Estrogen In Milk

[Dhair]

I have been saying that native cow's milk may be 100% safe, yet it's the process of homogenization that facilitates large peptide persorption. You can still have you 'sacred cow,' as long as you can view homogenization as a modern modification of a naturally-safe product—a process inspired by vanity, not safety, as separation is just an esthetic concern.

Is this why goat milk is generally much better?
I buy the Summerhill Dairy brand of goat milk, and it feels consistently positive for me. I don't think that it has ever caused me digestive problems. Can't say the same for commercial cow's milk. On their website, they describe goat milk as being "naturally homogenized," which, they say, is why they do not artificially homogenize it.

 

[Waynish]

Is this why goat milk is generally much better?
I buy the Summerhill Dairy brand of goat milk, and it feels consistently positive for me. I don't think that it has ever caused me digestive problems. Can't say the same for commercial cow's milk. On their website, they describe goat milk as being "naturally homogenized," which, they say, is why they do not artificially homogenize it.

I believe which is better & when would be a per-country issue with milk due to a variety of farming practices. I've heard Switzerland has some of the best dairy, but I don't know of any cross country comparison studies for types of dairy. Swiss companies do market some high-end colostrum.

 

[michael94]

Perhaps you really are sincere, but you're still wrong. Nothing better explains low cerebral spinal fluid folate concentrations concomitant with normal plasma concentrations of same, especially since these criteria are always accompanied by FRα antibodies.

You don't really ever truly think do you? You ought to read a few more studies if you're interested. You are selling yourself short by attaching so much weight to a Ray Peat one-liner, an offhand comment—especially since he's old, committed, and has been promoting milk for decades.

I have been saying that native cow's milk may be 100% safe, yet it's the process of homogenization that facilitates large peptide persorption. You can still have you 'sacred cow,' as long as you can view homogenization as a modern modification of a naturally-safe product—a process inspired by vanity, not safety, as separation is just an esthetic concern.

homeogenized fat is more easily digested in low bile conditions, it is not purely aesthetics but very practical with some drawbacks as you mentioned.

 

[MrSmart]

Hey Potato Guy, obnoxious troll, there are dozens and I have told you this many times. You are intentionally lying about this, just as you've lied about many other things in the past.

Ramaekers, Vincent T. "A milk‐free diet downregulates folate receptor autoimmunity in cerebral folate deficiency syndrome." Developmental Medicine & Child Neurology (2008)

Desai, A. "Prevention of behavioral deficits in rats exposed to folate receptor antibodies: implication in autism." Molecular psychiatry (2017)

Rossignol, Daniel A. "Folate receptor alpha autoimmunity and cerebral folate deficiency in autism spectrum disorders." Journal of Pediatric Biochemistry (2012)

Ramaekers, Vincent T. "Folate receptor autoimmunity and cerebral folate deficiency in low-functioning autism with neurological deficits." Neuropediatrics (2007)

Frye, R. E. "Cerebral folate receptor autoantibodies in autism spectrum disorder." Molecular psychiatry (2013)

Ramaekers, Vincent T. "Autoantibodies to folate receptors in the cerebral folate deficiency syndrome." New England Journal of Medicine (2005)

Frye, Richard E. "Blocking and binding folate receptor alpha autoantibodies identify novel autism spectrum disorder subgroups." Frontiers in neuroscience (2016)

Ramaekers, Vincent T. "Role of folate receptor autoantibodies in infantile autism." Molecular psychiatry (2013)

Al-Baradie, Raidah S. "Diagnosis and management of cerebral folate deficiency: A form of folinic acid-responsive seizures." Neurosciences (2014)

Frye, Richard E. "Folate receptor alpha autoantibodies modulate thyroid function in autism spectrum disorder." North American Journal of Medicine and Science (2014).

Moretti, Paolo. "Brief report: autistic symptoms, developmental regression, mental retardation, epilepsy, and dyskinesias in CNS folate deficiency." Journal of autism and developmental disorders (2008)

Frye, R. E. "Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial." Molecular psychiatry (2016).
​

A similar amount of studies have been published concerning these autoantibodies and their capacity to cause birth defects by binding/blocking placental folate receptors. If anyone doubts that FRα do in fact block human folate receptors with high affinity, what's implied by its name, there are a good many studies conducted by disciplined biochemists and immunologists on just that. Now, is the rest of you're comment worth reading? Probably not, but I suppose I will. [...]

'...and Ramaekers et al. somehow forgot to measure whether folate levels (N5 -methyltetrahydrofolate) differed after their milk intervention, allthough [sic] they measured the number of blocked folate receptors. You might argue that they simply forgot about looking into this important fact, or ran out of funding - or you might suspect that they did measure it and didn't really like the results.' —Kartoffel​

He had 'forgot,' really? Do you realize how cerebrospinal fluid is obtained? If so, do you think this is a routine procedure that should be done on children?

'The study that Travis cited above (2007) actually doesn't have anything to do with milk, and doesn't include the words milk or bovine even once. The one study that he bases his whole milk-folate theory on is this one.' —Kartoffel​

Oh my god people! These folate receptor autoantibodies could have come from anything . . . like pineapples!!! [lol, not]

'The one study that he bases his whole milk-folate theory on is this one.' —Kartoffel​

You are a liar, and that is one of the reasons why I usually avoid you. Most people consider the practice of lying to be both offensive and undemocratic, Kartoffel, so you should stop doing it.

And another thing: This is not merely a 'theory,' and it is not solely 'mine' either. These antibodies are proven realities, and so is cerebral folate deficiency. The only novel aspect that I had contributed to this was the potentiation of autoimmunity by homogenization, an idea strongly supported by older science concerning the encapsulation of milk xanthine oxidase and subsequent persorption.

And why do you think, is this not part of mainstream media? Is it because the dairy industry is keeping a closed lid, or generally the medical field's indifference to market their research in the absence of a useful product?

 

[Kartoffel]

You don't really ever truly think do you? You ought to read a few more studies if you're interested. You are selling yourself short by attaching so much weight to a Ray Peat one-liner, an offhand comment—especially since he's old, committed, and has been promoting milk for decades.

I am not. My position doesn't rest on his comment, I have come to my own conclusions after reading the literature and considering the material you have posted. I merely asked for his comment out of curiosity, and posted it so that you might stop insulting everyone (well, mostly me) that doesn't completely agree with you on this. By the way, I don't think that Peat is an old, senile fool just yet, and I would think him capable of reconsidering his positions, if he saw relevant evidence.

Perhaps you really are sincere, but you're still wrong. Nothing better explains low cerebral spinal fluid folate concentrations concomitant with normal plasma concentrations of same, especially since these criteria are always accompanied by FRα antibodies.

That's not true. As the correlation graph from your paper shows, you can have fairly low cerebral spinal fluid folate concentrations without any antibodies, and without having the disease. On the other side, you can have the antibodies and significantly more cerebral folate than controls.

Nevertheless, you can't rely deny the involvement of the antibody peptides in folate deficiency. What you can, and should, debate is the cause for the autoimmunity. The immunglobulin that was present in the people with folate deficiency was IgG, which is the most prominent antibody in the human body. I admit that I probably know very little about antibodies compared to you, but as far as I know IgG is not a specific product of a reaction to FR from milk or other peptides found in it, and many other foreign substances can trigger an autoimmune reaction evoking the production of it.

If it is the autoimmune reaction to folate "receptor" proteins in milk that is the only reason for folate deficiency, why don't we all get folate deficiency when we drink our mother's milk? The amount of pmoles folate receptor blocked is "only" 30% higher for bovine milk than for human milk. That's still significant, but the amount should still be sufficient to cause the disease, if the role of FR peptides is as central as you claim. Now, of course, you can say "It's all about the homogenization" but this would just be another assumption on top of many assumptions, and there is no study that has looked at it in this context.

Finally, if milk as an environmental factor was the main reason for the formation of autoantibodies, why are these antibodies so "prevalent in affected families with similar distribution in parents, normal siblings and affected children?" (Quadros et al. 2018). You can propose that drinking milk runs in the family, but that would just be another vague assumption, and I think it should rather encourage us to think about other things that might be going on.

Autism Res. 2018 May;11(5):707-712. doi: 10.1002/aur.1934. Epub 2018 Feb 2.
Folate receptor autoantibodies are prevalent in children diagnosed with autism spectrum disorder, their normal siblings and parents.
Quadros EV1, Sequeira JM1, Brown WT2, Mevs C3, Marchi E2, Flory M4, Jenkins EC2, Velinov MT2, Cohen IL5.
Author information
Abstract
Folate deficiency can affect fetal and neonatal brain development Considering the reported association of Folate receptor alpha (FRα) autoantibodies (Abs) with autism and developmental disorders, we sought to confirm this in families of 82 children with ASD, 53 unaffected siblings, 65 fathers, and 70 mothers, along with 52 unrelated normal controls. Overall, 76% of the affected children, 75% of the unaffected siblings, 69% of fathers and 59% of mothers were positive for either blocking or binding Ab, whereas the prevalence of this Ab in the normal controls was 29%. The Ab was highly prevalent in affected families including unaffected siblings. The appearance of these antibodies may have a familial origin but the risk of developing ASD is likely influenced by other mitigating factors since some siblings who had the antibodies were not affected. The antibody response appears heritable with the blocking autoantibody in the parents and affected child increasing the risk of ASD. Autism Res 2018, 11: 707-712. © 2018 International Society for Autism Research, Wiley Periodicals, Inc.

LAY SUMMARY:
Folate is an essential nutrient during fetal and infant development. Autoantibodies against the folate receptor alpha can block folate transport from the mother to the fetus and to the brain in infants. Children diagnosed with autism and their immediate family members were evaluated for the prevalence of folate receptor autoantibodies. The autoantibody was highly prevalent in affected families with similar distribution in parents, normal siblings and affected children. The presence of these antibodies appears to have a familial origin and may contribute to developmental deficits when combined with other factors.

 

[MrSmart]

That's not true. As the correlation graph from your paper shows, you can have fairly low cerebral spinal fluid folate concentrations without any antibodies, and without having the disease. On the other side, you can have the antibodies and significantly more cerebral folate than controls.

I'm fairly neutral on the issue, but you clearly have a difficult time reading graphs. The results of Ramaekers, Vincent T., et al. "A milk‐free diet downregulates folate receptor autoimmunity in cerebral folate deficiency syndrome." Developmental Medicine & Child Neurology 50.5 (2008): 346-352 are quite clear. And it's unscientific to say "you can have", there can be lots of things in the world, you can have short NBA players, or rich people born poor, but there is a thing called statistical significance that must be observed.

Folate receptor autoantibodies are prevalent in children diagnosed with autism spectrum disorder, their normal siblings and parents.

Quadros EV1, Sequeira JM1, Brown WT2, Mevs C3, Marchi E2, Flory M4, Jenkins EC2, Velinov MT2, Cohen IL5.
Author information
Abstract
Folate deficiency can affect fetal and neonatal brain development Considering the reported association of Folate receptor alpha (FRα) autoantibodies (Abs) with autism and developmental disorders, we sought to confirm this in families of 82 children with ASD, 53 unaffected siblings, 65 fathers, and 70 mothers, along with 52 unrelated normal controls. Overall, 76% of the affected children, 75% of the unaffected siblings, 69% of fathers and 59% of mothers were positive for either blocking or binding Ab, whereas the prevalence of this Ab in the normal controls was 29%. The Ab was highly prevalent in affected families including unaffected siblings. The appearance of these antibodies may have a familial origin but the risk of developing ASD is likely influenced by other mitigating factors since some siblings who had the antibodies were not affected. The antibody response appears heritable with the blocking autoantibody in the parents and affected child increasing the risk of ASD. Autism Res 2018, 11: 707-712. © 2018 International Society for Autism Research, Wiley Periodicals, Inc.

LAY SUMMARY:
Folate is an essential nutrient during fetal and infant development. Autoantibodies against the folate receptor alpha can block folate transport from the mother to the fetus and to the brain in infants. Children diagnosed with autism and their immediate family members were evaluated for the prevalence of folate receptor autoantibodies. The autoantibody was highly prevalent in affected families with similar distribution in parents, normal siblings and affected children. The presence of these antibodies appears to have a familial origin and may contribute to developmental deficits when combined with other factors.

First of all, Travis outlined a relationship between Autism and FRAbs, which seems to hold no matter how you look at it. In addition, there seems to be even a stronger relationship, I assume, if the study used CFDS as their dependent variable instead of autism but there clearly is a relationship between all three. Now with regards to milk, that doesn't mean some populations have naturally higher (or even present) FRAbs than others, as you have outlined above, but in all cases, a milk-free diet lowers their presence, and milk-containing diets raises them, even from absolute zero in non-affectted populations.

There is a much stronger significance to blocking antibody types than binding ones on risk of ASD, and naturally the presence of such as much more statistically different and significant compared to controls. The previous test study on milk did not specify which of them had that effect, although I would assume it's the blocking type based on the absence in some post-results data.

Lastly, that doesn't mean you will develop temporary autism drinking a cup of milk, but there can be cognitive implications nonetheless, and autism is indeed a spectrum that everyone is on. And if drinking no milk improves you on that spectrum, then by all means, cut it out completely.

 

[Kartoffel]

I'm fairly neutral on the issue, but you clearly have a difficult time reading graphs. The results of Ramaekers, Vincent T., et al. "A milk‐free diet downregulates folate receptor autoimmunity in cerebral folate deficiency syndrome." Developmental Medicine & Child Neurology 50.5 (2008): 346-352 are quite clear. And it's unscientific to say"you can have", there can be lots of things in the world, you can have short NBA players, or rich people born poor, but there is a thing called statistical significance that must be observed.

Why do you think I can't read the graph? Travis said "are always accompanied". I picked out single points from the graph (which represent single people) to show that this is not true, that doesn't have anything to do with beeing unscientific. I know what statistical significance is, but it is completely irrelevant for the point I was making. Seems you have a hard time reading an argument.

Now with regards to milk, that doesn't mean some populations have naturally higher (or even present) FRAbs than others, but in all cases, a milk-free diet lowers their presence, and milk-containing diets raises them, even from absolute zero in non-affectted populations.

Well, that remains to be seen and confirmed by more studies, and studies that have blinded control groups, and a more controlled environment. The term "relationship" can mean many things ranging from correlation to clear causation. And how do you know that it holds in all cases and all populations "even from absolute zero in non-affectted populations"? Have I missed several studies repeating the milk experiment for different populations? In the experiment we're talking about here they used 24 preselected people that already had high antibodies! Your statement is absolutely without any evidence.

Since Travis doesn't seem eager to answer these questions, maybe you can: Why did the levels of antibodies increase so drastically in the control group even though they just "remained on their normal diet containing milk products." (347)? How do you know that the milk-free diets in the intervention group didn't change some other signifcant factor? They probably received a completely different diet designed by dieticans, which constitutes a whole new environment. Unfortunately we can't know what exactely they ate because it wasn't a controlled intervention and they provide no data. Milk "products" can contain a lot of things.

"The parents were instructed by a dietician on maintaining the patient on a milk-free balanced diet repletewith essential nutrients and protein-calorie requirement" (ibid)​

Why do the FR in human milk (which block 12 pmoles folate recoptor vs 15 for bovine milk) not produce very similar symptoms?

And if drinking no milk improves you on that spectrum, then by all means, cut it out completely.

Can't argue with that. However, if "poorer cognitive function and an increased risk of vascular dementia (VaD) were found to be associated with a lower consumption of milk or dairy products" (Solfrizzi et al. 2011) it might not be such a good idea.

 

[MrSmart]

Why do you think I can't read the graph? Travis said "are always accompanied". I picked out single points from the graph (which represent single people) to show that this is not true, that doesn't have anything to do with beeing unscientific. I know what statistical significance is, but it is completely irrelevant for the point I was making. Seems you have a hard time reading an argument.

Yes he did say always, and yes if you go back and look at the study, there is always a presence of blocking FRAbs with low CSF/serum folate ratio.

Well, that remains to be seen and confirmed by more studies, and studies that have blinded control groups, and a more controlled environment. The term "relationship" can mean many things ranging from correlation to clear causation. And how do you know that it holds in all cases and all populations "even from absolute zero in non-affectted populations"? Have I missed several studies repeating the milk experiment for different populations? In the experiment we're talking about here they used 24 preselected people that already had high antibodies! Your statement is absolutely without any evidence.

You don't need a randomized control group without any CFDS, the control group, in this case, was the milk-containing diets that the other group had. Does that predict the levels in intervention of milk on FRAbs in unaffected populations? No. But the effect on the already affected populations had reduced their levels to normal controls, which is obviously, zero. Why would do you think milk's effect on a randomized population would be different? Because there is no reason to.

Since Travis doesn't seem eager to answer these questions, maybe you can: Why did the levels of antibodies increase so drastically in the control group even though they just "remained on their normal diet containing milk products." (347)? How do you know that the milk-free diets in the intervention group didn't change some other signifcant factor? They probably received a completely different diet designed by dieticans, which constitutes a whole new environment.

Because they were children? And secondly, because it was a 24mo followup, and it wasn't entirely evident when did they make the switch from human milk to bovine milk during the period, at least nothing that I could pinpoint.

Unfortunately we can't know what exactely they ate because it wasn't a controlled intervention and they provide no data. Milk "products" can contain a lot of things.

Now you're being retarded. This info was enough:

"The parents were instructed by a dietician on maintaining the patient on a milk-free balanced diet repletewith essential nutrients and protein-calorie requirement" (ibid)​

If something else eliminated the Abs response besides the presence of milk, it would be a clear second followup study, but it wasn't because likely, the children didn't have controlled diets either, except for the absence of milk.

Why do the FR in human milk (which block 12 pmoles folate recoptor vs 15 for bovine milk) not produce very similar symptoms?

Folate receptors are not my specialty,

"The cross-reactivity of the blocking autoantibodies with antigen from different sources is consistent with the significant homology in the native structure of these proteins. FR is well conserved across species, with more than 90% amino acid sequence homology between human FRα and bovine FRα, 15,16 and this could contribute to common antigenic epitopes and cross-reactivity of the autoantibodies. The antibody showed better reactivity with the FR from bovine milk than with the FR from human placenta, human milk, or goat milk, suggesting bovine FR as the likely primary antigen. Quantitatively, there was more cross-reactivity with FR purified from human milk than with FR from human placenta. This discordance may be due to the presence of both the α and β isoforms of FR in human placenta, whereas milk contains only the FRα isoform;16,17 this would support the conclusion that the autoantibodies react better with epitopes on FRα, the putative antigen for the initial immune response. Most of the FR autoantibodies belong to the IgG4 subclass, and the switch to this class of antibodies seems to be influenced by repeated exposure to the antigen over a prolonged period,18,19 which supports the conclusion that repeated exposure to milk FR in the digestive tract is the likely mechanism for autoantibody generation." – (Ramaekers, Sequeira, Blau, & Quadros 2008)​

 

[Kartoffel]

You don't need a randomized control group without any CFDS

If you want to make the claim that you made, or if you want to claim (like Travis) that dairy, because of the folate receptors antibodies, is the main cause for mental impairments in the Western world, then of course you do!

Why would do you think milk's effect on a randomized population would be different? Because there is no reason to.

I have explained in detail why I'm not convinced there is any causal effect demonstrated in this study, so your question is redundant, and since you talked about beeing unscientifc earlier - saying there is no reason to assume that things might be different in different populations after one trial- well, that is unscientific. The reason we test things repeatedly in science, with different populations and different samples is to confirm theories (or try to falsify hypotheses if you are a Popperian), and to rule out potential errors and faulty reasoning.

Because they were children? And secondly, because it was a 24mo followup, and it was entirely evident when did they make the switch from human milk to bovine milk during the period, at least nothing that I could pinpoint.

You just listed a lot of the things introducing elements of uncertainty and potential confounding variables.

If something else elminated the Abs response besides the presence of milk, it would be a clear followup study, but it wasn't because likely, the children didn't have controlled diets either, except for the absence of milk.

I don't understand your point. What dou mean by "it would be clear"? Of course, it would not be clear, since their study design and the uncontrolled environment allow for various confounding variables, especially since one group was at least partly controlled by dieticians while the other was not. That's like Lustig's recent study showing that kids eating hotdogs, pizza, and spaghetti automatically lose weight, while those eating sugar get fat and sick.
If you eliminate all milk products, you don't just eliminate milk and the presumed causative agent in it, you also remove lots of other things that are in "milk products". You know how many terrible junk food items contain milk? Carragenan and other gums, for example, are in many milk products, and would have been eliminated in the milk free diet, and that's just one of the destructive substances that you would cut out in a diet without milk products. How do you know that the children in the control group didn't have controlled diets, except for the absence of milk? I think this statement pretty clearly indicates that the dieticians did not simply control that they didn't consume any milk (products), but also told them what to eat instead to get the same amount of protein, nutrients, etc.

The parents were instructed by a dietician on maintaining the patient on a milk-free balanced diet replete with essential nutrients and protein-calorie requirements.
​

Edit: Forgot your first point.

Yes he did say always, and yes if you go back and look at the study, there is always a presence of blocking FRAbs with low CSF/serum folate ratio.

No, there isn't. Many of the healthy controls without antibodies have comparatively low CSF folate compared to the ones with antibodies, so this already tells us (even in a small sample) that you can have antibodies and high folate, and no antibodies and comparatively low folate. Below 50mmoles/l you don't see people w/o antibodies any longer, but even in this segment you have large variation ranging from 0.5 mmol to almost 5 mmol, with three aberrations dsitorting the picture.
And if you want to take from that that this demonstrates that you just need small amounts of antibodies to create the effect on folate, then you go right back to the questions of why some poeple with antibodies have significantly more CSF folate than controls, or why you should assume that human, or goat milk is any safer.

 

[SOMO]

My .02, I was drinking three gallons of milk a day for a period of three months in an effort to put on weight and completely shrug off three years of malnutrition(vomit/fecal losses). It worked, but I became very sensitive to any potential BS contained within the milk due to the fact that it was a good chunk of my calories(9000kcal). Walmart milk gave me terrible hives at 2L, Deans at 1 gallon, Organic(all the same) at 2 gallon, and Roundy's Select(Kroger/Mariano's) gave me no strange red spots or any other issues. My friend bought me a Trader Joe's milk, I drank a liter and told him it was garbage. Another note on the Walmart milk is that it gave someone I was working out with an ulceration on their bicep that disappeared upon stopping walmart milk(4 days).
N=5 since the group I train martial arts and go to the gym with wondered how I put on weight after being sick. Same results(some cheaped out on milk) and interesting results when someone ignored my recommendation to use lactase a certain way(at work too!).
Currently drinking Roundy's "Fat Free" milk and noticing much more heat loss from my body(higher temp) and focus. Let's hope everything stays nice and conjugated.

I think you would have reacted to ANY milk you tried.

DAIRY (not just milk) is known and has been convincingly shown to be both acne-genic/acne-forming and cause dermatitis/other skin eruptions.
Dairy, including the hormones naturally present it, still nourishes us, but Peatarians are delusional if they don't think that milk is a relatively allergenic food that although high in nutrition, can cause everything from diarrhea to skin issues. More likely, ANY milk you purchase will vary.

Grocery Store milk, including many of the organic brands, comes from a process called "pooling." This is where they take milk from cows on the farmer's land/the co-op and pool it in a big steel vat. It's just as likely, if not more, that the milk inside the milk carton comes from more than 1 cow.
I think you should continue drinking milk but perhaps consume YOGURT with it, seeing as how many lactose-intolerant people can still tolerate yogurt. I don't personally buy Lactaid/Lactose-reduced milks but I have tried them before and like the taste a lot. When consuming some yogurt with your milk, some "lactose-intolerant" people find they can temporarily tolerate larger amounts of dairy (leaky gut, by another name. RP also believes the small intestine is damaged in people who have supposed "Lactase-Enzyme deficiency.").

Even if you continue reacting negatively (physically) to milk, it's still nutritious and it's (reacting to dairy) possibly a barometer or gauge of one aspect of digestion.

 

[MrSmart]

If you want to make the claim that you made, or if you want to claim (like Travis) that dairy, because of the folate receptors antibodies, is the main cause for mental impairments in the Western world, then of course you do!



I have explained in detail why I'm not convinced there is any causal effect demonstrated in this study, so your question is redundant, and since you talked about beeing unscientifc earlier - saying there is no reason to assume that things might be different in different populations after one trial- well, that is unscientific. The reason we test things repeatedly in science, with different populations and different samples is to confirm theories (or try to falsify hypotheses if you are a Popperian), and to rule out potential errors and faulty reasoning.



You just listed a lot of the things introducing elements of uncertainty and potential confounding variables.



I don't understand your point. What dou mean by "it would be clear"? Of course, it would not be clear, since their study design and the uncontrolled environment allow for various confounding variables, especially since one group was at least partly controlled by dieticians while the other was not. That's like Lustig's recent study showing that kids eating hotdogs, pizza, and spaghetti automatically lose weight, while those eating sugar get fat and sick.
If you eliminate all milk products, you don't just eliminate milk and the presumed causative agent in it, you also remove lots of other things that are in "milk products". You know how many terrible junk food items contain milk? Carragenan and other gums, for example, are in many milk products, and would have been eliminated in the milk free diet, and that's just one of the destructive substances that you would cut out in a diet without milk products. How do you know that the children in the control group didn't have controlled diets, except for the absence of milk? I think this statement pretty clearly indicates that the dieticians did not simply control that they didn't consume any milk (products), but also told them what to eat instead to get the same amount of protein, nutrients, etc.

The parents were instructed by a dietician on maintaining the patient on a milk-free balanced diet replete with essential nutrients and protein-calorie requirements.​

Did you also read Berrocal-Zaragoza, Maria Isabel, et al. "High milk consumers have an increased risk of folate receptor blocking autoantibody production but this does not affect folate status in Spanish men and women." The Journal of nutrition 139.5 (2009): 1037-1041 ?

Folate receptor protein in cow’s milk contaminated vaccines (e.g. DTap) can cause the development of FRAbs that block folate uptake and cause autism.

1. Frye RE, Sequeira JM, Quadros E V, James SJ, Rossignol D a. Cerebral folate receptor autoantibodies in autism spectrum disorder. Mol Psychiatry. 2012;18(3):369–81
2. Arumugham V. Autism Spectrum Disorders: A special case of vaccine-induced cow’s milk allergy? 2017
3. Kattan JD, Cox AL, Nowak-Wegrzyn A, Gimenez G, Bardina L, Sampson HA, et al. Allergic reactions to diphtheria, tetanus, and acellular pertussis vaccines among children with milk allergy. J Allergy Clin Immunol. 2011;Conference(var.pagings):AB238.

Injected proteins cause the development of allergies, which is the same thing as persorption of homogenized proteins such as those in bovine milk. We know that as the IgE antibody mediated allergy. Repeated injection of bee venom proteins causes the development of IgE mediated bee sting allergy. Injecting influenza virus proteins causes the development of IgE mediated allergy to influenza viral proteins. Injected egg proteins cause the development of egg allergy.

 

[Kartoffel]

Did you also read Berrocal-Zaragoza, Maria Isabel, et al. "High milk consumers have an increased risk of folate receptor blocking autoantibody production but this does not affect folate status in Spanish men and women." The Journal of nutrition 139.5 (2009): 1037-1041 ?

No, but I will. Thanks. The title sounds like it is validating one of the suspicions I had about Ramaekers study - that there was no significant difference of 5MTHF in the two groups. If that's true, doesn't that throw the whole theory overboard?

Folate receptor protein in cow’s milk contaminated vaccines (e.g. DTap) can cause the development of folate receptor alpha antibodies (FRAA) that block folate uptake and cause autism.

1. Frye RE, Sequeira JM, Quadros E V, James SJ, Rossignol D a. Cerebral folate receptor autoantibodies in autism spectrum disorder. Mol Psychiatry. 2012;18(3):369–81
2. Arumugham V. Autism Spectrum Disorders: A special case of vaccine-induced cow’s milk allergy? 2017
3. Kattan JD, Cox AL, Nowak-Wegrzyn A, Gimenez G, Bardina L, Sampson HA, et al. Allergic reactions to diphtheria, tetanus, and acellular pertussis vaccines among children with milk allergy. J Allergy Clin Immunol. 2011;Conference(var.pagings):AB238.

Injected proteins cause the development of allergies, which is the same thing as persorption of homogenized proteins such as those in bovine milk. Today, we know that as IgE antibody mediated allergy. Repeated injection of bee venom proteins causes the development of IgE mediated bee sting allergy. Injecting influenza virus proteins causes the development of IgE mediated allergy to influenza viral proteins. Injected egg proteins cause the development of egg allergy

My point exactely. Almost everything can be persorbed and trigger an antibody reaction when the intestine is leaky, which is why I find it so hard to understand why you dismiss my points about the Ramaekers study out of hand.

 

[MrSmart]

No, but I will. Thanks.

My point exactely. Almost everything can be persorbed and trigger an antibody reaction when the intestine is leaky, which is why I find it so hard to understand why you dismiss my points about the Ramaekers study out of hand.

Why would the intestines of Children be leaky? And how does that explain the absence and reintroduction of milk on the FRAbs almost immediately in group 1, and the regressing markers in group 2? Surely they weren't feeding on trace milk containing cakes and brownies in their developmental stages? And I wouldn't even be so sure that all dairy products were cut in the milk-free group, only straight milk from either source in particular. Sadly, we will never know, but I have faith based on other indirect findings that the hypothesis is true.

 

[Kartoffel]

Why would the intestines of Children be leaky? And how does that explain the absence and reintroduction of milk on the FRAbs almost immediately in group 1, and the regressing markers in group 2? Surely they weren't feeding on trace milk containing cakes and brownies in their developmental stages?

Of children with folate deficiency. Even Rameakers et al. admit that to be the primary cause.

This indicates that the gastrointestinal tract is a likely route of exposure to the antigen and that a compromised immune barrier in this system can be considered as the potential cause of the autoimmune response (350)
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And how does that explain the absence and reintroduction of milk on the FRAbs almost immediately in group 1, and the regressing markers in group 2?

Can you rephrase that, please? I don't understand the sentence.

​

 

[MrSmart]

Of children with folate deficiency. Even Rameakers et al. admit that to be the primary cause. This indicates that the gastrointestinal tract is a likely route of exposure to the antigen and that a compromised immune barrier in this system can be considered as the potential cause of the autoimmune response (350)

Because homogenized milk proteins do not need a leaky intestinal tract to bypass, unlike leaky gut syndrome. Do you know of any other homogenized molecules that could have been included in children diets?

Can you rephrase that, please? I don't understand the sentence.

Assuming your claim was true, and I don't want to drag on a false assumption, how does leaky guts explain the rise in FARbs in group 1 in the study after milk was reintroduced by almost 3x? While group 2 continued to naturally deteriorate in the presence of milk?

 

[Kartoffel]

Because homogenized milk proteins do not need a leaky intestinal tract to bypass, unlike leaky gut syndrome. Do you know of any other homogenized molecules that could have been included in children diets?

Would you mind providing a reference showing that in vivo consumption of homgenized milk leads to the persorbtion of proteins? Also, the question is redundant, since the role of a compromised intestinal barrier in mental disorders is well etsablished and not even questioned by Rameakers et al.

Assuming your claim was true, and I don't want to drag on a false assumption, how does leaky guts explain the rise in FARbs in group 1 in the study after milk was reintroduced by almost 3x? While group 2 continued to naturally deteriorate in the presence of milk?

Thanks, now I understand it. Looking at the orignial sentence again, you will probably agree that it was hard to comprehend your meaning. I think the answer to your question is already in several of the replies i wrote. The increase in group 2 is interesting, though, since the antibody levels continue to increase way above what they were before the trial. This is especially striking since the data shows that we shouldn't expect to see a continuous rise of antibodies as the patients get older. Before the experiment there was only one patients (and remember they all were on their standard milk-containing diets before) with an autoantibody titer above 3. Most of them were below 1 or slightly above (no correlation with age). And, then, suddenly half of the guys in group two have an autoantibody titer of 3 or greater, and only one that has a titer of 1, with the others ranging between 2 and 3.
Isn't that curious? Why do you think their antibodies increased when their diet didn't change and the baseline data tells us that we shouldn't excpect any linear increases?

To phrase that more clearly, there is nothing that indicates that they normally "naturally deteriorate in the presence of milk" in the sense that antibodies continue to rise.

 

[MrSmart]

Would you mind providing a reference showing that in vivo consumption of homgenized milk leads to the persorbtion of proteins? Also, the question is redundant, since the role of a compromised intestinal barrier in mental disorders is well etsablished and not even questioned by Rameakers et al.

Yes but the discussion is for children which you would confidently assume that no compromised intestinal barrier exists.

I can't waste any more time on that while managing billions of dollars, you would have to wait for @Travis to continue following the breadcrumbs with you.

 

[Kartoffel]

I can't waste any more time on that while managing billions of dollars, you would have to wait for @Travis to continue following the breadcrumbs with you.

Lol, ok go manage your billion dollar company. So, no last reply to my last point? It's really sad that business is calling just as you seem to run out of answers, especially since those points are not breadcrumbs but very unexpected results that requiring explaining. Come on, anyone managing a billion dollar company can surely explain this striking difference, where there was originally no large variation in the children consuming the same milk-diet.

 

[MrSmart]

Lol, ok go manage your billion dollar company. So, no last reply to my last point? It's really sad that business is calling just as you seem to run out of answers, especially since those points are not breadcrumbs but very unexpected results that requiring explaining. Come on, anyone managing a billion dollar company can surely explain this striking difference, where there was originally no large variation in the children consuming the same milk-diet.

View attachment 9998

What is this supposed to prove exactly? That you're wrong?

What about this:

 

[Kartoffel]

What is this supposed to prove exactly? That you're wrong?

I just explained that to you - twice.