Dark Roast Coffee Is Not Only Bad, It's Disrespectful

[Travis]

...paranoid...beeing stalked or insulted...hysterical...

Kartoffel, it is plainly obvious to me that you: (1) follow me around, (2) send me personal messages, and (3) harass me. You are insulting me with denials and you're attempts of framing me as delusional.

So how does hyperglycemia cause tiredness in one instance, yet can cause agitation and excitability in another?

I think the receptor-displacement of ligands can actually explain paradoxical results, depending of course on whether or not the μ-receptor had been initially occupied by an opioid? Caffeoyl quinide could also block intestinal μ-receptors, known to be present and active in that location, thereby allowing increased passage of dietary-derived exorphins. The nullifying of high-affinity binding sites would logically increase the mobility of other ligands.

And I don't get angry at all alternate ideas, only when they are contrived just to spite me—as was obviously done in this case.

 

[General Orange]

Ooooh yes indeed! I drink it every evening as it puts me straight to sleep. I always assumed it had to with adrenaline sensitivity/blood sugar. I am sensitive to adrenalin and often get nightmares. But not when I have my evening coffee

It is seen with addiction, that a person who is about to get his fix, the body anticipates the potential response of the substance in question and tries to compensate for the high. The brain is trying to get back in homeostasis. This is why tolerance builds up with drug use. So a little bit of coffee in the evening can trigger a downer response, to counteract the stimulating effects. Also drinking coffee on regular times can trigger this counter acting downer effect.

 

[Travis]

• Del Campo, Martin. "Effects of naloxone on diurnal rhythms in mood and endocrne function: a dose-response study in man." Psychopharmacology (1994)

'As in all studies on man, both affective and endocrine responses to naloxone were quite highly variable between subjects.' ―Del Campo

'Our results suggest that diurnal sensitivity to drugs such as naloxone...' ―Del Campo

'The VAS showed increased depression in the afternoon, and heightened tension, sleepiness and reduced ability to concentrate at both times of day.' ―Del Campo

'VAS depression and tension were increased, and there were changes in sleepiness.' ―Del Campo

'Sleepy: subjects were sleepier in the morning (F = 10.42), but natoxone increased sleepiness irrespective of the time of day (F = 3.78).'

'Sleepiness was marginally increased by naloxone (F = 3.2), tiredness was increased by naloxone in the morning (F = 4.5), and subjects became less relaxed in the afternoon after naloxone (F = 4.7).' ―Del Campo

 

[Kartoffel]

Kartoffel, it is plainly obvious to me that you: (1) follow me around, (2) send me personal messages, and (3) harass me. You are insulting me with denials and you're attempts of framing me as delusional.

So how does hyperglycemia cause tiredness in one instance, yet can cause agitation and excitability in another?

Do you realize that the receptor-displacement of ligands can better explain paradoxical results, depending of course on whether or not the μ-receptor had been initially occupied by an opioid?

Nobody has to frame you as delusional, you do that yourself. Don't you remember how you wrote just a short while ago that the user MrSmart was "working for me" and that I have multiple accounts here just to "follow you around"? (You know very well that this was the only reason I sent you a personal message, and that I never contacted you before - I asked you to stop with false accusations). Tell me, how did that theory turn out? You still believe we are the same person? The simple truth is that you consider yourself so superior that your mind makes you believe that two people cannot possibly disagree with you at the same time, so they must be one and the same person trying to harrass you.
I hate writting about this nonsense in a public thread, but I will not simply let your ridiculous accusations of harassing and following you remain in the room, either. Also, you have shown this kind of aggressive behavior repeatedly in this forum. When people disagree with you, you accuse them of beeing paid internet trolls, morons, etc. Various examples of that can be found looking at your history. You even started portraying Peat as some kind of biased moron with a hidden agenda since it became clear to you that he doesn't really like your reductionist lock and key ideas.

As for the question at issue: I have nothing more to add. You are just elduding my criticism by ignoring any evidence I post, and asking pointless questions. The simple truth remains: You haven't provided any evidence for your central claim, which you already admitted to be hypothetical. I could just respond in kind now, and ask you why our brain requires (goes to) 8 hours of sleep/inhibition in regular intervals.

 

[Travis]

Nobody has to frame you as delusional, you do that yourself. Don't you remember how you wrote just a short while ago that the user MrSmart was "working for me" and that I have multiple accounts here just to "follow you around"? (You know very well that this was the only reason I sent you a personal message, and that I never contacted you before - I asked you to stop with false accusations). Tell me, how did that theory turn out? You still believe we are the same person? The simple truth is that you consider yourself so superior that your mind makes you believe that two people cannot possibly disagree with you at the same time, so they must be one and the same person trying to harrass you.
I hate writting about this nonsense in a public thread, but I will not simply let your ridiculous accusations of harassing and following you remain in the room, either. Also, you have shown this kind of aggressive behavior repeatedly in this forum. When people disagree with you, you accuse them of beeing paid internet trolls, morons, etc. Various examples of that can be found looking at your history. You even started portraying Peat as some kind of biased moron with a hidden agenda since it became clear to you that he doesn't really like your reductionist lock and key ideas.

As for the question at issue: I have nothing more to add. You are just elduding my criticism by ignoring any evidence I post, and asking pointless questions. The simple truth remains: You haven't provided any evidence for your central claim, which you already admitted to be hypothetical. I could just respond in kind now, and ask you why our brain requires (goes to) 8 hours of sleep/inhibition in regular intervals.

You are a provocateur and had contrived this entire scene. The only people who actually deny the known fact that industry trolls comment online are industry trolls themselves. The favorite defense of such is to present the accuser of being 'paranoid' and 'delusional,' words that you freely insult me with. You are bending reality to such an extreme, as you often do, that it only strengthens my point.

You are far more delusional because you deny: (1) established laws of immunology when milk is in dispute, (2) established facts about exorphins when milk is in dispute, and (3) the fact Zellweger's disease is a DHA-deficiency disease. You are delusional Kartoffel; you do follow me around and intentionally-provoke me, ostensibly to frame me as arrogant.

Have fun in you campaign to convince people that: (1) milk is not associated with autism, (2) DHA is not essential for the brain, (3) online paid commenters do not exists and the very idea is ridiculous, (4) that I'm arrogant because I realize what's going on and speak freely about dairy products. Good luck with that, potato guy.

 

[DaveFoster]

Indeed. Those heroes at huffpo know how to stick to the issues! I for one have simply had enough of these French/Italian Roast patriarchs thinking that just because their way has been around for 400 some odd years, it bears some kind of merit or standard....Well I say it STINKS!!

We should abolish all hierarchies because nature's evil.

 

[Travis]

At least the coffee snobs are not quite as extreme as wine snobs with their esoteric vocabulary and tasting methods. Even though 'cupping'—aspirating the drink—could reveal some otherwise-occult flavors, it wouldn't matter anyway because that's not how it's normally drunk. The ultimate result of cupping is just revealing the best tasting coffee when aspirated, and wouldn't necessarily apply to what tastes best when prepared as usual.

 

[Kartoffel]

(3) the fact Zellweger's disease is a DHA-deficiency disease.

No, it's not. Correcting DHA "deficiency" does nothing for Zellweger's patients.

Lab Invest. 2000 Jan;80(1):31-5.
Docosahexaenoic acid deficit is not a major pathogenic factor in peroxisome-deficient mice.
Janssen A1, Baes M, Gressens P, Mannaerts GP, Declercq P, Van Veldhoven PP.

Abstract
Docosahexaenoic acid (DHA), a major component of membrane phospholipids in brain and retina, is profoundly reduced in patients with peroxisome biogenesis disorders (Zellweger syndrome). Supplementing newborn patients with DHA resulted in improved muscular tone and visual functions. The purpose of this study was to investigate (a) whether DHA levels were also reduced in newborn PEX5 knockout mice, the mouse model of Zellweger syndrome that we recently generated; (b) whether these levels could be normalized by supplying DHA; and (c) whether this results in longer survival. The DHA concentration in brain of newborn PEX5-/- mice was reduced by 40% as compared with levels in normal littermates; in liver, no differences were noticed. The daily administration of 10 mg of DHA-ethyl ester (EE) to pregnant heterozygous mothers during the last 8 days of gestation resulted in a normalization of brain DHA levels in Zellweger pups. However, no clinical improvement was observed in these pups, and the neuronal migration defect was unaltered. These data suggest that the accretion of DHA in the brain at the end of embryonic development is not only supported by the maternal supply but also depends on synthesis in the fetal brain. Furthermore, the DHA deficit does not seem to be a major pathogenic factor in the newborn Zellweger mice.


Docosahexaenoic acid therapy in peroxisomal diseases
Results of a double-blind, randomized trial

A.M. Paker, MD, MPH, J.S. Sunness, MD, N.H. Brereton, MS, RD, L.J. Speedie, PhD, L. Albanna, EdD, S. Dharmaraj, MD, PhD, FRCS, A.B. Moser, BA, R.O. Jones, PhD, and G.V. Raymond, MD

Objectives:
Peroxisome assembly disorders are genetic disorders characterized by biochemical abnormalities, including low docosahexaenoic acid (DHA). The objective was to assess whether treatment with DHA supplementation would improve biochemical abnormalities, visual function, and growth in affected individuals.

Methods:
This was a randomized, double-blind, placebo-controlled trial conducted at a single center. Treatment groups received supplements of DHA (100 mg/kg per day). The primary outcome measures were the change from baseline in the visual function and physical growth during the 1 year follow-up period.

Results:
Fifty individuals were enrolled and randomized. Two were subsequently excluded from study analysis when it was determined that they had a single enzyme disorder of peroxisomal β oxidation. Thirty-four returned for follow-up. Nine patients died during the trial of their disorder, and 5 others were lost to follow-up. DHA supplementation was well tolerated. There was no difference in the outcomes between the treated and untreated groups in biochemical function, electroretinogram, or growth. Improvements were seen in both groups in certain individuals.

Conclusions:
DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders.

Classification of evidence:
This interventional study provides Class II evidence that DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders during an average of 1 year of follow-up in patients aged 1 to 144 months

 

[Travis]

No, it's not. Correcting DHA "deficiency" does nothing for Zellweger's patients.

Lab Invest. 2000 Jan;80(1):31-5.
Docosahexaenoic acid deficit is not a major pathogenic factor in peroxisome-deficient mice.
Janssen A1, Baes M, Gressens P, Mannaerts GP, Declercq P, Van Veldhoven PP.

Abstract
Docosahexaenoic acid (DHA), a major component of membrane phospholipids in brain and retina, is profoundly reduced in patients with peroxisome biogenesis disorders (Zellweger syndrome). Supplementing newborn patients with DHA resulted in improved muscular tone and visual functions. The purpose of this study was to investigate (a) whether DHA levels were also reduced in newborn PEX5 knockout mice, the mouse model of Zellweger syndrome that we recently generated; (b) whether these levels could be normalized by supplying DHA; and (c) whether this results in longer survival. The DHA concentration in brain of newborn PEX5-/- mice was reduced by 40% as compared with levels in normal littermates; in liver, no differences were noticed. The daily administration of 10 mg of DHA-ethyl ester (EE) to pregnant heterozygous mothers during the last 8 days of gestation resulted in a normalization of brain DHA levels in Zellweger pups. However, no clinical improvement was observed in these pups, and the neuronal migration defect was unaltered. These data suggest that the accretion of DHA in the brain at the end of embryonic development is not only supported by the maternal supply but also depends on synthesis in the fetal brain. Furthermore, the DHA deficit does not seem to be a major pathogenic factor in the newborn Zellweger mice.


Docosahexaenoic acid therapy in peroxisomal diseases
Results of a double-blind, randomized trial

A.M. Paker, MD, MPH, J.S. Sunness, MD, N.H. Brereton, MS, RD, L.J. Speedie, PhD, L. Albanna, EdD, S. Dharmaraj, MD, PhD, FRCS, A.B. Moser, BA, R.O. Jones, PhD, and G.V. Raymond, MD

Objectives:
Peroxisome assembly disorders are genetic disorders characterized by biochemical abnormalities, including low docosahexaenoic acid (DHA). The objective was to assess whether treatment with DHA supplementation would improve biochemical abnormalities, visual function, and growth in affected individuals.

Methods:
This was a randomized, double-blind, placebo-controlled trial conducted at a single center. Treatment groups received supplements of DHA (100 mg/kg per day). The primary outcome measures were the change from baseline in the visual function and physical growth during the 1 year follow-up period.

Results:
Fifty individuals were enrolled and randomized. Two were subsequently excluded from study analysis when it was determined that they had a single enzyme disorder of peroxisomal β oxidation. Thirty-four returned for follow-up. Nine patients died during the trial of their disorder, and 5 others were lost to follow-up. DHA supplementation was well tolerated. There was no difference in the outcomes between the treated and untreated groups in biochemical function, electroretinogram, or growth. Improvements were seen in both groups in certain individuals.

Conclusions:
DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders.

Classification of evidence:
This interventional study provides Class II evidence that DHA supplementation did not improve the visual function or growth of treated individuals with peroxisome assembly disorders during an average of 1 year of follow-up in patients aged 1 to 144 months

Those mice were not true 'Zellweger's mice' because they had been genetically-engineered to lack an enzyme not representative of the condition. Mice also lack the high intellectual capacities needed to discern differences in brain fatty acid content, and that study does not even put a dent in the sum evidence for DHA's involvement.

You are still clutching to that one study although there's plenty of clinical evidence directly demonstrating how DHA improves myelination in humans with actual Zellweger's disease.

And you have yet to give us a plausible mechanism of what could be 'the real cause of Zellweger's,' or even the 'actual antigen(s) behind FRα autoantibodies.' Let me guess: you think it's hypoglycemia that's responsible?

 

[Kartoffel]

there's plenty of clinical evidence directly demonstrating how DHA improves myelination in humans with actual Zellweger's disease.

No, there isn't. Please don't post that Martinez paper again, or I have to quote Paker et al. for a third time to show you what's wrong with not having a control group. Why don't we let that discussion rest for now, and let people talk about coffee. There are already two threads where people can read our discussion on DHA and Zellweger's, if they want to. In case you have any new evidence besides Martinez that you haven't cited yet, feel free to post it there and I will look at it and respond to you.

 

[Travis]

No, there isn't. Please don't post that Martinez paper again, or I have to quote Paker et al. for a third time to show you what's wrong with not having a control group. Why don't we let that discussion rest for now, and let people talk about coffee. There are already two threads where people can read our discussion on DHA and Zellweger's, if they want to. In case you have any new evidence besides Martinez that you haven't cited yet, feel free to post it there and I will look at it and respond to you.

Zellweger's is complex disease, yet there are some more fundamental considerations that appear undeniable:

• The sum of DHA + osbond acid = 14–17% in the brain grey matter.
• A cell's glucose flux is a direct function of its unsaturation index, and particularly its' DHA concentration.

Assuming a fixed sum, a lower amount of DHA (22∶6ω−3) necessarily would correspond to a higher amount of osbond acid (22∶6ω−6): This is an omega−6 elongation/desaturation product of linoleic acid formed with ostensible intent of maintaining the brain's unsaturation index when α-linolenic acid (18∶3ω−3) is unavailable, or displaced. Thus, DHA saves the brain from the more harmful omega−6 fatty acids.

This appears logical to me unless a person can find a brain analysis showing that the sum of DHA + osbond acid is not a fixed near-constant range.

Besides preventing ω−6 brain influx, docosahexaenoic acid is more effective than osbond acid in excluding sterols from cell membranes. In the brain: the sterols cholesterol, pregnenolone, and progesterone are needed for white matter myelination yet serve to inhibit glucose flux in grey matter membranes where it doesn't belong. All of these trends are implied in postmortem analysis, are proven in physicochemical studies, are all very strong, and since I have seen absolutely no exceptions I would consider them nearly 'laws.'

Disclaimer: I don't eat fish, sell fish oil, and believe that fish liver oil is dangerously-high in retinol. I think it's more important to avoid ω−6 fatty acids than to consume ω−3 fatty acids. Enzymes needed to elongate the shorter DHA-precursor omega−3 fatty acids are also occupied by omega−6 fatty acids. The solution to dysfunctional cell membranes is probably better seen as avoiding 'seed oils,' yet this explains why fish oil has been correlated with a reduction of certain diseases in some instances. Yet: long omega−3 fatty acids are unstable and would likely contribute to lipofuscin, meaning that the shorter precursor α-linolenic acid (18∶3ω−3) is likely safer: this fatty acid is found in leaves, grass-fed beef, grass-fed dairy, and is practically unavoidable.

 

[Kartoffel]

or even the 'actual antigen(s) behind FRα autoantibodies.

Regarding this I actually have two sincere questions: (1) Why should babies drink their mother's milk? Ramaekers et al. showed in their cross-reactivity analysis that FR antibodies from human milk block 12pmol of folate receptors (vs 15pmol for cow's milk). If "foreign" FR as an antigen are such a potent inhibtor of folate uptake and disrupt 5MTHF production in CSF, then the amount in human milk should be problematic. (2) Do you still stand by your recommendation that goat's milk is safer than cow's milk? According to the Nygren-Babo and Jägerstad paper you posted, goat's milk contains twice as many folate receptors as cow's milk. Even if they have a lower cross-reactivity, their potential to block folate receptors should still be higher for a given quantity of milk.

 

[Hemo]

I like dark roast.

best for enemas

 

[zewe]

I like my coffee tepid, like my men.

Oops! Did I say whaaat?

 

[Travis]

Regarding this I actually have two sincere questions: (1) Why should babies drink their mother's milk? Ramaekers et al. showed in their cross-reactivity analysis that FR antibodies from human milk....

The antibodies had actually come from human serum (Ramaekers, 2014).

...block 12pmol of folate receptors (vs 15pmol for cow's milk). If "foreign" FR as an antigen are such a potent inhibtor of folate uptake and disrupt 5MTHF production in CSF, then the amount in human milk should be problematic.

No, because human immune cells will not form antibodies against human FRα. If this actually did occur, the ingestion of human milk would matter little considering the FRα concentrations already present in the child's serum. I am of course assuming that the mother's milk is equally non-immunogenic.

Yet, there is of course a chance that human FRα could form antibodies when ingested by a human unrelated to it.

(2) Do you still stand by your recommendation that goat's milk is safer than cow's milk? According to the Nygren-Babo and Jägerstad paper you posted, goat's milk contains twice as many folate receptors as cow's milk. Even if they have a lower cross-reactivity, their potential to block folate receptors should still be higher for a given quantity of milk.

Are you sure? because that's not what Ramaekers data plainly indicates. This had been depicted in a bar graph directly adjacent to the the cross-reactivity data you had mentioned in point #1 above, making me question the statement directly proceeding that.

Jägerstad cited Swiatlo, who had determined the folate binding capacity of lypholized milk powder. This takes into account all three subtypes—i.e. α, β, and γ—of bovine and caprine folate receptors present. Since we are concerned with FRα because its found on the placenta and choroid plexus, the Ramaekers data should be considered more important for that reason alone. Ramaekers had also used whole milk.

Now assuming that both cow and goats' milk has equivalent proportions of all three subtypes—e.g. ¹⁄₃FRα, ¹⁄₃FRβ, and ¹⁄₃FRγ—and that these are exclusively responsible for the total folate binding capacity, the fact that Swiatlo's data had been expressed per unit mass lypholized milk powder means that less can be said of the whole milk in which it'd been derived. In the case of lypholized milk powder, the total folate binding capacity would reflect the ratio of all folate binding proteins to unevaporated solids. Both cow and goats' milk have near-identical protein∶fat ratios (Barłowska, 2011) so that's not a factor, yet this could be explained by folate affinity to unspecified proteins or a higher FR(β+γ)∶FRα ratio in goats. For immunological purposes, concentrations determined using ELISA towards the one specific protein of concern are indicated; the folate binding capacity used in nutritional research means little in comparison, for reasons outlined above.

Ramaeker's data had been expressed as FRα per unit volume milk while Swiatlo's data had been expressed as folate binding capacity per gram lypholized milk powder. When I say something to the effect of 'goats milk has a lower concentration of FRα,' I certainly don't mean simply that 'dry milk powder from goats binds more folate than from cows.'

 

[Kartoffel]

The antibodies had actually come from human serum (Ramaekers, 2014).

Sorry, I meant the antibodies formed in response to human milk.

No, because human immune cells will not form antibodies against human FRα. If this actually did occur, the ingestion of human milk would matter little considering the FRα concentrations already present in the child's serum. I am of course assuming that the mother's milk is equally non-immunogenic.

Ok, either I misunderstand the procedure that they used to determine cross-reactivity or the Ramaekers paper does show that human FRα is immunogenic. They incubated the isolated FRα from all the types of milk with human serum and then measured how much of the added folic acid was blocked from binding to the recptors to determine how many antibodies were formed. Since the addition of human milk to the serum resulted in 12pmols folate receptors blocked, I thought it's logical to assume that human milk is immunogenic in this sense.

Are you sure? because that's not what Ramaekers data plainly indicates. This had been depicted in a bar graph directly adjacent to the the cross-reactivity data you had mentioned in point #1 above, making me question the statement directly proceeding that.

Ok, I looked at the Ramaekers 2012 paper, and the first thing that I noticed is that the reported cross-reactivity for bovine milk is roughly three times greater than for human or goat's milk. It's only 25% greater in the 2008 paper. Why this large difference?
In this paper they report that the concentration of the FRα subtype is only 30% in goat's milk compared to bovine milk, so this would indeed explain the lower potential. In the 2008 paper they used a preadjusted amount of concentrated receptors, so this wouldn't have accounted for the total amount in a given quantity of milk.

The concentration of each purified FR from placental membranes, human milk, bovine milk, and goat milk was adjusted to bind about 10000cpm of [ 3 H]folic acid (0.34pmol of FR)​

Finally, camel milk seems to have an even greater reactivity with autoantibodies than bovine milk, yet there are numerous publications showing it to have benefical effects for autism patients, some of those papers have an observation period of several years. In the 2014 paper, Ramaekers et al. briefly mention this, but don't provide any possible solution for this puzzle. What's your opinion on that?

 

[Travis]

Sorry, I meant the antibodies formed in response to human milk.

Judging by their affinity towards bovine FRα and likelihood of prior exposure, those antibodies had most likely been formed in response to a product derived from cow's milk.

Ok, either I misunderstand the procedure that they used to determine cross-reactivity or the Ramaekers paper does show that human FRα is immunogenic.

The human folate receptor α had not been shown to generate antibodies in this study, and therefor the Ramaeker paper does not 'show that human FRα is immunogenic.' What Ramaekers had indeed shown was that antibodies derived from human serum—ostensibly raised in response to bovine FRα—would also bind human folate receptor α. The amount of folate that had been blocked by the antibody–hFRα interaction had been given the value of unity; the bar graph had been normalized to this value. All other values had been expressed in relation to human FRα blocking.

They incubated the isolated FRα from all the types of milk with human serum and then measured how much of the added folic acid was blocked from binding to the recptors to determine how many antibodies were formed.

This should also determine their affinity because folate blocking would be a function of antibody concentration and affinity.

Since the addition of human milk to the serum resulted in 12pmols folate receptors blocked, I thought it's logical to assume that human milk is immunogenic in this sense.

I think it's logical to assume that human milk had been used as a convenient source of human folate receptor α. This receptor, although not longer functioning as such, is identical to the ones found on the brain's choroid plexus—responsible for cerebral folate uptake. Ramaeker's data demonstrates that human antibodies bind human folate receptor α, earning them the designation of 'autoantibodies.'

Since these autoantibodies had a substantially more affinity for bovine folate receptor α, it would be logical to assume the former had originally been elicited by the latter.

As an afterthought; this also implies that the attachment of FRα autoantibodies would be temporarily-reduced by the ingestion of bovine FRα by providing them something to bind to, and something of higher affinity. Extrapolating from Ramaeker's data, this should result in a more profound decrease of brain folate upon the cessation of ingesting bovine FRα. Going further out on a limb, though on a solid one, this amelioration of AuAb–hFRα binding could induce the coincident amelioration of negative symptoms associated with it—such as: (1) low cerebral folate, and/or (2) the immunogenic attack by circulating neutrophils naturally attracted to antibody ends. This hypothetical sequence could induce a temporary relief in those with FRα autoantibody symptoms while acting to ensure the continuation of bovine FRα ingestion through positive reinforcement. This paradigm overlays with the the concept of 'allergy–addiction syndrome' propounded in popular books.

Ok, I looked at the Ramaekers 2012 paper, and the first thing that I noticed is that the reported cross-reactivity for bovine milk is roughly three times greater than for human or goat's milk. It's only 25% greater in the 2008 paper. Why this large difference?

Autoantibodies are very rarely characterized down to the atom. Antibodies of all types are large proteins having identical 'tails' yet variable 'heads.' The binding-end is specific to the protein to which it binds, and it is the antibody class and target protein that define the antibody. Folate receptor α contains 257 amino acids yet the amount of amino acids the antibody actually binds-to is far smaller, I would guess around twelve amino acids. This is enough protein to attach and also to ensure specificity; there are over twenty amino acids used in structural proteins. A random sequence of 12 amino acids would have 20¹² possibilities, demonstrating both the powerful selectivity of antibodies and the reason why autoantibodies rarely form against random proteins. Autoantibodies generally form in response to a protein that is similar, yet still different-enough, to the host protein in which it binds. Caprine folate receptor α is roughly 20% homologous to the human form and bovine FRα is ~80% homologous.

Finally, camel milk seems to have an even greater reactivity with autoantibodies than bovine milk, yet there are numerous publications showing it to have benefical effects for autism patients, some of those papers have an observation period of several years. In the 2014 paper, Ramaekers et al. briefly mention this, but don't provide any possible solution for this puzzle. What's your opinion on that?

This is indeed perplexing, yet could be confirmation of my hypothesis that the process of homogenization increases the immunogenic risk via the liposomal-encapsulation of FRα antigen. Goat's milk is never homogenized because the naturally-small diameter of its' liposomes precludes separation. Milk from camels could also be exempt from separation for the same reason, and if so it would be unlikely to have been homogenized because doing so would be illogical.