furuki Y., 1983; J. L. Meyerhoff et al., 1988; Kapcala LP, Weng CF, 1992). Immune cells also have the ability to synthesize beta-endorphin.

There's a direct μ‐opioid antagonist in coffee similar in strength to naloxone,⁽¹⁾ yet you take a more indirect approach to arrive at the same receptor. Besides being highly circuitous and entirely unnecessary—in light of caffeoyl quinide's presence—it doesn't even concord with observations; and here's why:

Exhibit A: Brown, S. R. "Effect of coffee on distal colon function." Gut (1990)

In this two‐part study, Doctor Brown administered a questionnaire to some and a rectal probe + coffee to others. He had also examined the effects of decaffinated coffee in the same subjects:

'Twenty nine per cent (63% women) claimed that coffee induced a desire to defecate.' ―Brown

'Coffee has been shown to have profound effects on the gastrointestinal system;' ―Brown

'Intraluminal pressure in the rectum and distal sigmoid colon were recorded using a 5 lumen, flexible, manometric assembly (od 5 mm)...' ―Brown

coffee.png


'Both regular and decaffeinated coffee contain exorphines that can bind to opiate receptors. Opiate receptors, both in the brain and within the gut wall, mediate important effects on colonic motility; Sun and his colleages have shown that opiate receptors are necessary for the colonic response to food.' ―Brown

'A similar increase was seen after drinking decaffeinated coffee in all coffee responders tested. No increase in rectosigmoid motility was seen after a drink of hot water.' ―Brown

'In conclusion, our results confirm the common belief that coffee promotes the desire to defecate. This response, which can also be induced by decaffeinated coffee, is seen in about a third of the population...' ―Brown

Thus: the laxative agent in coffee could not be removed through the decaffination procedure, adding even more proof—as if it needed any more—that caffeoyl quinide is primarily responsible for these effects.

[1] Boublik, J. H. "Coffee contains potent opiate receptor binding activity." Nature (1983)
 

Nighteyes

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There's a direct μ‐opioid antagonist in coffee similar in strength to naloxone,⁽¹⁾ yet you take a more indirect approach to arrive at the same receptor. Besides being highly circuitous and entirely unnecessary—in light of caffeoyl quinide's presence—it doesn't even concord with observations; and here's why:

Exhibit A: Brown, S. R. "Effect of coffee on distal colon function." Gut (1990)

In this two‐part study, Doctor Brown administered a questionnaire to some and a rectal probe + coffee to others. He had also examined the effects of decaffinated coffee in the same subjects:

'Twenty nine per cent (63% women) claimed that coffee induced a desire to defecate.' ―Brown

'Coffee has been shown to have profound effects on the gastrointestinal system;' ―Brown

'Intraluminal pressure in the rectum and distal sigmoid colon were recorded using a 5 lumen, flexible, manometric assembly (od 5 mm)...' ―Brown

View attachment 8466

'Both regular and decaffeinated coffee contain exorphines that can bind to opiate receptors. Opiate receptors, both in the brain and within the gut wall, mediate important effects on colonic motility; Sun and his colleages have shown that opiate receptors are necessary for the colonic response to food.' ―Brown

'A similar increase was seen after drinking decaffeinated coffee in all coffee responders tested. No increase in rectosigmoid motility was seen after a drink of hot water.' ―Brown

'In conclusion, our results confirm the common belief that coffee promotes the desire to defecate. This response, which can also be induced by decaffeinated coffee, is seen in about a third of the population...' ―Brown

Thus: the laxative agent in coffee could not be removed through the decaffination procedure, adding even more proof—as if it needed any more—that caffeoyl quinide is primarily responsible for these effects.

[1] Boublik, J. H. "Coffee contains potent opiate receptor binding activity." Nature (1983)

What are the authors referring to with the part pasted below? Are they saying that the opiate receptors are needed for the bowel to move after eating? And do they mean “response” as in activation of the opiate receptors?

Sun and his colleages have shown that opiate receptors are necessary for the colonic response to food.' ―Brown
 

Travis

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What are the authors referring to with the part pasted below? Are they saying that the opiate receptors are needed for the bowel to move after eating? And do they mean “response” as in activation of the opiate receptors?

Sun and his colleages have shown that opiate receptors are necessary for the colonic response to food.' ―Brown
Well, it's well known that opiates cause constipation. I think this is either an evolutionary adaption to milk, or the milk had evolved to match the receptor. Besides the milk of cow, human casein also contains β-casomorphin (referred to as human β-casomorphin to avoid confusion). This is slightly different than bovine β-casomorphin, differing by one amino acid; hovever, it is identical to soymorphin found in soy (from the concanavalin A protein). The one found in A1 cow's casein is stronger than the human form; it is the strongest one besides morphine.

Both morphine and β-casomorphin bind the μ-opiod receptor, and both the wheat (gluten exorphin) and leaf (rubiscolin exorphin) opiates bind the δ-opioid receptor. Also ligands for our δ−opioid receptors are the enkephalins, a class of endogenous opiates. Morphine has led to the discovery of β-casomorphin—the endogenous μ-ligand—in a way similar to how cannabinoids led to the discovery of 2‐arachidonylglycerol, the endogenous activator of our cannabinoid receptors.

So you would expect nonfermented soy and A1 dairy to slow intestinal transit time. The ability of A1 to do this is no secret. Besides being a common observation, the ability of dairy products to do this has been experimentally confirmed.

➝ Daniel, H. "Effect of casein and β-casomorphins on gastrointestinal motility in rats." The Journal of nutrition (1990)

Conversely, you would expect naloxone and other antagonists of the μ-opioid receptors to have opposing effects. Since coffee has a powerful μ-antagonist formed upon roasting you would expect an increased intestinal motility from drinking such—an effect completely independent of its caffeination status, exactly as found.
 
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Wagner83

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Conversely, you would expect naloxone and other antagonists of the μ-opioid receptors to have opposing effects. Since coffee has a powerful μ-antagonist formed upon roasting you would expect an increased intestinal motility from drinking such—an effect completely independent of its caffeination status, exactly as found.
You (and many others) said that coffee lost its stimulant properties over time, do you know if the pro-digestion effects of coffee would disappear with regular use?

Not necessarily. This is primarily an effect from eating 100% sugar, like soda‐drinking. Not even candy bars would do this since they often have enough protein to replace that pulled into the cells. Fernstrom had found this phenomenon to occur only with pure carbohydrate, although very low protein fruit juice could do the same.

Although fruit is seen as 'low protein' on charts, the water content can give a false impression. Also, most fruits have a low glycemic index which prevents the insulin spike which is actually the primary cause (it's not sugar per se). Even potatoes and rice, with their higher glycemic index, have enough protein to prevent this from happening; it's really only a practical hazard in those who bolt soda and/or refined fruit juice all day (or honey + coffee).

This phenomenon is only the result of an insulin spike and only when the subject had consumed a negligible amount of protein.
@haidut I know you love your pepsi so that could be interesting for you.
 
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