Sunday, May 10, 2015

Got Milk? Part 4: Into the Rabbit Hole!

A genetic trait, known as lactase persistence (LP), allows carriers of the gene to drink milk after they are weaned. The 'dairy councils' of the world, with the backing of the medical profession, want everyone drinking MOAR MILK. Our very own Gabriella Kadar, DDS, made the connection that possibly this lactase persistence gene was the root cause, or co-factor of a modern disease, multiple sclerosis.

Gabriella recently discussed this phenomenon with Gemma. Gemma, per usual, dug up many good papers and connected some dots that got Gabriella really scared! Possibly there's even more to the story than MS...


From Gemma:

A couple of weeks ago Gabriella mentioned to me that she suspects lactase persistence gene / status has something to do with susceptibility to multiple sclerosis, a hypothesis she researched a few years ago, out of pure curiosity. Gabriella said she had noticed that all people with multiple sclerosis she knew were drinking milk.  

An original hypothesis on a disease with unknown cause? A purely human disease, with no exact animal equivalent? A modern day disease, first described in 1868? An autoimmune disease, with  very long latency up to 20 years? A disease, when a body is attacking its own tissues? A disorder of altered T-cell homeostasis? No single pathogen responsible for MS was ever found, no single causal gene was ever identified, HLA genes and vitamin D status cannot explain all, hygiene hypothesis is not enough, and the causes seem to be epigenetic, humans are the only mammals that keep LP after weaning... and MS might start in the gut (2014).

More reading:
The story of multiple sclerosis 
Multiple Sclerosis Review (2012)
Multiple Sclerosis: A Disorder of Altered T-Cell Homeostasis (2011)
Nutrition Facts in Multiple Sclerosis (2015)

Should be fun to research, I thought. In the worst, our findings would simply join the very long line of hypotheses, all exposing a gap in understanding of multiple sclerosis causality. The scientists managed to come up with many theories so far, some quite esoteric indeed. Is it exposure to domestic cats? Is it a lack of exposure to domestic cats? Is it house dogs? Is it volcanogenic microelements? No, we don't think so. So, we set out to explore the cause of multiple sclerosis.

Here is what we found so far:

LCT gene and Chromosome 2 

First we had a look at Gabriella's suspicion that lactase gene (LCT) is just a red herring, that there is actually another faulty gene in its surrounding, in an area called 2q21, on a longer arm of the chromosome 2. This chromosome is very suspicious, since it is considered to be a fused chromosome, and the remnants of the ancient centromere are exactly in our region of interest, close to 2q21 where LCT is located. Human Chromosome 2 "is widely accepted to be a result of an end-to-end fusion of two ancestral chromosomes, as evidenced by the presence of a vestigial centromere. Normally a chromosome has just one centromere, but in chromosome 2 there are remnants of a second centromere. Moreover, in chromosome 2 there are additional telomere sequences in the middle."

More reading:
Origin of human chromosome 2: an ancestral telomere-telomere fusion. (1991)

Such a region might be a bit unstable and some more frequent mutations could be there. We found crazy many interesting genes at 2q21 or nearby, some even suspected to be involved in the pathogenesis of multiple sclerosis this way or another, but no single gene seemed to be The One. That does not mean that a deleterious mutation hitchhiking together with a positively selected allele for LP is not there, waiting to be discovered. 

GWAS studies looking for a causal gene(s), implicated in MS

Was LP gene ever identified as suspicious in MS? Genome-wide association studies (GWAS) are often used to study the DNA of groups of people. Comparisons are made between people with a particular disease and those without to see what genetic clues can be learned. Funny fact is that LCT gene is a strong confounder in GWAS studies for multiple sclerosis (MS), and as such removed from considerations.  This points to something that Gabriella picked up on.

More reading:

Some scientists are starting to "see the light" at the end of the tunnel, as far as LP and lactose is concerned, but we are faster!

 The implications of lactase persistence

Another thought we had reflected an idea that MS might be connected to the lactase gene being used and turned ON, even after weaning. So our attention turned to milk drinking and LCT gene itself, and we started to explore what it is actually good for, and why humans developed lactase persistence (LP) beyond weaning age. Some facts summarized in Part 1 and Part 2 of this series.

More reading:
T-13910 DNA variant associated with lactase persistence interacts with Oct-1 and stimulates lactase promoter activity in vitro. (2005)
Analysis of a SNP linked to lactase persistence: An exercise for teaching molecular biology techniques to undergraduates (2011)

Consult wiki or other literature, if you need to learn more about lactose (the milk sugar, a disaccharide sugar derived from galactose and glucose) or lactase, "also known as lactase-phlorizin hydrolase, or LPH, a part of the β-galactosidase family of enzymes, is a glycoside hydrolase involved in the hydrolysis of the disaccharide lactose into constituent galactose and glucose monomers."

But what exactly made LP possible? Was natural selection in play? And who is the puppet master controlling evolution and the genome change? Seems it is our beloved microbes...

The hologenome theory of evolution

Role of microorganisms in the evolution of animals and plants: the hologenome theory of evolution. (2008)
We present here the hologenome theory of evolution, which considers the holobiont (the animal or plant with all of its associated microorganisms) as a unit of selection in evolution. The hologenome is defined as the sum of the genetic information of the host and its microbiota. The theory is based on four generalizations: (1) All animals and plants establish symbiotic relationships with microorganisms. (2) Symbiotic microorganisms are transmitted between generations. (3) The association between host and symbionts affects the fitness of the holobiont within its environment. (4) Variation in the hologenome can be brought about by changes in either the host or the microbiota genomes; under environmental stress, the symbiotic microbial community can change rapidly. These points taken together suggest that the genetic wealth of diverse microbial symbionts can play an important role both in adaptation and in evolution of higher organisms. During periods of rapid changes in the environment, the diverse microbial symbiont community can aid the holobiont in surviving, multiplying and buying the time necessary for the host genome to evolve. The distinguishing feature of the hologenome theory is that it considers all of the diverse microbiota associated with the animal or the plant as part of the evolving holobiont. Thus, the hologenome theory fits within the framework of the 'superorganism' proposed by Wilson and Sober.


Natural selection and the immune system

Why do organisms adopt new genetic changes? Natural selection favors those who have more viable offspring, showing reproductive fitness, in other words. Fitness also stands for an ability to resist pathogens, so the immune system continuously evolves too, as yet another new pathogen shows up and tries to out-trick us. Gene network involved in the immune system function can be seen as a result of eons of battles, losses and victories against age-old pathogens that we are not perhaps facing in our modern times any more. But the immune system is still ready to fight them, in case they show up, or more importantly, when it perceives they might have shown up. Our immune system watches for signals that something is wrong, it watches for signals of stress and danger.

More reading:
A holobiont birth narrative: the epigenetic transmission of the human microbiome (2014)
The gut microbiome shapes intestinal immune responses during health and disease (2009)

What does milk have to do with the immune system? Well, a lot! We know that milk is packed with compounds not only feeding and nourishing a neonate, but protecting and defending the infant whose immune system is not yet fully developed. Some researcher even suggest that the nutritional role of milk evolved secondarily to its immune function, see: Evolution of the mammary gland from the innate immune system? (2006).

We said that immune system is watching for signs of stress. And as we know, our commensal microbiota is watching too, from the point of view of the superorganism, and evaluating: "is that what we together agreed upon, when adopting a new genetic change, still respected?"

In other words: does  adoption of LP into the human genome mean the microbiota, the puppet master, says: "OK, my dear human, you can continue to eat some dairy even after weaning, but make sure that all that the toxins are neutralized and do not affect us! Make sure that toxic lactose is hydrolyzed, so that we both can enjoy some more easily digestible sugars and benefit from more energy. Have some lactose metabolizing microbes around, just in case something bad happens to your own lactase enzyme. But we are telling you, do not dare to lose both, and do not bomb us with toxins. It would make us quite hungry. And angry too."

Is milk a suspect in multiple sclerosis?

Let's go back to the autoimmune disease we are researching: multiple sclerosis. Have other researchers ever explored milk and MS connection? This paper seems promising, but no satisfactory explanation is offered...

Milk consumption and multiple sclerosis--an etiological hypothesis. (1986)
Epidemiological studies of Multiple Sclerosis (MS) in the United States have shown an association with urban living and higher socio-economic groups and a higher incidence and earlier age at onset of symptoms in women. This study is based on the proposition that these trends may be a consequence of differences in exposure to an etiological factor around 15 years of age. As a result of variations in related United States and New Zealand data and other pertinent observations the possibility of a link between high childhood milk intake followed by a large or sudden reduction during the adolescent growth spurt, and the subsequent incidence of MS in young adults is proposed. The possible involvement of calcium and lead metabolism is also discussed. It may be that the elusive environmental variable associated with the incidence of MS is partly a behavioural one related to western social attitudes.

Here is another paper, getting a bit closer, but still identifying a wrong target, in our opinion:

Correlation between milk and dairy product consumption and multiple sclerosis prevalence: a worldwide study. (1992)
Multiple sclerosis (MS) epidemiology suggests that different factors are involved in the clinical expression of the disease. Alimentary cofactors have already been considered, but mainly theoretically. We have studied the relationship between MS prevalence and dairy product consumption in 27 countries and 29 populations all over the world, with Spearman's correlation test. A good correlation between liquid cow milk and MS prevalence (rho = 0.836) was found; this correlation was highly significant (p < 0.001). A low but still significant correlation was obtained with cream or butter consumption (rho = 0.619 and rho = 0.504, respectively). No correlation was found for cheese. These results suggest that liquid cow milk could contain factor(s) - no longer present in the processed milk - influencing the clinical appearance of MS. The possible role of some dairy by-products is discussed in the light of a multifactorial etiology of MS.

This paper from 1992 identifies the highly significant trigger present in liquid milk, but suggest that the milk component responsible for triggering MS is, surprisingly, butyrate. This conclusion made us laugh, really. No, it cannot be our beloved butyrate. So, which other factor present in liquid milk, and not anymore present in processed milk, could it be?

Innocent lactose?

We are mainly interested the immunomodulatory function of milk, so let's have a closer look at it. What is one of the strongest inducers of innate immunity in mammalian milk? This new research suggests that it is our milk sugar of interest, lactose. We have mentioned that lactose is selectively toxic to gut flora. On the other side, baby gut flora, namely Bifidos, enjoy lactose quite a lot, actually so much that they metabolize lactose preferably over glucose. But what about other microbes? Oh, oh...This paper revealing hitherto unknown function of lactose in innate immunity says:

Lactose in Human Breast Milk an Inducer of Innate Immunity with Implications for a Role in Intestinal Homeostasis (2013)
Postpartum, infants have not yet established a fully functional adaptive immune system and are at risk of acquiring infections. Hence, newborns are dependent on the innate immune system with its antimicrobial peptides (AMPs) and proteins expressed at epithelial surfaces. Several factors in breast milk are known to confer immune protection, but which the decisive factors are and through which manner they work is unknown. Here, we isolated an AMP-inducing factor from human milk and identified it by electrospray mass spectrometry and NMR to be lactose. It induces the gene (CAMP) that encodes the only human cathelicidin LL-37 in colonic epithelial cells in a dose- and time-dependent manner. The induction was suppressed by two different p38 antagonists, indicating an effect via the p38-dependent pathway. Lactose also induced CAMP in the colonic epithelial cell line T84 and in THP-1 monocytes and macrophages. It further exhibited a synergistic effect with butyrate and phenylbutyrate on CAMP induction. Together, these results suggest an additional function of lactose in innate immunity by upregulating gastrointestinal AMPs that may lead to protection of the neonatal gut against pathogens and regulation of the microbiota of the infant.

 Some other interesting facts, worth noting:

It is well known that lactose is first hydrolyzed into its glucose and galactose moieties by lactase, located in the mucosa of the small intestine [32]. Our results demonstrate no detectable levels of lactose in fecal samples of both one and four week old infants (Table 1). This suggest an efficient hydrolysis of lactose in the small bowel, which is in agreement with previous reports [33]. However, we cannot rule out the possibility that a part of the lactose is internalized by the colonic epithelial cells.
In addition to lactose, the levels of galactose were determined in the same feces samples and were found to be 1–7 g/l (Table 1), revealing an incomplete absorption of this monosaccharide in the gut. Interestingly, we observed that an equimolar concentration of a combination of glucose and galactose induced CAMP gene expression to the same extent as lactose. Furthermore, our results indicate that also maltose induced CAMP gene transcript to the same extent as lactose and that trehalose can even surpass lactose in CAMP gene-inducing capacity on an equimolar basis.

Now, what exactly is cathelidicin (also called CAMP or LL-37)? A very ancient antimicrobial peptide, acting as endogenous antibiotic, produced by the innate immune system. So ancient that the pathogens learned to live with it, and sometimes can even hijack its action to promote their own survival.

"So what?" you say. LL-37 can be upregulated by many other factors. What else can induce expression of  LL-37? Well, for instance, bacterial products, butyrate, or vitamin D, among others. Is upregulated LL-37 good or bad? It depends. It is good if you need to fight an infection and kill the pathogenic microbes. But what if they are not there?

More reading:
Little peptide, big effects: the role of LL-37 in inflammation and autoimmune disease (2013)
The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis. (2014) 

Immune system in overdrive?

Can it get any worse? What else can the innocent milk sugar lactose do, when it escapes digestion either by low/no activity of endogenous lactase, or by missing gut flora? Note that this is seen as a defect, it should not really happen too often. If there is too much lactose around, our immune system might think that something is wrong, and start an attack! Or, a smart commensal microbe afraid of lactose or of the imaginary pathogen might do the same...

See this in vitro research:
Lactose inhibits regulatory T-cell-mediated suppression of effector T-cell interferon-γ and IL-17 production (2014)

Our interest in lactose as an immunomodulatory molecule results from studies showing that lactose binds to galectin-9, which has been shown to have various regulatory functions in the immune system including regulation of T-cell responses. Impaired regulation of T helper (Th)1 and Th17 type immune responses and dysfunction of regulatory T cells (Treg) have been implicated in many human immune-mediated diseases. In the present study, we investigated the effects of lactose on immune regulation using co-cultures of human peripheral blood mononuclear cell (PBMC)-derived Treg and effector T cells (Teff) obtained from twenty healthy adults. Treg, i.e. CD4+CD25+CD127, were isolated from PBMC by immunomagnetic separation. The fraction of CD4+CD127 cells that was depleted of CD25+ cells was used as Teff. Treg and Teff at a ratio 1:5 were activated and the effects of lactose on the secretion of interferon-γ (IFN-γ) and IL-17 were analysed using ELISA for protein and quantitative RT-PCR for mRNA. Treg down-regulated the secretion of both IFN-γ (8·8–3·9 ng/ml, n 20, P= 0·003) and IL-17 (0·83–0·64 ng/ml, n 15, P= 0·04) in co-cultures, while in the presence of lactose the levels of secreted IFN-γ and IL-17 remained high and no down-regulation was observed (16·4 v. 3·99 ng/ml, n 20, P< 0·0001, and 0·74 v. 0·64 ng/ml, n 15, P= 0·005, respectively). We showed that lactose inhibits human Treg-mediated suppression of Th1 and Th17 immune responses in vitro.

Let's sum it up: 

This basically describes the altered T-cell homeostasis, mentioned as one of the MS attributes. Per previous paper, lactose can induce expression of endogenous antibiotic (LL-37) and at the same time induce pro-inflammatory response and block the anti-inflammatory Tregs that are important in the maintenance of immune homeostasis. Autoimmunity landscape par excellence.

The authors conclude with these points:
  • is plausible that in individuals susceptible to chronic inflammatory diseases, dietary lactose could induce harmful inflammatory responses by disrupting Treg-mediated regulation...
  • The incidence of autoimmune diseases, chronic inflammatory disorders and allergy has increased during the last few decades, especially in Western societies, and cannot be explained by changes in genetic predisposition.
  • Uncontrolled Th1 and Th17 immune responses and the inability of Treg to down-regulate immune responses have been implicated in the pathogenesis of many human immune-mediated diseases.
  • ...the role of dietary lactose in the exacerbation of allergic inflammation in individuals with food allergy should be considered.
  • In populations with a high proportion of lactose-tolerant individuals, due to the high frequency of lactase gene mutation contributing to the persistent intestinal lactase production during adulthood, lactose intake from the diet is relatively eminent.
  • Interestingly, the incidence of some immune-mediated diseases is high among these populations.
  • It is also possible that the intestinal problems associated with genetic lactose intolerance may not always be caused by lactose-related osmotic changes, but could be of immunological origin.
  • Taken together, lactose has strong immune-modulating properties, which we have demonstrated in the present study in vitro in human subjects...
  • Physiological relevance of our preliminary results and effects of dietary lactose on the human gut immune system and health need to be studied further.

Can inappropriate lactose signaling during dysbiosis, or in the absence of pathogens, cause an inappropriate immune response? Back in the "good old days" when we were surrounded by pathogens and forced to eat dirt with our meals, perhaps an immune system in overdrive was advantageous. Now, in our semi-sterile lives, drinking milk is still a signal that keeps our immune system in hyperdrive.

Babies are full of Bifidobacteria. Bifidobacteria is associated with a healthy baby. Before we started drinking the milk of other species, we were forced to develop an adult microbiota. Continually feeding our gut bacteria "baby food" may have profound implications when attempting to shift the gut flora from that of a baby's to that of an adult.

More reading:
The contribution of natural selection to present-day susceptibility to chronic inflammatory and autoimmune disease. (2014)
Regulation of osteoclastogenesis through Tim-3: possible involvement of the Tim-3/galectin-9 system in the modulation of inflammatory bone destruction. (2014) 

Evolution has no eyes to the future!*

*(Williams GC. Adaptation and Natural Selection. Princeton, New Jersey: Princeton University Press; 1966.)

Selective pressure does not look kindly upon humans acting against their own genes. Over the past several million years, we've perfected our immune systems and physiology. Now these mismatches in milk drinking, on a very new genotype, are creating "weak points" in our lives. We drink lactose, signalling a need for an immune boost, but with few pathogens present.  Perhaps when we had a high pathogen load, bellies filled with helminths and H. pylori, being LP was truly advantageous and milk allowed us to thrive.

But, no traditional means of milk processing gave anyone much lactose. Traditional methods all were lactose reducing. Cheese, fermented milk, and even the occasional drink of raw, not pasteurized or cooled and stored milk were the methods of dairy consumption that allowed humans to become LP. Nowadays, we drink all manner of processed, high-lactose milk products whenever we like. As Gabriella noticed, the LP genotype/status plays a BIG ROLE in susceptibility to modern inflammatory/autoimmune diseases, not only to multiple sclerosis. Researchers noticed it, too, but only at the genetic level, never connecting the problems with the lactose itself.

What Gabriella has hypothesized makes perfect sense. A gene or haplotype with a role in reproductive fitness connected to an ability to digest milk past the age of weaning. Milk is simply an external input to our innate immune system. Babies get their first microbes from their mothers, the mother also fuels their immune system with milk.

When Gabriella noticed the connection between the veritable milk orgy we've been engaged in since the advent of pasteurization and an explosion of MS, she was seeing a nasty trick of evolution at play. What was protective for humans when we were living a hard-scrabble life of recently liberated hunter-gatherers is deadly for modern humans. When the immune system ramps up for no good reason, it attacks anything it perceives as a threat. In auto-immune disease, that threat is us.

Some thoughts...

Dr. Kadar brilliantly noted a connection that few researches have seen. That lactose and the drinking of milk by entire populations of people without regard to the genetics of LP or LNP is most likely causing the MS we see in the world today, and possibly other autoimmune diseases too. What is T1D, anyway? We're calling for research in this area! The data has mostly been collected, it just has not been screened for this scenario.
We further hypothesize that the drinking of fluid, pasteurized milk in quantities only seen since the 1800's has overridden the genetic ability of our immune system to use lactose as a signalling molecule, and we suggest that the lactose is the problem. 

Does Multiple Sclerosis start in the gut, is microbiota involved?

We think so. But not in the way researchers tend to look at it, searching for a unknown evil pathogen with a causal role. We have stated that our immune system watches for signals that something is wrong. But so does our guardian microbiota that has co-evolved in tight relationship with us and our immune system. Therefore, we hypothesize that an ordinary, commensal microbe may have a causal role in autoimmunity.

Molecular Mimicry Revisited: Gut Bacteria and Multiple Sclerosis (2006)
Molecular mimicry is a possible explanation for autoimmune side effects of microorganism infections. Protein sequences from a particular microorganism are compared to known autoimmune immunogens. For diseases such as multiple sclerosis (MS), where the infectious agent is unknown, guesses to its identity are made. Mimics are assumed to be rare. This study takes a radically different approach. Reported sequences from all known human bacterial and viral agents were searched for autoimmune immunogen mimics. Three encephalitogenic peptides, whose autoimmune requirements have been studied extensively, were selected for comparison. Mimics were seen in a wide variety of organisms. For each immunogen, the mimics were found predominantly in nonpathogenic gut bacteria. Since the three immunogens used in this study are related to MS, it is suggested that a microorganism responsible for autoimmune activity in MS could be a normally occurring gut bacterium. This would explain many of the peculiar MS epidemiological data and why no infective agent has been identified for MS and supports recently found MS gut metabolism abnormalities.

But a microbe and the immunogen is not enough...

For molecular mimicry to work the immunogen must be “visible” to the immune system. It has therefore been assumed that it must be located on the surface of a protein that is either excreted by the microorganism or is on its surface. This is not necessarily true. The microorganism itself can initiate an immune response. Cells are hydrolyzed, and their contents are released. A great amount of digestive enzyme activity is present. All this can “expose” potential immunogens (23). It certainly happens within active EAE lesions. These “new” immunogens can be processed by the already-present immune cells.

And what else is missing?

Why is the incidence of MS so low? Although both the immunogen and adjuvant molecules are present, they must be processed in such fashion that the correct units are made in high enough concentration to form the complex. This will depend entirely upon the nature of the gut and its hydrolytic enzymes. The gut is a dynamically evolving biosystem whose bacterial content is changing and therefore the concentrations and types of hydrolytic enzymes continually vary.

Conclusions and open questions

We propose that an innocent commensal microbe, perturbed by lactose signalling during dysbiosis, starts a causal cascade to autoimmune disease.  Which one? Does it matter? Does bacterial beta-galactosidase play a role too? What is the initial trigger setting a stage for autoimmune attack on myelin? We do not know, we only have some wild ideas... But we hope for more research in this area soon!



  1. A very thoughtful piece. It brings up some intriguing questions regarding milk and MS. I think the environment in which the mother is living at the time of the birth of the baby is important. Why does one child get MS and not the others? Why does it affect women more than men? I was born early on during the Second World War and my bother towards the end of the war. Food shortages was high and everything was on coupons. We were breastfed and weaned onto solid foods as quickly as possible. What was the quality of her milk at the time? I remember my mother saying that my brother was weaned on brown beans and apple sauce (at the start of the “hunger winter” in 44/45). Sufficient breast feeding is important as I have learned, on hearing of my father’s plight when he was a baby. He was born a twin at the beginning of the last century. When he was about 6 months old, my grandmother took him to the doctor, because something was not right. It turned out that his twin brother would wake up first, put to the breast, and by the time my father woke up the breast was nearly empty. If my grandmother had gone to the doctor 2 months later, my father would have died of malnutrition. My grandmother was told to put both babies to the breast at the same time. As a result my father was a head shorter than his brother, and skinny as a rake. Bottle feeding wasn’t around then, at least not like in the 60’s and 70’s when bottle feeding became the norm. Babies aren’t getting the benefits of breast milk any more, at least not like they used to. What would the gut biomes of my mother and grandmother have been like? My grandmother suffered badly from rheumatoid arthritis and my mother died young from cancer, which started in the womb. Their immune systems would have been in terrible shape.

    Jo tB

    1. To clarify: what affect did it have on the development of my father's immune system? What affect did the food shortages have on our immune systems?
      I don't remember my parents drinking milk, but we were definitely encouraged to do so, because "the white motor" is so healthy for us.

      Jo tB

  2. I guess my question is why are you singling out MS? Couldn't this also be related to any immune related disease. And who knows how or why the immune system decides to attack in a certain place. That is what I want to know. When I did 23 and Me I found that some gene that worked with the immune system made me at higher risk for an immune disease.. Which made sense to me. The majority of my family has immune related diseases. I have a sister with Lupus and brother with Celiac. Two of my children have Autism. Gene chances with sususeptabilty to immune disregulation + gut dysbiosis + environmental pathogen (milk or whatever) = immune disease. I see lots of families with Autism have higher rates of all kinds of immune related diseases.

    1. @Allison

      "why are you singling out MS?"

      Because this way it is easier to investigate, you know? Thanks for your comment.

    2. Exactly. We could have easily expanded this to all auto-immune diseases, and everything we say of MS fits very well with T1D. But milk and MS have a long connection in the scientific research papers, and Gab made some personal connections with MS as well, so we all dug in and saw what we could find.

      This could easily be a never-ending series and I have no doubt a "Wheat Belly" type expose' will one day pop up telling us all how bad milk is.

      The research is there, I assume the milk industry is biting their nails hoping no one sees the connections.

      As to auto-immune diseases, they seem to grow by the day, and every one seems somehow related to the gut. There's even an Autoimmune Disease is their list of AI diseases:

    3. Autoimmune and Autoimmune-Related Diseases

      Acute Disseminated Encephalomyelitis (ADEM)
      Acute necrotizing hemorrhagic leukoencephalitis
      Addison’s disease
      Alopecia areata
      Ankylosing spondylitis
      Anti-GBM/Anti-TBM nephritis
      Antiphospholipid syndrome (APS)
      Autoimmune angioedema
      Autoimmune aplastic anemia
      Autoimmune dysautonomia
      Autoimmune hepatitis
      Autoimmune hyperlipidemia
      Autoimmune immunodeficiency
      Autoimmune inner ear disease (AIED)
      Autoimmune myocarditis
      Autoimmune oophoritis
      Autoimmune pancreatitis
      Autoimmune retinopathy
      Autoimmune thrombocytopenic purpura (ATP)
      Autoimmune thyroid disease
      Autoimmune urticaria
      Axonal & neuronal neuropathies
      Balo disease
      Behcet’s disease
      Bullous pemphigoid
      Castleman disease
      Celiac disease
      Chagas disease
      Chronic fatigue syndrome**
      Chronic inflammatory demyelinating polyneuropathy (CIDP)
      Chronic recurrent multifocal ostomyelitis (CRMO)
      Churg-Strauss syndrome
      Cicatricial pemphigoid/benign mucosal pemphigoid
      Crohn’s disease
      Cogans syndrome
      Cold agglutinin disease
      Congenital heart block
      Coxsackie myocarditis
      CREST disease


    4. Essential mixed cryoglobulinemia
      Demyelinating neuropathies
      Dermatitis herpetiformis
      Devic’s disease (neuromyelitis optica)
      Discoid lupus
      Dressler’s syndrome
      Eosinophilic esophagitis
      Eosinophilic fasciitis
      Erythema nodosum
      Experimental allergic encephalomyelitis
      Evans syndrome
      Fibrosing alveolitis
      Giant cell arteritis (temporal arteritis)
      Giant cell myocarditis
      Goodpasture’s syndrome
      Granulomatosis with Polyangiitis (GPA) (formerly called Wegener’s Granulomatosis)
      Graves’ disease
      Guillain-Barre syndrome
      Hashimoto’s encephalitis
      Hashimoto’s thyroiditis
      Hemolytic anemia
      Henoch-Schonlein purpura
      Herpes gestationis
      Idiopathic thrombocytopenic purpura (ITP)
      IgA nephropathy
      IgG4-related sclerosing disease
      Immunoregulatory lipoproteins
      Inclusion body myositis
      Interstitial cystitis


    5. Juvenile arthritis
      Juvenile diabetes (Type 1 diabetes)
      Juvenile myositis
      Kawasaki syndrome
      Lambert-Eaton syndrome
      Leukocytoclastic vasculitis
      Lichen planus
      Lichen sclerosus
      Ligneous conjunctivitis
      Linear IgA disease (LAD)
      Lupus (SLE)
      Lyme disease, chronic
      Meniere’s disease
      Microscopic polyangiitis
      Mixed connective tissue disease (MCTD)
      Mooren’s ulcer
      Mucha-Habermann disease
      Multiple sclerosis
      Myasthenia gravis
      Neuromyelitis optica (Devic’s)
      Ocular cicatricial pemphigoid
      Optic neuritis
      Palindromic rheumatism
      PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus)
      Paraneoplastic cerebellar degeneration
      Paroxysmal nocturnal hemoglobinuria (PNH)
      Parry Romberg syndrome
      Parsonnage-Turner syndrome
      Pars planitis (peripheral uveitis)
      Peripheral neuropathy
      Perivenous encephalomyelitis
      Pernicious anemia
      POEMS syndrome
      Polyarteritis nodosa


    6. Type I, II, & III autoimmune polyglandular syndromes
      Polymyalgia rheumatica
      Postmyocardial infarction syndrome
      Postpericardiotomy syndrome
      Progesterone dermatitis
      Primary biliary cirrhosis
      Primary sclerosing cholangitis
      Psoriatic arthritis
      Idiopathic pulmonary fibrosis
      Pyoderma gangrenosum
      Pure red cell aplasia
      Raynauds phenomenon
      Reactive Arthritis
      Reflex sympathetic dystrophy
      Reiter’s syndrome
      Relapsing polychondritis
      Restless legs syndrome
      Retroperitoneal fibrosis
      Rheumatic fever
      Rheumatoid arthritis
      Schmidt syndrome
      Sjogren’s syndrome
      Sperm & testicular autoimmunity
      Stiff person syndrome
      Subacute bacterial endocarditis (SBE)
      Susac’s syndrome
      Sympathetic ophthalmia
      Takayasu’s arteritis
      Temporal arteritis/Giant cell arteritis
      Thrombocytopenic purpura (TTP)
      Tolosa-Hunt syndrome
      Transverse myelitis
      Type 1 diabetes
      Ulcerative colitis
      Undifferentiated connective tissue disease (UCTD)
      Vesiculobullous dermatosis
      Wegener’s granulomatosis (now termed Granulomatosis with Polyangiitis (GPA)

    7. As Gemma said......

      Type 1 diabetes probably has the same sort of aetiology. There a autoimmune diseases that have zero geographic distribution. They can't be tracked at all. Like Hashimoto's Thyroiditis. That probably starts in the gut too.

      Some diseases have been getting better potential risk assessments, like Coeliac. There's apparently 6 genes but having them does not guarantee that a person will develop the disease. Fasano has done a lot of longterm research on first degree relatives of Coeliac patients.

      With Coeliac disease, a doctor in the Nethelands noticed that during the war, little children were not dying from failure to thrive and after the second world war, again they were. He identifed bread as being the reason. There bread before the war, not during the war and then again there was bread after the war. He didn't know what about bread was killing children, he just figured out that something was.

      Are you aware that no one give Aspirin to children with fever anymore because of Reye Syndrome? ? ASA has never been proven to the causative and Reye syndrome still does happen but Baby Aspirin is gone. In 1980 there were 555 cases of Reye Syndrome.

    8. Allison Hurst,

      YOU SAY********The majority of my family has immune related diseases. I have a sister with Lupus and brother with Celiac(<--------------KEYS FACTORS HERE<---------------------------. Two of my children have Autism. Gene chances with sususeptabilty to immune disregulation + gut dysbiosis + environmental pathogen (milk or whatever) = immune disease. I see lots of families with Autism have higher rates of all kinds of immune related diseases ( and I bet you see many have problems with milk,soy gluten........or the reverse high OXALATE FOODS

      My family the same--- lupus , type 2 diabetes, crohns and colitis , stomach problems.. After 3.5 years thousands of dollars.. picking apart my roots Italian many NON standard tests... (rome mountians -- half---- the other eastern sea coast-) all Mothers side and her parents and fathers side german , irish and British( his parents ) 23and me is good.... but dig further , run your data file the top right corner in 23andme.. download and take it( your data file) over to genetic genie and then mtthr report.. find out more what genes you have defective. 23andme cant tell you this due to the FDA , they dont want you to know. Look at your blood type... your ubiome ..what bacteria you have and also what yeast (great plans lab ) OAT and comp stool. the real test genetic test ( labcrop for celiac genes) many of these genes also ---you guessed it link to diabetes, lupus and other diseases ...imagine that<-------- Lab corp which is the lab that runs your 23andme :) test your HLA DQ in more detail. learn what genes you have in the ALPHA and BETA for HLA DQ here youll see and piece it all together. your blood type... what bacteria you have (low bifido) high yeasts.. many dont play happy with yeast with ALPHA and beta gluten genes... many processed foods have added molds to add to shelf life.. Citric acid is aspergillus mold.(it has to say FRUIT citric acid to be real)many foods even juice, lunch meat etc etc add it..even teas bottled with no sauce made with aspergillus mold, corn syrup (fermented with bacillus & aspergillus mold ) antibiotics you first get penicillin mold , you wont find a test at your hospital to tell you what your mold /fungus level is. OH the doc says antibiotics are worries.... right??? Most sinus problems are due to fungus... eat foods with mold , you may ramp up your immune system due to your genes. many with European descent carry gluten genes. that doesnt mean you will get celiac --- but you need an alpha and beta to have issues. I argue -- many of these diseases are really responses to mold/fungus types. bakers brewers candida or aspergilluis . As stated a healtly baby will start off life HIGH in bifido longum... which uses the milk sugar...IF you dont have any bifido... conman sense -----> something else uses it.... Id be happy to pick through your stuff, as my many seems close..except no ADHD...

      many with European desent have mixed.....we are muts (like dogs) add in different genes alphas and betas some have just betas some just alpha some a set---which allows you to get celiac it also is the number 1 factor in auto immune diseases .. if you have a set , an alpha and beta and fun this is me HLA dq2.5 Trans you also dont have to have celiac antibodies tTG to be sick... some dont get damage on the villi... this is my case..I got sick but never got celiac diease ...I became intolerant , when your intolerant your thrown under the bus... because 99% of doctors have no clue or understand it.. let alone genes , bacteria and yeasts. The biggest Ass clown is your allergy office... and there testing

  3. > "lactose and the drinking of milk by entire populations of people without regard to the genetics of LP or LNP is most likely causing the MS we see in the world today, and possibly other autoimmune diseases"
    > "the drinking of fluid, pasteurized milk in quantities only seen since the 1800's has overridden the genetic ability of our immune system to use lactose as a signalling molecule, and we suggest that the lactose is the problem."

    It's important to search for examples that don't fit one's hypotheses. The Mongols don't fit neatly with these hypotheses. Their very low rates of MS despite heavy milk consumption and despite low rates of LP suggest that there's more to the effects of dairy on MS and health in general than lactose consumption and lactase persistence. Interestingly, they reportedly have high rates of vitamin D deficiency, which also doesn't fit neatly with current popular hypotheses.

    1. If lactose is an important factor in MS, then some possible factors that may account for the negligible rate of MS among Mongols could include not pasteurizing (instead consuming milk either raw or boiled), fermentation, seasonality and stage of pregnancy of the milked animals (see, not using modern hormones and antibiotics, using the milk of older and more varied species of animals, adding other foods like tea, salt, millet or butter to the milk (and historically, sometimes blood), and possibly other differences.

    2. "Species" should be "species and breeds" and by "older" I mean more ancient and/or less domesticated.

    3. @Paleo Phil

      Very true. My opinion is that it is not dairy per se, just the way it is used in Western populations nowadays.
      Plus that what Dr. Ayers commented below: "milk, adult gut flora (lacking beta-galactosidase) and persistence of lactase results in an immune response."

      I was wondering: when reading about ancestral traditions, have you ever come across any dietary recommendations for pregnant women related to milk/dairy intake? (One paper modelling MS causal cascade suggests that the first environmental trigger happens very early in life, close to the birth, possibly even in utero).
      But it probably does not help much, if the pasteurization and homogenation, not used by traditional societies, is a factor.

    4. Paleo Phil-------Their very low rates of MS despite heavy milk consumption and despite low rates of LP suggest that there's more to the effects of dairy on MS and health in general than lactose consumption and lactase persistence. Interestingly, they reportedly have high rates of vitamin D deficiency, which also doesn't fit neatly with current popular hypotheses.

      Now im sure they dont sit there and pasteurize there milk, they have low vit d levels..... Interestingly, they reportedly have high rates of vitamin D deficiency..

      So does that mean they have more cases of osteoporosis, generally all with low d have high osteoporosis , one is given high doses of vit d2 ( mold based aspergillus ) 50,000 IU when sick with disease and osteo. yet they never get better. Vitd2 lowers vitD3 levels.. Im sure Mongols get SUN.... and the raw milk they use breaks down the milk.. so theres real no comparison

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    8. Sorry for the deleted comments.

      @Gemma, Indeed I have come across recommendations by traditional societies and Weston Price / WAPF ( for milk/dairy for pregnancy, fertility, lactation, growth and development (including of young male herder-warriors), and even as medicinal therapeutics (my grandmother taught me about the traditional Irish remedy of milk with a bit of home-brewed whiskey aka poitin added -, spiritual aids/protection and as a food of the gods. The notion of dairy being the cause of disease is foreign to traditional pastoral societies (I'll bet that someone suggesting it to rural Mongols or Himba might be regarded as potentially crazy :) ).

      To understand dairy, it helps to look at not only lab studies and modern populations, but also some traditional pastoral societies, such as the Maasai, rural Irish (as recently as my grandparents' generation), Scottish Highlanders, Mongols, Turkic peoples, Samburu, Zulu, Tuareg, Kapsiki, Wodaabe, Dinka, Himba, Amhara, biblical Hebrews and so on. If you do, you'll discover common traditional dietary practices among peoples separated by great distances that have survived for millenia.

      I was rather surprised to learn some time ago about the low levels among Mongols of the phenotype connected to lactase persistence in Europeans, despite thousands of years of consuming dairy as a staple food and nonetheless drink some fresh unfermented milk daily during milking season, though perhaps they have another form of LP phenotype that hasn't been discovered yet. I was also surprised to learn that the Hadza have roughly 50% lactase persistence ( despite being thought to never have consumed dairy as a staple food (though perhaps they are descended from pastoralists). As so often is the case, things are much more complicated than they at first seem.

      @edward belschner, Correct, Mongol herders don't pasteurize their milk.

      The Mongolian rate of osteoporosis may be approaching that of the USA, based on an extrapolated estimate (

      Regarding the low rate of the LP phenotype among milk-drinking Mongols and Chinese, there was this hypothesis: "Some mechanisms other than lactase persistence may allow people to tolerate lactose, such as non-specific hydrolysis of the disaccharide. The lactase gene -13910T allele can not predict the lactase-persistence phenotype in north China" (

      However, the failure of hydrolyzed formula to prevent T1D that Gabriella Kadar reported suggests that explanation may also be missing something (such as the importance of microbes, perhaps?).

      Rather than wait for the scientists to figure it all out, I have tried various dairy products myself and found that I tolerate best the oldest, most traditional types (with a suprisingly wide range of effects and tastes within types).

    9. @Paleo Phil

      Thanks for the WAPF link, in fact I searched something a bit older. Never mind.

      "The notion of dairy being the cause of disease is foreign to traditional pastoral societies"

      I tend to agree and we should be asking why.

      "I was also surprised to learn that the Hadza have roughly 50% lactase persistence"

      OK, here some clarification. Hadza passed so called lactose tolerance test (LTT). But they were up to now not found to have any allele that would keep LP after weaning. Yet their gut flora was able to deal with the lactose load. Why? The authors speculate it is due to the enzymatic role of lactase enzyme, that serves not only in hydrolyzing the milk sugar, lactose, BUT other such bonds. The enzyme is in fact called "lactase-phlorizin hydrolase".

      Read this:

      "For example, our data showed that 47% of the Hadza, a Tanzanian hunter-gatherer population with no history of dairy production and with no known LP-associated variants, were classified as having the LP trait on the basis of the LTT. It is known that LPH, in addition to having lactase activity, has a second enzymatic activity at a different position—phlorizin hydrolase, which uses phlorizin as a substrate.9,52 Phlorizin is a bitter natural product found in bark, roots, and the stems of pear, apple, cherry, and other fruit trees that belong to the Rosaceae family and is present worldwide, including Tanzania, the homeland of the Hadza.52–55 Phlorizin has also been used as traditional medicine to treat fever and infectious diseases, particularly malaria.55,56 Hence, it is possible that the LPH activity in the Hadza hunter-gatherers might have been selected for a broader and more complex role than simply digesting lactose. However, further investigation of this hypothesis is needed."

    10. "Regarding the low rate of the LP phenotype among milk-drinking Mongols and Chinese, there was this hypothesis: "Some mechanisms other than lactase persistence may allow people to tolerate lactose, such as non-specific hydrolysis of the disaccharide. "

      I don't know what "non-specific hydrolysis" is. It is rather cared for gut flora that is able to hydrolyze lactose. Think Bifido, but not only.

      In an ideal case of LP person, you have your own lactase active and your gut flora ready to express lactase enzyme (the enzymatic system is called lactase operon, discovered in E. coli). As Dr. Ayers remarked, the genes are exchanged and the ability is shared among species. So the species don't matter much.

      And conversely, there maybe a genetically LNP person, with a backup gut flora, able to deal with lactose.

      But, both may be lost! The part of intestine that produced lactase enzyme may get damaged (think celiac etc.), and dysbiosis (antibiotics, infections) may cause loss of beneficial gut flora. That's a problem.

    11. "However, the failure of hydrolyzed formula to prevent T1D that Gabriella Kadar reported suggests that explanation may also be missing something (such as the importance of microbes, perhaps?)."

      There were theories that casein is responsible for T1D. This study followed a large group of infants, some fed with formula containing hydrolyzed casein, the other part had normal formula. The results were the same, the same number of T1D cases. So it seems that casein in milk is not responsible for T1D.

      It had nothing to do with hydrolyzed lactose, if you understood it that way.

    12. @Gemma, Yes, I do see that they hydrolyzed casein in the formula, rather than lactose, so that doesn't actually undercut this hypothesis re: milk-drinking Mongols and Northern Chinese after all. I think I provided the wrong link with it and now can't find where I got the full text:

      "Some mechanisms other than lactase persistence may allow people to tolerate lactose, such as non-specific hydrolysis of the disaccharide. The lactase gene -13910T allele can not predict the lactase-persistence phenotype in north China"

      Here's a link to the abstract:

      Perhaps the hydrolysis they are talking about could be due to gut flora like you suggest.

  4. Here are the traditional "FIVE KINDS OF FOOD" of the essentially MS-free Mongols:

    "White- diary products
    Red- Meat products
    Green - Plants and vegetable
    Yellow - Butter and oil
    Black - Water and distilled milk vodka [airag]"

  5. I have gone through a lot of the autoimmune diseases on your list and searched the literature to find out the protein of the tissue that is targeted by the antibodies diagnostic for the disease. Thus, the "autoantigen" targeted by celiac antibodies is tTG. It then makes sense that celiac is a risk factor for Hashimoto's thyroiditis and vitiligo, because tTG is also an autoantigen for those diseases. Celiac sets up the gut inflammation and Treg deficiency that is the basis for autoimmunity and the tTG is one of several dozen proteins that make good antigens. All of the proteins that interact with nucleic acids, i.e. nuclear proteins have the features (triplets of basic amino acids) needed to make good autoimmune antigens and I have found that many of the autoantigens for diseases listed are targeted by antibodies.

    The point I am making is that milk, adult gut flora (lacking beta-galactosidase) and persistence of lactase results in an immune response against some protein in the gut that is also present in the myelin sheaths of the brain. The antibodies produced in MS are anti-MOG and anti-MBP. The unusual modern condition that dramatically promotes autoimmune diseases is a gut flora that is inflammatory and causes Treg deficiencies. Most modern pharmaceuticals have the same side effects: they have antibiotic activities that kill gut bacteria, cause inflammation and reduce Tregs. Processed foods have the same effects. Allergies and food intolerance have related origins.

    Fortunately, most autoimmune diseases can be prevented or stopped by repairing gut microbiota.

    By the way, as you can see, all of the autoimmune diseases will be related to genes involved in inflammation, Treg production and antigen presentation (HLAs). I personally think that searching for personal genetic risks for autoimmune diseases is a waste of time, since that can all be avoided by diet, gut flora, sleep and exercise. Autoimmune diseases that run in families usually have nothing to do with family genes (don't fit expected genetic patterns) and everything to do with family diet and shared/inherited gut flora.

    1. I agree with you, autoimmune diseases has everything to do with family diet and similar gut flora. Circumstances, like the great depression (not being able to buy food) and WW2 (food shortages) will effect the mother's diet during pregnancy and pass any deficiencies onto her offspring.

      The BBC recently had a program called Back in Time for Dinner, where a family lived again in the 50's, 60's, 70's, etc. It was fascinating to see just how much the British social, cultural and eating patterns changed, how packaged foods were introduced. It made me realise how much my own eating pattern had changed without me realising it. Most of my food choices came out of packets, tins, etc. Not much fresh foods like my mother used to make with the limited choices she had.
      What did we know about gut bacteria and autoimmune diseases in the 50's? Nothing, if I'm a general example.

      Jo tB

    2. Dr. Art Ayers

      I disagree personally , YOU say --- I personally think that searching for personal genetic risks for autoimmune diseases is a waste of time, since that can all be avoided by diet, gut flora, sleep and exercise. Autoimmune diseases that run in families usually have nothing to do with family genes (don't fit expected genetic patterns) and everything to do with family diet and shared/inherited gut flora. I feel ones genes play with and how they deal with auto immune disease(due to bacteria and YEASTS) -- take HLA DQ genes take mine...

      some keys
      HLA-DQB1 Molecular analysis, 0201
      HLA-DQB1 Molecular analysis 0602
      HLA-DQB1 Molecular analysis 0302
      HLA-DQA1 Molecular analysis 0501
      HLA-DQA1 Molecular analysis 0505
      All three
      FUT2/card 15 genes defective RED mutated
      If you look at my alpha and betas you see the links to auto immune diseases.. I personally carry HLA DQ 2.5

      all in my family have had lupus , crohns colitis , IBS , tyroid problems migraines.. bad arthritus.. BAD sinus.. heart issues. Many multiple problems. Personally most of my genes -- that I have I track back to the side that had all these issues Italian side. When they got here they were fine.. and healthy. as time went on they all dropped off. The great grandparents had 8 kids and those kids each had 4 to 7 kids. You can follow diease down the line today. Yet all who stayed behind in italy both side of the original families -- all live to well in there 90's.. No one here.. They all drop dead in there mid 60's some as early as 50's all getting the above I listed. all falling apart......this started to happen to me at 38

      If one picks apart the diet of a mountain sheep harder in the mountains of rome or the eastern seaboard coast you dont see a diet even close to here( USA) a diet low in yeasts in many. My blood type is also type O most type O's are low in bifido... they also have more yeasts. and dont play well with yeasts. Crohns people tend to be low in bifido...and high in yeast.. If you have no bifido...milk doesnt playwell with you

      I became gluten intolerant after 1.5 months of MOLD based penicillin( yes this killed off good bacteria ), I also had sinus issues my whole life. after the antibotics for my dental crown my sinus got did my hemorrhoids.. I got colitis , then crohns with an abscess, lived my life before with hemorrhoids.. after waking up , and researching.. you will find products available here in the USA are not the same. Wheat is a animal of 42 chromosomes.. with a alpha chain that sticks to MY genes above. A lab made wheat which actually fungus likes.,.. why we see so much stem rust. research this. Europe blocks USA 42 wheat.. ALL of europe is 14 or 28 chromosome wheat. ALL 14 chromosome wheat has no alpha chain. Half of all 28 wheat is missing it as well. people naturally made 28 wheat by picking the best seeds. ALL corn and usa wheat is high in fungus and attracts fungus due to the clear GMO engineering to make it grow better in heat and water. Follow the FDA there using 14 chromosome wheat , EINKORN to pull its genes to try and make USA wheat prevent stem rust. (going on right NOW) Its old old school wheat has almost no stem RUST and no alpha chain. Drink a shitty USA milk product of High cassien which can easily convert to hackers are doing this now. Eat tons of soy products , you get your added aspergillus mold. Citric acid ..lab mold...vitd2 lab mold( aspergillus) corn syrup --aspergillus mold. Corn naturally attracts MOLD...look to the mexicans they cut the mold off and eat it.. breeding has changed corn as well.. in the past corn was not a solid color... of yellow.. they made a lab bullshit version to grow well and look pretty. Most of all crops are picked and stored in a large dam silo... sitting in high heat or wet damp drums..growing more mold which produce toxins

    3. in order to feed everyone.. more disease has been created. Not all people can handle added specific bacterias or molds added to food for shelf life. I got sick and heard every bull shit thing from my johns hopkins trained doctors. when I started to research.. reading actual studies. I quickly found out how clueless 90 percent of docs are. They can repair an organ or push a FDA pill...but cant tell you shit on genes.. let alone understand them. Bacteria or yeast... I smile when I hear my docs talk about antibiotics. If your sick for example--in the hospital your first drug in your IV today is ZYSON... look this up ....your a kid penicillin

      until I dig , modified things..downed yeast..upped bacteria ...reduced yeast. mold foods... I strangely got better. last year I visited the mountains of rome.. Looked at the grave markers and chatted with family. No one is sick there.... they live long

      Your statement """be avoided by diet, gut flora, sleep and exercise.""""" is somewhat right... The problem what doctors are trained in at the street level is out dated. My GI's told me what to eat... which thru gene testing and other means NON standard testing , I modified my yeast levels...bacteria levels etc , to an extent your right. ( but your forgetting yeast)

      These people made me SICKER.... today I have no crohns , no colitis , no ibs , no hemorrhoids, no migraines, I can eat gluten again... drink beer.. and ally my docs --trained by hopkins are lost.. At some point I will share my story at the head hospital and be a PIN cushion for testing. I KEEP my yeast low... and specific bacteria UP...I now have no problems. from what I found. Coming here to the USA killed my family it was due to genes and the food available.

      I eat Einkorn wheat now.. and drink europeon beer I limit my yeast intake --- I dont have a problem. I stay away from USA milk products,, and wheat. as well soy ( all brands or choices)

      Follow the foods in the BLUE zone of sardina -- other than wine grenache.. with some yeast , highest anti oxidant wine there diet is low in yeast. There milk is sheep and goat --unpasteurized If you follow wine , different wines in general are made in a different ferement process High wines they add back WILD yeasts...candida etc ... light whites and light reds lacto .bacteria to CUT the yeasts down drop the alcohol %. Look at foods... in Sardinia bread is flat bread no yeast or risen with bacteria. All foods that are healthy are a mix of lacto bacteria and yeast. kraut, cheese, wine, some beer REAL bread not store yeast risen bread ...a real starter is yeast and bacteria for several hours..

      Disease starts in the upper gut...In my case I never had good amounts of bifido ..which I say due to yeasts past down from my mother. I know for a fact she had lots of yeasts infections. My blood type and my genes played a role. I had intestinal problems at the start.. If you have low to no lacto bacteria and no have a rough start. antibiotics KILL the lacto in your upper gut where they should be living --I say fermenting with yeast to produce health. Bifido... as well. you see key examples of oxaltes and lacto /bifido. ALL mental people have high yeast levels....ADHD ... yeasts ,and over run bad bacteria ... soy milk dairy problems. or the add oxalte.

      I d be happy to chat with you , you seem to be an interesting bird :) I plan to do something interesting my im up to almost 4 years now perfect. I plan to re genetic test myself.. ( today my bacteria and yeast levels are completely different)

      in the future when I test ...If my genes flip... CARD15 /fut2 from red to yellow or GREEN... """""will call bullshit on current science""""".. and say yeasts play a larger role. with bacteria and gene expression. But this is a guess .. time will tell NO one has documented there life in disease as detailed in testing, as I have standard , genes, non standard etc , FOOD etc

    4. Art, they tried hypoallergenic baby formula to prevent type 1 diabetes. Doesn't work.

  6. Replies
    1. Gemma

      Yes ........too me a double edged sword I say.... the milk is RAW -- the sheep or goat.. you also have bacteria to break it down... THE bacteria<--- and enzymes.. why i say its low in yeast. because the bacteria most likely work with the yeast breaking down. to me no different then bread.. or all fermented food

      take some store MILK--- with VIT D2 pasteurized (aspergillus mold added in) as well inject the MS person with 50,000IU of D2 Im pretty sure they would NOT get better... studies already prove D2 isnt helping anyone

      Its a JOINT effort -- bacteria-- breaking and working with yeast. All this stuff is really based on COW milk and pasteurized milk D2 fortified people fight about theres no acturate basis to me

      Read your study ----> total of """6 genera""" and 15 species of fungi. Among the 6 identified genera Geotrichum spp., Candida spp., Phaeosphaeriopsis spp., Pestalotiopsis spp. and Cladosporium spp. belong to the phylum of Ascomycota, while Cryptococcus spp. is part of the phylum of Basidiomycota. In particular, two genera (Pestalotiopsis and Phaeosphaeriopsis) and two species (Plectosphaerella cucumerina and Pryceomyces carsonii) have never been reported in dairy ecosystems before. Results provide evidence that several moulds and yeasts, previously described only in ovine cheeses, are transferred directly from raw milk.

      I would bet , bacteria work with these...and MAKE a healthy product.. my relatives in italy eat cheese and some milk.. not COW.. they use there own starter for bread.. and not 42 USA wheat..

      SO back to yeasts...theres value in yeasts..I ate a diet low in yeasts and MOLDS to gain my life back.. But I say loosing my life --was due to ASPERGILLUS molds added to food.. you dont see this listed above. its added to all foods , soy, cirtric acid. drinks and VITd2 --- it grows on CORN and wheat.. and is used to make corn syrup. Yeasts seem to control and regulate cholesterol. When one looses all good bacteria-- the natural candida yeasts goes wild..making you sick. you need yeast in your body. What im saying I should be more clear -- is removing many products with aspergillus and created yeasts. As well products that have no bacteria that break yeasts down. Most of the yeasts in foods now are added MOLD..from a lab. Ive had sick people around me for years.. watching them crumble apart. currently I have a friend falling she gets 50,000IU weekly I ve watched her also get sicker..Not the first example.

      again real products real bacteria and real yeasts....working handed to hand we see this in healthly people and SARDINA is a good example. ASPERGILLUS following the trail I say

    2. as well..... your adding LAB created aspergillus mold to food.....the food doesnt rot or grow mold on it...

      I wonder what it does in your stomach....Im sure it doesnt DIE if it makes food last 1 year

    3. Also for Gemma

      Look at the bacteria ....and yeast forming bread(jointly here--read the yeast and bacteria.... Heres a good link you see sardina as well... SOUR-DOUGH KEY bacteria and YEASTs,,,

      here you see many of the same bacteria---> Evolution and identification of lactic acid bacteria isolated during the ripening of Sardinian sausages

      Raw milk cheese....has yeasts BUT raw-milk Pecorino cheese example sardina is HIGH in a heterogeneous lactic acid bacteria population, which includes strains with metabolic characteristics of technological interest

      A cheese link... It may also be...when you pasteurize MILK...your killing yeasts and bacteria --- you ll see a note in this article These white molds produce enzymes that break down the milk proteins of the curds,

      with the presence of LACTIC ACID bateria during fermentation---the maxium growth rate of yeast is REDUCED...<-----------------
      BUT with --------> no effect of final cell counts .. *************ethanol is decreased yeast ferementation here favors production of mannitol and acetic acid by lactic acid bacteria<------

    4. the line ---deals with bread( sour dough) Sardinia
      Pecorino Romano is More Than Good for the Heart

      Generally, Italian foods are thought to be healthy. Sardinia’s very own Pecorino Romano cheese is no different. Made from"""" sheep or lambs"""milk, it has been revealed to be some sort of a wonder Italian food that is effective in keeping people in tip top shape and in preventing a host of illnesses.<------------------------------

      Compared to cow’s cheeses, Pecorino Romano cheeses contain 3-5 times higher amount of CLA which validates the team’s study that regular consumption of Pecorino Romano cheese contributes a set of bioactive elements capable of doing the following: a.) Considerably lower the risk of acquiring cardiovascular diseases and b.) Enhance the immune system

      (Sardinia – Italy) in cooperation with a team of doctors from the United States, it has been confirmed that Pecorino cheeses contain high levels of Conjugated Linoleic Acid (CLA) and Omega-6 polyunsaturated fatty acid naturally found in certain food groups and which shows bioactive properties for humans.

      Why I point to COWs milk...and trash(USA milk d2 mold --cassien) being sold as to adding to MS...
      Gemmas yeast points to it( better yeasts) ... My bacteria and both playing together ( in a role ) good yeasts and bacteria.....I still point to genes in there relation to specific MOLDs in many immune diseases. Science has chased bacteria for 40 years now.. and people are sicker. more antibiotics and more lab created molds

    5. Sardinia is a Blue Zone, but isn't it also an MS Hot Zone?

    6. Anonymous

      that would really be interesting if so :) then they have one of the highest longevity living cycles ...but HIGH MS... maybe those that have defects...the very yeast destroys them due to defects in genes or a Band yeast/fungus getting into the milk or products made

      from Gemmas link ---- """"""""The relationship between intestinal fungi and bacteria is not well understood."""""""""

      One study reported a correlation between intestinal fungi and bacteria, such as Prevotella and Bacteroides46 Candida species have been shown to induce production of carbohydrates, which subsequently reduce the ratio of Bacteroides.46 In our study, although both C. kefyr and S. cerevisiae increased the proportion of Lactobacillus species, Saccharomyces species did not reduce the ratio of Bacteroides (data not shown). Thus, C. kefyr may have significant effects on the Bacteroides ratio through a mechanism that is distinct from that of S. cerevisiae.

      In conclusion, C. kefyr decreased the ratio of Bacteroides and the production of IL-6 in the intestines, which contributed in part to the induction of regulatory dendritic cells and the suppression of EAE. Therefore, modulation of microflora by dietary yeasts may be an option to prevent and treat MS. <------------------------------- NOW he knowledge of fungal consortia inhabiting sheep raw milk is a particularly relevant issue because several species are directly involved in cheese making and ripening, determining the typical aroma. On the other hand, spoilage yeasts and molds are involved in anomalous fermentation of cheese and may be responsible for considerable economic losses and-----> serious risks for consumers' health which maybe why many benefit in the blue zone of Sardinia--LACTOS and yeast ... then also such high MS --bad strains getting in of mold giving MS --- why I point back to soy,cassien and gluten( simular to molds/yeasts

      For my self , getting sick.. I find it odd I had high AMCA...most with immune disease will have ASCA high or AMCA high.. ASCA --equals brewers yeast or bakers yeasts-- Saccharomyces species AMCA --candida / I believe aspergillus falls here as well. In advanced testing nothing you get at an allergy office or hospital in my blood I had problems with l levels reported with responses to yeast and lactoglobulin, milk dairy , apples , collard greens and buck wheat. the last two (collard and buckwheat Im lost) apples..are high in arbinose --which yeast produce. milk and dairy cassien --converts to yeast Here you can see phosphate linkage in casien , soy ,yeasts and lactoglobulin in this link For me as shit failed I got osteoparsis the last thing im working on fixing...Ive taken no (D2 injections ) and have not increased my calcium. As I feel they feed yeast.. so far all areas that use to hurt are fine... I test again later this year. In OAT pee testing my bone metabolites have increased...(phosphoric) from 1035 to 1702 Normal range 1000-4900 I predict even high this year

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    8. Now in fecal gut testing... nothing again you can get at the hospital or local lab...I had super high markers for GLUTEN and SOY... milk just above normal but high also high.. and CORN high... and these products are loaded with or can have bad fungus strains growing on them or in them. I didnt have MS but at my worst part I had shaking hands... and nerves firing. Both my mom dead...67 and grandmother... 68 dead.. both had bad arthritis and neurological issues. As well colitis , migraines sleeping problems... and tyroid issues. For myself... once I got a handle or removing things... lowering what ever it was candida or aspergillus building up good bacteria..a large break form several foods my immune system has RESET... and several foods do not bother me. One thou that does SOY sauce..which is aspergillus mold. I mainly stay away from citirc acid and aspergillus well as any fortified food with d2

    9. Yes, the link with high MS rates and Sardinia is present. It is rather interesting. It was discussed some in Part 3 of this series, but the map is a little blurry. It was also discussed in the comments section of the Magic Mushrooms . Here is one older study, but there are many available :

      Multiple sclerosis epidemiology in Sardinia: evidence for a true increasing risk.

      Repeated epidemiological assessments of MS in Sardinia over decades have shown that the island is at high risk for MS. The present work highlights that MS incidence in Sardinia has been increasing over time. Although a substantial and widely spread improvement in MS case ascertainment can be postulated as the reason for such observations, a comparison between our data and those recently reported from a more industrialized province in Northern Italy seems to prove an at least partially real increase in MS risk among Sardinians and favours the hypothesis of a MS "Sardinian focus" as related to its latitude

    10. So what did you eat to regain your health?

    11. what I did....from using different tests first remove things that responded to my testing ...gut fecal , oat (pee) Amgut, U biome, Ibd expanded panel blood test. formulated a diet from my results.. -- which ended in all low starch veggies.. fish, chicken pork, lamb , buffalo and cow. as well all other seafood.. I then used products to lower yeast.. olive leaf..oil of oregano , grapefruit seed extract pau d'arco tea..and many others .. Worked first on sinus. as most have yeast/fungus in the sinus even thou the ENT is clue less. (Ive seen 5 in 38 years-- same speech same non working protocol. You re infect your gut. over time I worked on both sinus and gut. Then heavy on the gut. as time went I added many different lacto strains.. as well bifido.. I did no soil based SBO's (personally I think all the magic starts in the upper gut-- between YEAST and bacteria. If you read most lacto lives in the upper gut...The first to die from poor eating or antibiotics. Yeast also live here. loose the balance yeast spread.. loose the bacteria lacto.. other cridders crawl up and move in. (hence acid reflux and problems indigestion in my eyes. Yeast can move on and live all the way to your anus..aka hemorrhoids.. look at a baby- you put zinc cream on there ass. If you get a polyp in your nose --the ENT actually sites yeast. If you get one in your Gi...tract (its the fault of red meat.) per the medical experts. Personally for my case i cant say all....most vitamins probiotics , yogurt kefir etc have milk, soy or gluten in them... A key I found..I need probiotics and vitamins free of all three. after 2 years of adding several strains building up I was able again eat foods that bugged me. I could go on and write a book..but there no room for detail in a short paragraph. Be happy to supply the many photos I took of what happen to me in stages...stool...eyes... hands... toe nails... skin color , crap from nose..lung and ears.. All checked by GI , ENT and regular docs before hand as normal. I was also loosing my hearing,,, all normal now.

      food can resemble bacteria or yeast from my testing.. as well many products /vitamins or probiotics have things your immune system may be ramped up to.

    12. Good stuff, Eddie - Keep talking! It's great that you do these type posts so we can look back at them as you progress in your journey. I can't wait until you get enough data collected to get your doctors to listen to you.

      Point to make, you were not just randomly adding and removing foods, you were doing so based on tests and symptoms.

      Good job!

    13. Yes... I formulated my diet based on my results...Not just blood... but gut stool fecal testing <-----fecal stool blood I tested IGE allergy office was a complete waste of time for me prick test and cap raast. I even drank lactose All came back negative. Yet when I drank the lactose scores were normal but lips tingled. All Ige both caprast and prick were normal. The allergy lady said I was crazy.. and to make a food chart .I said F&Ckyou :) you people are crazy. She said make a chart as to what bugs you. I said How I do know not all seem to bug me and it could be delayed. I moved on to ELSIA/ACT bio here I got more answers some call this bull shit... I dont because it helped. pin point things I then also did Greatplans lab OAT then stool of the best ---->stool ... I took charge and became my own doc...My local doc came on board and let me run the show. I quickly saw results. I then ran my Amgut.. laid all results on a table and came to conclusions linking all sides. You can have your gut(stomach), your blood-- several different antibodies not just antibodies IgE, sinus (think ENT ear nose and throat) as well lungs and gut me stomach and GI are different. I began to system ly work on each area. Reading studies ...looked at my APO type...blood type .. what kinds of bacteria I had living in me.. how many bad types from RNA testing Ubiome and Amgut.. as well the cultures from great plans. I quickly found how worthless local hospital and lab testing was. I used the OAT pee test from great plans, and stool to look at yeasts... micro yeasts. I ran my 23andme. got my genetics , took over to genetic genie and mthr report and picked them apart..Figuring out all defects. I Ran IBD panels and IBD expanded panels from labcorp and HLA -DQ gene tests for gluten. Laying it all out-- massive defects with FUT2/card15 all three genes RED ....Several gluten genes alpha and beta ...Type O blood, No bifido ... bad bacteria overloaded and extremely high yeasts .. Type O and card15/ fut2 dont play nice with yeasts. Or do gluten genes. For myself I found yeasts/fungus , most likely in the way aspergillus or candida activate and """"express""" my genes (gluten and card15) As time went on I retested many of these tests. I had large amounts of micro yeasts...which then dropped off. My diet was very limited as I tested. To this day I eat a regulated diet. As I continually test. (4 years now) My Doc is lost , yet amazed. I have no crohns no ass problems (HAHAH) or sinus... joint ,headaches great sleep... good general blood work etc -- I cardiac calcium scored last year was a (1) in one area , also had neck and chest ultra sounded clear... Hearing checked and fine now. ENT also lost. my nose would always randomly blood the first 38 years of my life. same with my ass (hemmroids ) gone.... I carry genes that predispose me to auto immune disease.. I dont harp... getting sick like the rest in my family was the best thing that happen to me. It allowed my to track there history dating back to 1900. and to pick my self apart. I also have longevity genes...many I belive in epi-genetics as things flip and express genes. Just because you have bad genes from your parents doesnt mean your going to have what your family had -- as you can alter or take a different path.. to keep the switch off. This is what I have done. In the end I hope to prove , by changing your bacteria and YEAST make up.. changes your genes(exression).. as seen in your breakout report from genetic genie or mtthr report. I will roll the dice and say many of my card15/fut2 RED mutated genes will flip yellow or green... If so I have something for science to see.

    14. I point to some sort of yeast -- mixing in and altering my genes <--- this is just my theory. You need yeast in your system as well bacteria. But no one knows what kind of yeast or fungus or HOW MUCH-- like food some are good and some produce sickness and waste of products when making..No different then food production. If one looks at the liver , you can see yeasts /fungus control cholesterol. If you slice your arm open.. its role CHOLESTEROL is to go to the site of the wound. What amazes me put sugar on a open cut. or honey it will quickly clot. outside of the USA they use specific honey for burn wounds. Ive cut myself and played with this(yes im a little nutty). If you have surgery get your cholestrol checked before hand. Then after it you will see a rise(but get the NMR lipo profile which looks at particles) Science has only to begin.. I wonder if reallly ones blood type is really determined by the type of yeast one has. Crohns people tend to have no bifido and other specfic bacteria. yet they also high higher amounts of yeast. Right now theres studies going on...where they have changed blood type by using bacteria.

      I have crazy photos of my EYE,,, hands etc as I lowered my internal yeasts my hands between my fingers turned red. All areas where I had osteoparsis hurt...when I added antifungal drugs. something I documented and lost my doctor. What also interests me is almost anyone who has surgery, in an area dealing with joints ligaments and bone later gets arthritis<------- playing sports Ive had right knee surgery football and left ankle basketball.. The ankle ligaments and bone chip. When I took antifungals the chip site hurt. If any area get any pain I put magnesium oil...or nizarol cream on instant success.. So it begs me to wonder the role of yeast in wound healing. and surgery location site once cut open. as well see everyone getting arthritis

      In all of the thousands I have spent ,I also tracked my cholesterol but in advanced testing of particles NMR lipo profile. When I was sick my cholesterol was lower 155 total at my sickest point. Today healthy and fine 221 total..<--- but OH my some say this is bad. But if you look at my break out my HDL is in the upper 60's my small LDLp is low. but my total LDL particles are high.. As I got better and felt better my total LDL particles keep going up. Experts in cardio have two sides.. some say low small LDL-P is the choice .....while others say total LDL particles should be low. then you have some small LDL p should be low and total LDL particles low. What has happen to me is my small LDL-P dropped low.. insulin resistance is low. and my total LDL particles shot up high way over the so called limit.

      Now testing 6 months ago.. I added almond milk with chalk in it..and D2 made from mold. as I drank it.. my small -LDL P rose up and up , the higher the small LDL-p the higher chance of heart disease and heart attack. 6 months later.. later in the summer I test again. I already know what the results will be... lower small-LDL p SILK alond milk is chalk<-- almonds , vanilla bean and d2 (aspergillus mold) which contributes to heart disease

  7. Replies
    1. LOL

      Have you finished reading about Gamma delta T-cells, Tim?

    2. Shhhhhh! You are giving away the plot of Part 13!

  8. Mike from SarasotaMay 12, 2015 at 5:02 PM

    Really fascinating stuff. My father has MS, my mother has Hashimoto's and I have RA and Hashimoto's. We were never a huge dairy household as both my father and I also have asthma which it aggravated. My mother still consumes it to this day, my father very sparingly and except the occasional serving of ghee I've had none in the last 10 years. I've spent so much time researching Autoimmune diseases and it seems like the more I read the more confused I end up.

    Curious as to how much, if any, dairy Tim, Gemma and Gabriella consume?

    1. Interesting, Mike. That's quite a cluster of auto-immune issues! I've read that AI hits something like 5-8% of the population, so an entire family should be eye-opening. And once it afflicts you, it seems nearly impossible to shake.

      Not sure if diet will ever cure some AI's though others may respond. To me, research needs to focus on mass prevention rather than targeted cures.

      I don't drink milk, never have. Hated it in school and my Mom tired of trying to make me drink it by about age 8 or 9. I eat cheese most every day, yogurt several times per week, sour cream every now and then. I use butter for cooking occasionally.

    2. Mike, I don't think it's relevent, but I'm viciously lactose intolerant. So I put lactose free in my tea. I can eat well fermented yoghurt (I buy a tub of live culture and leave it in the fridge unopened for a couple of weeks). Hard cheese is okay.

      I tried the 'eat yoghurt or kefir' every day and see what happens..... nothing. Still lactose intolerant. I can't drink even 200 ml regular milk evert day and get away with it. Three days is the limit.

      My kids can put milk in their coffee but other than that they eat yoghurt and kefir. The whole family is lactose intolerant. Most of my cousins as well.

      For whatever reason, one of my cousins was born lactose intolerant. She was raised on buttermilk. I don't know the details of what my aunt had to do with the buttermilk, add sugar or what. Dilute it a bit? Don't know.

      There are families in eastern Finland who have this genetic 'flaw'. They cope. We're not Finnish though, so ??? who knows.

    3. Mike, it seems what's important is 'where someone has lived' for the first 15 years......I think it's more like what they drank if it was fluid milk.

      Wahls' protocol is interesting that she eliminates all dairy, eggs and grains. I think she may be overshooting on eliminating all dairy. She doesn't like eggs so that's not a big deal for her. I don't like that she eliminates potatoes. Daily megadoses of vegetables: at least she can poop (maybe).

    4. @Mike from Sarasota

      I only learned about the milk and autoimmunity connection from Gabriella a month ago.

      But I do not thank it changes my attitude to dairy, which is: yogurt, kefir often (daily), goat kefir from a nearby farmer. Raw cow milk from another nearby farmer. Not pasteurized, not homogenized, though cooled. I put it in my coffee, though sometimes I do have a warm cup of milk with honey, or occasionally some golden milk (boiled milk + turmeric + black pepper + honey). Butter. Various cheeses, preferably from unpasteurized milk (= imported Italian, Swiss). I make my own sour cream, and ghee for cooking. I really, really should make my own kefir.

      But not that you think I live on dairy only. More vegetables etc.

    5. @Mike
      I am a highly functional (I, think!) RA sufferer. I drive myself crazy with the amount of reading I do on autoimmune disease. So I am right there with you in being confused. What haven't I tried!

      The only milk I drink is the homemade kefir I make. And I do eat cheese occasionally but I try to buy goat, sheep or unpasteurized cow. I have been using coconut milk for everything else. I buy it by the case from import It is preservative free. The cans you find in Asian grocery stores all contain preservatives.

      Exercise (and yoga) have been my saving grace. Maybe it's the endorphins! I eat about as natural as one can but have only been able to keep my RA contained. Am well aware it's with me, though!

    6. Mike,,,

      What are your genes.....

      DQ2.5 and the linked DR3 are associated with probably the greatest frequency of autoimmune occurrence relative to any other haplotypes. The haplotype is positively associated with coeliac disease, dermatitis herpetiformis, juvenile diabetes, Lambert-Eaton myasthenic syndrome (LEMS), Sjögren's syndrome, and autoimmune hepatitis (although significant proportion of the risk is secondary to coeliac disease). DR3 and/or ***********DQ2.5******** are linked to the following diseases: Moreen's ulceration,[5] "bout onset" multiple sclerosis,[6] Grave's disease[7] and systemic lupus erythematosus.[8

      HLA dq 2.5 ----> has arthritis link

      fungus has been linked to thyroid diease People with Hashimoto thyroiditis have an increased risk of developing other autoimmune disorders, including vitiligo, rheumatoid arthritis, Addison disease, type 1 diabetes, """""""multiple sclerosis""""", and pernicious anemia. many also link to fungus Variations in several genes have been studied as possible risk factors for Hashimoto thyroiditis. Some of these genes are part of a family called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders (such as viruses and bacteria)

      Gluten-free diet

      Preliminary studies have suggested a correlation between Hashimoto's thyroiditis and celiac disease.<--------------- where your back up to the genes HLA DQ 2 -- and above you see HLA DQ 2.5 worst possible mix

      90 celiac patients, which found that thyroid-related serum antibodies tended to reduce during a gluten-free diet ... Soy , cassien (milk) and gluten are similar in aspects of molds/yeasts

    7. Eddie - You may not be crazy after all! A recent study shows that 25% of people's genes "flip" between summer and winter, explaining why people get sick less in summer and gain weight in winter among other things. These epigenetic changes were once thought to be impossible, but now we are seeing they are common-place. I hope your gene testing shows you made some positive changes!

      I have not yet seen the full study, but here is one of many articles popping up:

    8. That has interesting implications for many of these studies and tests. Now, you need to track what season the study was done in.

      This was from NPR for those who prefer an audio review LOL.


    9. Wow, that's fascinating! I'm going to have a lot of fun with that rabbit hole. Thanks Tim.

    10. And think about ---what makes your immune system change other then the general cold<-----.... pollen --->seasonal , mold---> seasonal two large factors and there piles of medicines in the pharmacy --wow imagine--ones asthma UP ticks in these times...

      Why not food as they add molds etc for shelf life ...this is what ive seen in my self.. then think -------->********Lower levels of aspergillus molds in celiac patients blood while following a yeast free diet specifically avoiding bakers and brewers yeast has shown lowered gluten sensitivity disease activity

      Ergosterol which ( D2) is made from... is an irritant to respiratory tract. Ingestion of large amounts can cause hypercalcemia Vitd2 is made from MOLD -----in a lab ergosterol. Also ---bacteria Protozoa as well.....uses ergosterol. """"vitD3""" is made mostly from lanolin
      a sterol, C 30 H 50 O, formed from squalene epoxide, that is a precursor in the biosynthesis of --->cholesterol and is a component of lanolin
      lanosterol under enzyme catalysis leads to the core structure of steroids. 14-Demethylation of lanosterol by CYP51 eventually yields cholesterol

      Vit D2 given to most with health problems is made from Ergosterol is a sterol found in cell membranes of fungi and protozoa, serving many of the same functions that cholesterol serves in animal cells.many fungi and protozoa cannot survive without ergosterol

      Vit d is import but from SUN light --D3 which makes you WONDER if in its natural form Sun its drawing in and converting to a natural STEROID to lower inflammation

      vit d2 vitamin D2 is less well absorbed and utilized by the body, and it also interferes with, and actually reduces, levels of circulating D3 in the body. This conclusion is confirmed again by a very recent study released in February of 2014. But this study added one further bit of bad news when it was revealed that vitamin D2 was also linked to causing muscle damage after intense exercise. D2, while it did not cause the muscle damage that the last study discussed did, it still reduced blood levels of D3 and offered no benefits.
      poor bioavailability and potential toxicity are not enough to scare you off of vitamin D2, consider also that double blind, placebo controlled studies have found that taking D2 actually lowers blood levels of D3.

    11. Protozoa, including Trichomonas and Leishmania are inhibited by drugs that target ergosterol synthesis and function
      lyme disease is a ----->protozoa all with it loose VIT D and are given D2 yet dont get better

    12. Gabriella Kadar @<------

      your lactose intolerant *** how do you know you dont have a problem with cassien as well or lactalbumin or lactoglobulin theres more things in MILK

      do you even know what bacteria you have or have you done any yeast tests. I used this test for foods..... out all gave me the most....

      Give you an example... when I was sick..I thought like you. eat more yogurt.(i need the probiotic effect). I made my own.. from a yogumart machine. 1 billion good bacteria right .. I ate every day.. felt fine I thought. When I did this test . It showed I had problems with lactalbumin , lactoglobulin ,apples and ,yeasts .Many fruits have wild yeasts ...some more then others or some HIGH amounts --certain fruits are high in arbinose which Yeasts can produce.... I tossed the yogurt and went to dairy free probiotic pills ( RENEW LIFE 50 billion) soy free gluten free. I did this test I plan to do again next month after first doing it 3 years ago(after 3 years changing my flora yeast and bacteria--I will guess it will be different). Once your system resets , many foods can be brought back in like a baby first learning to eat. (Some call this test bullshit) but it helped me better then the allergy office .. This round I plan to zoom in more the test above and (all yeasts and molds ) my guess aspergillus will come back for me and penicillium.

      many with penicillan allergry cant do EGGS aspergillus is in many foods (added citric acid) soy sauce and corn syrup . most foods addivites for shelf live have bacillus or aspergillus loaded in them

      I can eat eggs....but not dairy soy sauce KILLS me , its loaded with aspergillus .. I cant eat chocolate or a KINDbar with soy lecthin in it. no problem. Most dont realize soy is loaded in foods as well. the molds test I will do

    13. I meant 1 trillion not billion in making my own yogurt

    14. eddie I eat very little yoghurt. Not a regular dairy consumer except for the lactose free in the tea. Some sour cream occasionally. Rarely eat cheese although I did for a few days recently because my daughter brought some over. I make kefir but other people drink it. I'll have a few sips now and then, that's all I don't notice anything adverse happening from any of this stuff.

      But regular milk is a no no. Cream cheese is a partial no no depending.

      I used Gemma's recipe for 'golden milk' but instead cooked the turmeric and black pepper into a paste. Added a bit of honey and mixed it into yoghurt instead. (added some low sugar cranberry sauce and it was great. Too good. ;( Ate two bowlsful.....Maybe I have a weird 'taste' but it was awesome.)

    15. gabriella kadar,

      look toward your genes.(I ll help you here).... do you consume soy??? how much wheat.. what type of wheat USA wheat??? 42 chromosome wheat..There all not the same....having many gluten genes.I personally laugh now at the gluten FREE crazy. try 14 wheat...EINKORN. I noticed nothing from butter...kefir ,or yogurt but my test results said other wise.. (for blood)

      When I got sick...i headed to the hippy store and started buying gluten free. What I noticed was its all just rice, potato ,soy and dairy...your just screwing your in a different way. Many of these are similar ( close ) You may feel better eating gluten free.....BUT ONE never fixes the issues -broken gut with intolerance or celiac. Why I say it not the gluten per say. Yes it adds to the problem and is easly seen. Having the worst gluten genes and having intolerance happen first hand.....I got to experience what people say....but then others piled on SOY dairy then starch problems. Today I can eat gluten and even the worst crappy USA wheat.. I can eat dairy with no issues but im in the process of testing to prove and document no more issues, Soy, I ll never eat again

      Do you have your genetic file( raw data) ??? have you run genetic genie...mtthr report and promethous ???? Look to these to find your HLA DQ and HLA DR links... whats your blood type ????

  9. Mike

    buy some ketoconzole antifungal cream rub it on your arthritis area ...give it a try

  10. antifungal drugs

    Amphotericin B, an antifungal drug, targets ergosterol.<-------------------------It binds physically to ergosterol within the membrane, thus creating a polar pore in fungal membranes. This causes ions (predominantly potassium and protons) and other molecules to leak out, which will kill the cell

    Miconazole, itraconazole, and clotrimazole
    work in a different way, inhibiting synthesis of ergosterol from lanosterol Ergosterol is a smaller molecule than lanosterol; it is synthesized by combining two molecules of farnesyl pyrophosphate, a 15-carbon-long terpenoid, into lanosterol, which has 30 carbons. Then, two methyl groups are removed, making ergosterol. The "azole" class of antifungal agents inhibit the enzyme that performs these demethylation steps in the biosynthetic pathway between lanosterol and ergosterol.[citation needed]

  11. Hey all, um, how is lactose getting to the large intestine of a lactase persistent individual? Lactose would be well digested by the time it reaches the large intestine, no? That is probably why researchers have summarily dismissed lactose as any causative agent.

    I suppose your answer is going to be milk drinkers are overwhelming their body's ability to generate sufficient LPF? Any data to support that contention? If I drink 4 oz of milk, how much, if any, lactose reaches the large intestine? What if I drink 16 oz? I'd think there would be data on how much lactose a human can metabolize at a time. Or maybe not since lactase persistence is particularly human-specific, and measuring the amount of lactose reaching the large intestine doesn't sound at all like an easy thing to accomplish?

    I suppose one last parting thought is that even if this hypothesis is true, there are millions of milk drinkers without ALS. Milk might be necessary, but certainly is not sufficient. I'm not giving up milk if I am over 30 (OK, I am... :) ) and otherwise without health problems. For children, I might choose to go easy on their milk consumption -- hey it's not water -- but to give it up in whole or in part because of a 2.2 per 100,000 risk factor?? Smoking, milk ain't.

    Best Regards.

    1. Allan, probaby add type 1 diabetes to it as well. Depending on which population you are looking at as to risk. It's only 2.2 per 100,000 in India. And that's the whole country. It's about 55 per 100,000 in northwestern India although probably under-reported. And it's significantly higher than that in Scandinavian countries. 203/100,000 in Norway. Anyone with their ancestry in Scotland, England, Ireland, Germany, Scandinavia is at much higher risk.

    2. Just my 2 cents...

      It's hard for me to make any recommendations on milk drinking, but it does truly appear that milk is behind MS and many other AI diseases. Why is not every milk drinker affected? Who knows? But if this connection is eventually proven beyond a shadow of a doubt, you can bet there will be high-level recommendations for certain people to avoid lactose, just as they have recently banned baby aspirin due to only a few cases of Reye's Syndrome.

      Maybe the deciding factor of who gets MS or AI disease is related to the condition of the gut/gut bacteria. We'll touch on this Friday in part 5. More than likely it's not so much that milk is evil and will cause you harm, the point of this was to show the connection of lactose/lactose persistence genes/and MS. As we dug into this idea, we quickly realized we were looking at something huge, and as this post's title implies, a very deep and twisting rabbit hole.

      So, what happens if it's proven that milk causes MS when folks have dysbiotic guts? Do we ban milk or fix guts? It's probably safe to say that a large percentage of babies have dysbiotic guts due to antibiotics and formula, then low fiber foods. Does that make milk safe for most babies?

      I know if I suddenly became a new father, I'd think very hard before giving li'l Tatertot any milk. But cheese, yogurt, kefir all would be on the menu regularly.

    3. I didn't follow the links to double-ckeck, but Wikipedia quotes the following incidence rates:

      "In Europe, the disease affects about 2.2 people per 100,000 per year.[5] In the United States, more than 5,600 are diagnosed every year and up to 30,000 Americans are currently affected [OK, out of 330M & assuming 70%(?) are caucasian, that is ~13:100k -af]. ALS is responsible for two deaths per 100,000 people per year.[82]"

      2-10 per 100k is a personal "meh" as far as a risk factor influencing my behavior. 200 per 100k, granted, has more of my attention. Anyway, it was just my parting thought, especially as regards the inevitable dairy-scare. (sigh, what's bacon, butter, & coffee this week? :) ) I certainly don't want to come across as taking away from the importance of the new hypothesis, if true. I know finding the cause for ALS is one of medicine's holy grails.

      As for T1D, I thought celiac's was virtually off the charts for co-morbidity? To me, that points more in the direction of wheat than milk, unless of course lactose-intolerance is doubly-so for co-morbidity? I don't know.

      But, alas, through entirely my own fault we have digressed… how does lactose even get to the large intestine of a LPF producing individual? (Apologies if it's been covered and I missed it.)

    4. @Allan

      "Hey all, um, how is lactose getting to the large intestine of a lactase persistent individual?"

      So much was written in Parts 1-4, and we probably did a bad job, and probably did not stress this enough. The lactose metabolism may be compromised. MS follows a certain causal cascade, and the idea was that compromised lactose status plays a role, that it is one of the necessary triggers. One has to be extremely unlucky to get MS.

      "I suppose one last parting thought is that even if this hypothesis is true, there are millions of milk drinkers without ALS."

      Are you talking ALS or MS? These posts talk MS since there is enough data to connect some dots.

      "That is probably why researchers have summarily dismissed lactose as any causative agent"

      Have I missed anything? What do you mean?

      "For children, I might choose to go easy on their milk consumption"

      This is my personal guess: it is not the milk consumption per se. It may well be the modern form of pasteurized milk consumption, and/or without balance of naturally fermented dairy.

      I am purposefully neglecting all the other stuff we might mention re modern way of milk production and consumption: cows hybridized so that they give milk even in high state of pregnancy, availability of milk the whole year round, all the hormone and miRNA signalling, stem cells passed via milk, al that... but it would just get too complex.

    5. Thanks for the clarifications Gemma.

      RE: ALS vs. MS. Ops, yeah, my bad. Long story on why I have a tendency to get those two crossed.

      RE: "That is probably why researchers have summarily dismissed lactose as any causative agent" That was my take-away from the section "Is milk a suspect in multiple sclerosis?" Perhaps too much inference on my part.

      RE: "purposefully neglecting all the other stuff we might mention" Yeah, the classic problem with science, every question answered results in three to five more asked.

      Finally, I ended up re-reading the last couple sections and the case for lactose made a little bit more sense to me, especially the molecular mimicry.

    6. Allan and Gabriella,

      My genes and all this hoot I talk about.... I have many longevity genes.. -but many gluten alpha and beta genes
      DQ2 (DQA1 0501/0505,DQB1 02XX)

      HLA-DQB1 Molecular analysis, 0201
      HLA-DQB1 Molecular analysis 0602
      HLA-DQB1 Molecular analysis 0302

      HLA-DQA1 Molecular analysis 0501
      HLA-DQA1 Molecular analysis 0505

      DQA1*0501 : DQB1*0201. DQ2.5 is one of the most predisposing factors for autoimmune disease. DQ2.5 is encoded, often, by a haplotype associated with a large number of diseases.

      I have high risks For MS and type 1 diabetes... as well :) many family
      My gene pull is German, Irish ,British , Italian --with tiny greek and sardiana more then half of my make up just italian being . Think of us a a MUTT dog(most dont want a mutt) ..a mix when you mix several genes ---say alpha and beta's from all German, Irish ,British , Italian they dont mix well. Some alpha s and betas dont play well( making a match--gluten problems and auto immune disease) ... when I dig I see alphas from my grand mother , betas from my grand father and alphas from my italian side ... why my DAD was fine. he got only one side only alphas

      One gene above gives you narcolepsy in HLA there are genes in the HLA DR you only need one. I had sleeping problems when these actived. My DAD and sister as well my fathers father (grandfather ) had sleeping problems. today I sleep well... with no alarm clock.. from 39-42 I havent needed one.

    7. take a look ,,,, As I say learn your genes and play with your genes make up..make them happy :)

      I also have massive defects in FUT2/card15 most of all people are secretors Me being card15/fut2 I am a-----> NON secretor making my mucus lining different( bifido dont like NON secretors ....why you see milk problems in crohns as well. Kids missing bifido and non secretor status have it bad... Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn's disease

      I know my weakness and ways around my genes.... Ive learned yeast.....bifido , I wont say what other specific strains of probiotics as well b12 The b12 is due to being a non secreter. As well FUT2 low bifido due to blood type 0 , blood type also plays bad with yeasts. low bifido allows yeast to expand. having several genes in the HLA - for diabetes...MS and gluten etc,,,when you dig you see the tie. gluten is simular to yeast/fungus --as well cassien and soy .. Today I have all stumped because one I ve worked around my genes. filling in and making up for the defects in specfic strains of bacteria , and limiting specfic foods... certain foods extremely high in folates and b12 oxalate help me as well foods low in yeasts. I would speculate if someone else ate my diet. they would not handle the high amount of oxaltes well . I will guess due to my genes I dont need any more yeasts...because oh the amount my blood carries. which studies show crohns people sensitive to yeasts( you have to dig). Being sensitive to yeasts most fruits etc are HIGH in excess wild yeasts. Or produce arbinose--what yeast produce.... Foods resembling yeasts are no different for me SOY and cassien. Not a fan of the blood diet.. but if you dig and look this matches somewhat well for type O blood (me) As well I have many ties in my HLA genes for type 1 diabetes. Starch is a problem , for it converts to sugar.

      Keeping my starch low also helps in the fact with my yeasts. Several specific strains of bacteria has helped limit this effect. the higher my internal yeasts the more problems I have. The lower and up regulated / side step of specific bacteria keeps me in balance and NO disease

      T*******To me theirs no way to pick apart MILk, MS etc as each persons case is specific due to there gene make up..until you pull in this in a testing the result to me are VOID..

  12. Gemma wrote: "I am purposefully neglecting all the other stuff we might mention re modern way of milk production and consumption: cows hybridized so that they give milk even in high state of pregnancy, availability of milk the whole year round, all the hormone and miRNA signalling, stem cells passed via milk, al that... but it would just get too complex."

    Thanks indeed for the clarifications. The problem with just using "milk" is that we can't tell from that single word that you mean all those other things, and I was confused by the articles until that was clarified by Tim and you. The desire for simple terminology is understandable. So what is needed is a different term that will explain what you mean and still be relatively simple. How about "modern milk" or "unfermented pasteurized milk"? The latter term doesn't literally incorporate all the factors, but they tend to go with those two factors.

  13. Milk.....
    Skim low fat D2 added (mold injected) pasteurized all living useful things killed
    Whole milk D2 added (Mold mold injected) pasteurized all living useful things killed
    Raw , loaded with bacteria , yeast enzymes

    grain feed......grass feed (omega 3 , omega 6 )



    all comletely different animals

  14. Yup, and my most beneficial dairy product I have tried so far (one particular goats milk kefir) is not the lowest in lactose. I fare better with it than with lactose-free kefir, so there does indeed seem to be much more to the dairy story than lactose content, at least for me.

    1. Phil, this wasn't about what you eat. This was about a hypothesis for what kids are being fed.

    2. This comment has been removed by the author.

    3. Of course, and I didn't say the articles were about what I eat. I was just sharing my personal experience and not saying that it necessarily applies to anyone else (YMMV). For me, lactose-containing goat kefir has appeared to be more beneficial than lactose-free dairy products (which doesn't necessarily mean that lactose content isn't a factor, just that it doesn't appear to be the only or primary factor in health effects for me).

      I also find the Mongols and other traditional pastoral societies that consume fluid milk and other dairy products while remaining relatively free of MS to be an interesting piece of the puzzle. My experience seems to fit pretty well with theirs.

  15. Good write-up. Interesting comments. While reading the last two posts on this topic here, I began to think about children who would be breastfed beyond the lactose persistence period (up into the five-seven year-old range). What cultures do this? Do any cultures still do this much? What is the incidence of AI disease (MS, etc) in these cultures? Does the lactose in the milk have detrimental effects on them? How would this contribute to your thoughts here? Would it? Would it not? Probably a dead end. But thought about it a little.

    I'd love to see Edwards' journey written up in a very organized fashion, almost outline form. (I'm an MD who stepped out for who knows how long to raise kids and discovered this "voodoo" stuff with some success in our family. Now just watching. Observing. Soaking stuff up now. To do what, don't know. But love to learn from others who have success.) What his specific tests were, why he ordered them, what they look for, and how he used them to make changes. I read about all these alternative tests, and I'm like, "Geesh. Whatever. Another $250-500 for patients to spend. Ching. Ching. Ching. You need these ten tests..." So it's nice to hear someone who feels he did use them and got success. ~~Terri F

    1. @Terri

      Lactase persists longer, into adolescence (in LNP). So its expression does not stop with weaning.

      Breastfeeding till 7 y? I doubt it.

      Here some info if you like to study more:
      Hunter-Gatherer Infancy and Childhood

      Prevalence of MS in traditional populations that consume high dairy is very low or null.

  16. Thanks. Good to hear your thoughts. Will read article. Terri

  17. informative post. thanks for sharing. Actually milk is a complete food item for our health

    1. @Custom thesis writing service (why is the world so lazy and outsources everything?)

      Thank you for your deep thoughts and oh-so-careful use of the word "milk".