Genes and Diabetes

Here is a great resource for anyone who is has some ambition to do some digging on the cause(s) of diabetes (both Type 1 and 2).

It is fascinating and fairly comprehensive, albeit technical, in its scope. Though it would help to be familiar with all that is ‘genetic’ related, this site gives some interesting insights into the genes that can be affected along with describing where among our chromosomes different functions of our respective blueprints are cached.

Have a look and, hopefully, you will glean some useful information!

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Gluten Sensitivity Revisited

I am among the many that believed that the effects of gluten sensitivity were confined to the gastrointestinal tract. However, if you watch this video you will hear the speaker describe quite a different situation. This is quite a fascinating revelation. Please take the time to watch it and process it all.

Also, here is a list of the ‘gluten cross reactive foods’ that are mentioned in the video. Hope this helps!

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Resolving Inflammation-An Update

I recently performed the ‘bleach sniff test’ to evaluate for oxidative tissue damage. The test was positive. The test was negated by cross checking with unsaturated fatty acids and minerals. Exactly which mineral(s) is/are required remains to be determined. But, the positive test was also negated by “therapy localizing” (touching) the Neurolymphatic reflexes for the Stomach, Small Intestine, and the Pancreas, which signifies that these are the organs/glands involved. So, a protocol was followed to alleviate the reaction to the bleach sniff test itself. The full benefit will truly be realized when the fatty acids and necessary mineral(s) are supplemented. However, this is an appropriate interim solution.

I also did some testing using similar methods and found that the Herpes Zoster and Rubella viruses were affecting the Pancreas Neurolymphatic reflex. I plan on further investigating to see if other Neurolymphatic reflexes are being affected. (This was accomplished using homeopathic vials with the viruses in dilutions of 30x.) Unfortunately, I ran out of time to continue this research. I will continue to pursue this (and other) methods of eliminating inflammation and restoring the gut and the immune system to optimal health.

A big thanks goes out to Ian M. for all of his help with this!

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Resolving Inflammation

Up to this point the focus of this blog has centered on the causes of Type 1 DM. It is time to turn the page and start examining how a cure can be reached. I have been deliberating on how best to resolve this and it has become apparent that the inflammation and how the immune system fails to resolve it is paramount in making any inroads to being diabetes free.

Having been exposed to a lot of interesting alternative interventions, I have continually come back to several protocols devised by Walther H. Schmitt and Kerry McCord, two ICAK diplomates. These two gentlemen are Chiropractors who have created a comprehensive clinical protocol that treats all aspects of the body. I am interested to conduct the ‘bleach sniff test’, which is a screen for free radical pathology to see the results. In the ‘Quintessential Applications’ protocol it notes that symptoms of free radical pathology include autoimmune diseases. I am also interested to use ‘injury recall technique with offending agents’, which in this case would be foods, to the Neurolymphatic reflexes for my organs and glands. I hope that this too will achieve the result of decreasing any aberrant immune activity as well as decrease any inflammation. Although I have made it a habit to avoid any foods that I have determined provoke an immune response by the GI tract, I am curious to see if my situation improves by neurologically disassociating these foods from any inflammatory processes.

Also after reading this article it has become even more apparent that there is potential for many foods to provoke inflammatory responses, which I have to suspect contributes to the maintenance of the immune mediated destruction of the beta cells. I am planning on going back to yams and sweet potatoes in place of white/russet/yukon gold potatoes as a regular source of carbohydrates so as to avoid any potential inflammation on that front. It also seems that I need to focus on ensuring that I am getting my EFAs (essential fatty acids) and, perhaps more importantly, that my body is capable of using these fatty acids in the right places to curb inflammation and restore and repair cellular membranes. However, this will be addressed with the ‘bleach sniff test’ as it involves testing different nutrients involved with regulating inflammatory processes to see which ones negate a positive test, should that be the case.

Another source of inflammation is infection. In the case of T1D (Type 1 Diabetes) it would seem that enteroviruses are culprits worthy of investigation. Particularly interesting is the coxsackie (B) virus, which can affect the pancreas (meaning inflammation). Some suggest that it is what leads to T1D. Perhaps it is a contributing factor. It seems as though there are myriad potential causes but no definitive, singular cause. Cow’s milk seems to be a recurrent suggested cause but, it doesn’t effect the development of diabetes on it’s own. Some suggest that genes are the cause but, if you read this article or this article it suggesst that even when one identical twin has T1D, the other develops Type 1 at best 50% of the time. That would imply that genes are at best half of the reason someone develops T1D.

So, since this is my blog I will posit a theory: Type 1 Diabetes Mellitus begins with the development of a leaky gut. With the degradation of the integrity of the intestinal walls, immune protection against foreign invaders is compromised and, with digestion impaired the semi or undigested food passes into the blood stream, triggering immune responses that compound the situation. This amounts to considerable inflammation/oxidative tissue damage. If there is a leaky gut, it may have been provoked (at least, in part) by a lack of antioxidants which mean good fats and a number of nuts, vegetables and fruits. Or, the condition may have been exacerbated by a lack of antioxidants, which will ultimately lead to an ongoing cycle of oxidative tissue damage. Plus, if previously digested proteins (i.e bovine serum albumin) are now no longer being properly digested and the immune system is overburdened, it may, because of the similarity in conformations of the beta cells and BSA, resort to destroying the beta cells in error in an attempt to control the situation. And/or, an enterovirus affects the pancreas and the free radicals released by the immune system wind up damaging the beta cells. (There is also the gene aspect but, I will leave that aside for now.) This makes sense to me because the leaky gut seems to be the tie that binds between many autoimmune disease like MS, T1D, Crohn’s, Celiac disease and others. If one considers that the GI tract has the enteric nervous system, which has been likened to a second brain it becomes apparent that the body’s response pathogenesis and/or being bombarded with foods that it is sensitive/allergic to, the immune system may respond in unpredictable and complex ways.

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Suspected Causes of Type 1 diabetes: Milk

Milk. “It does a body good” is what the ads used to say. I never doubted that as a kid. But, it has become a centerpiece in the debate on the potential causes Type 1 diabetes. Personally, I drank tons of milk through my childhood and on into early adulthood. I would drink several glasses full of milk with each meal. But, as the years have gone by, milk has taken on a different image. In fact, after having stopped drinking milk at the advice of my ND, my severe seasonal allergies were greatly reduced. With the introduction of proper food combining, I no longer suffer from seasonal allergies. And, to invoke one of the most common observations made when it comes to drinking milk, we are the only species on earth that a) continues to do so after our infancy and b) drinks the milk of another species.

The following quotes have been taken from

“Studies have suggested that bovine serum albumin is the milk protein responsible for the onset of diabetes… Patients with insulin- dependent diabetes mellitus produce antibodies to cow milk proteins that participate in the development of islet dysfunction… Taken as a whole, our findings suggest that an active response in patients with IDDM (to the bovine protein) is a feature of the autoimmune response.”

New England Journal of Medicine, July 30, 1992

“In lieu of the recent evidence that cow’s milk protein may be implicated in the pathogenesis of diabetes mellitus, we believe that the Committee on Nutrition should clarify whether cow’s milk is ever appropriate for children and whether or not infant formulas that are based on cow’s milk protein are appropriate alternatives to breast milk.”
Pediatrics, July, 1992: 89 

“Antibodies to bovine beta-casein are present in over a third of IDDM patients and relatively non-existent in healthy individuals.”

LANCET, October, 1996, 348 

“Cow’s milk proteins are unique in one respect: in industrialized countries they are the first foreign proteins entering the infant gut, since most formulations for babies are cow milk-based. The first pilot stage of our IDD prevention study found that oral exposure to dairy milk proteins in infancy resulted in both cellular and immune response…this suggests the possible importance of the gut immune system to the pathogenesis of IDD.”

LANCET, Dec 14, 1996 

“Introduction of dairy products and high milk consumption during childhood may increase the child’s risk of developing juvenile diabetes.”

Diabetologia 1994;37(4):381-387 

“These new studies, and more than 20 well-documented previous ones, have prompted one researcher to say the link between milk and juvenile diabetes is ‘very solid’.”
Diabetes Care 1994;17(12) 

These passages are taken from Ch. 9 Autoimmune Diseases (pg. 186-201) in “The China Study” by T. Colin Campbell., PhD and Thomas M. Campbell II.

“…It so happens that some of the foreign invaders that our soldier [immune] cells seek out to destroy look the same as our own cells. The immune system “molds” [antibodies] that fit these invaders [in this case, antigens] also fit our own cells. The immune system then destroys, under some circumstances, everything that fits the mold, including our own cells. This is an extremely complex self-destructive process involving many different strategies on the part of the immune system, all of which share the same fatal flaw of not being able to distinguish “foreign” invader proteins from the proteins of our own body.
What does all of this have to do with what we eat? It so happens that the antigens that trick our bodies into attacking our own cell may be in food. During the process of digestion, for example, some proteins slip into our bloodstream from the intestine without being fully broken down into their amino acid parts. The remnants of undigested proteins are treated as foreign invaders by our immune system, which sets about making molds to destroy them and sets into motion the self-destructive autoimmune process.
One of the foods that supply many of the foreign proteins that mimic our own body proteins is cow’s milk. Most of the time, our immune system is quite smart. Just like an army arranges for safeguards against friendly fire, the immune system has safeguards to stop itself from attacking the body it’s supposed to protect. Even though an invading antigen looks just like one of the cells in our own body, the system can still distinguish our own cells from the invading antigen. In fact, the immune system may use our own cells to practice making molds against the invader antigen without actually destroying the friendly cell.
…When our immune system is working properly, we can use the cells in our body that look like the antigens as a training exercise, without destroying them, to prepare our soldier cells to repulse the invading antigens…
…The immune system uses a very delicate process to decide which proteins should be attacked and which should be left alone. The way this process, which is incredibly complex, breaks down with autoimmune diseases is not yet understood. We just know that the immune system loses its ability to differentiate between the body’s cells and the invading antigen, and instead of using the body’s cells for “training”, it destroys them along with the invaders.


In the case of Type 1 diabetes, the immune system attacks the pancreas cells responsible for producing insulin. This devastating, incurable disease strikes children, creating a painful and difficult experience for young families. What most people don’t know, though, is that there is strong evidence that this disease is linked to diet and, more specifically, to dairy products. The ability of cow’s milk protein to initiate Type 1 diabetes is well documented. The possible initiation of this disease goes like this:
-A baby is not nursed long enough and is fed cow’s milk protein, perhaps in an infant formula.
-The milk reaches the small intestine, where it is digested dow to its amino acid parts.
-For some infants, cow’s milk is not fully digested, and small amino acid chains or fragments of the original protein remain in the intestine
-These incompletely digested fragments may be absorbed into the blood.
-The immune system recognizes these fragments as foreign invaders and goes about destroying them.
-Unfortunately, some of the fragments look exactly the same as the cells of the pancreas that are responsible for making insulin.
-The immune system loses its ability to distinguish between the cow’s milk protein fragments and the pancreatic cells, and destroys them both, thereby eliminating the child’s ability to produce insulin.
-The infant becomes a Type 1 diabetic, and remains so for the rest of his or her life.

This process boils down to a truly remarkable statement: cow’s milk may cause one of the most devastating diseases that can befall a child. For obvious reasons, this is one of the most contentious issues in nutrition today.
One of the more remarkable reports on this cow’s milk effect was published over a decade ago, in 1992, in the New England Journal of Medicine. The researchers, from Finland, obtained blood from Type 1 diabetic children, aged four to twelve years. Then they measured the levels of antibodies that had formed in the blood against an incompletely digested protein in cow’s milk called bovine serum albumin (BSA). (Bold my own). They did the same process with non-diabetic children and compared the two groups (remember, an antibody is the mirror image, or “mold” of a foreign antigen). Children who had antibodies to cow’s milk protein must have previously consumed cow’s milk. It also means that undigested protein fragments of the cow’s milk proteins had to have entered the infant’s circulation in order to cause the formation of antibodies in the first place.
The researchers discovered something truly remarkable. Of the 142 diabetic children measure, every single one had antibody levels higher than 3.55. Of the seventy-nine normal children measured, every single one had antibody levels less than 3.55.
There is absolutely no overlap between antibodies of healthy and diabetic children. All of the diabetic children had levels of cow’s milk antibodies that were higher than those of all of the non-diabetic children. This implies two things: children with more antibodies consumed more cow’s milk, and second, increased antibodies may cause Type 1 diabetes.
These results sent shock waves through the research community. It was the complete separation of antibody responses that made this study so remarkable. This study, and others even earlier, initiated an avalanche of studies over the next several years that continue to this day.
Several studies have since investigated this effect of cow’s milk on BSA antibody levels. All but one showed that cow’s milk increases BSA antibodies in Type 1 diabetic children, although the responses were quite variable in their magnitude
Over the past decade, scientist have investigated far more than just the BSA antibodies, and a more complete picture is coming into view. Very briefly, it goes something like this: infants or very young children of a certain genetic background who are weaned from the breast too early onto cow’s milk and who, perhaps, become infected with a virus that may corrupt the gut immune system, are likely to have a high risk of Type 1 diabetes. A study in Chile considered the first two factors, cow’s milk and genes. Genetically susceptible children weaned too early onto cow’s milk-based formula had a risk of Typer 1 diabetes that was 13.1 times greater than children who did not have these genes and who were breast-fed for at least three months (thus minimizing their exposure to cow’s milk). Another study in the U.S. showed that genetically susceptible children fed cow’s milk as infants had a risk of disease that was 11.3 times greater than children who did not have these genes and who were breast-fed for at leas three months. This eleven to thirteen times greater risk is incredibly large (1,000-1,200%!); anything over three to four times is usually considered very important. To put this in perspective, smokers have approximately ten times greater risk of getting lung cancer (still less than eleven to thirteen times risk here) and people with high blood pressure and cholesterol have a 2.5-3.0 times greater risk of heart disease.
So how much of the elven to thirteen times increased risk of Typer 1 diabetes is due to early exposure to cow’s milk, and how much is due to genes? These days, there is a popular opinion that Type 1 diabetes is due to genetics, an opinion often shared by doctors as well. But genetics alone cannot account for more than a very small fraction of cases of this disease. Genes do not act in isolation; they need a trigger for their effects to be produced. It has also been observed that after one member of identical twin pairs gets Type 1 diabetes, there is only a 13-33% chance of the second twin getting the disease, even though both twins have the same genes. If it were all due to genes, closer to 100% of the identical twins would get the disease. In addition, it is possible that the 13-33% risk for the second twin is due to the sharing of a common environment and diet, factors affecting both twins.
…Cow’s milk consumption by children zero to fourteen years of age in twelve countries shows an almost perfect correlation with Type 1 diabetes. The greater the consumption of cow’s milk, the greater the prevalence of Type 1 diabetes. In Finland, Type 1 diabetes is thirty-six times more common than in Japan. Large amounts of cow’s milk products are consumed in Finland but very little is consumed in Japan.
As we have seen with other diseases of affluence, when people migrate from areas of the world where disease incidence is low to areas of the world where disease incidence is high, they quickly adopt the high incidence rates as they change their diet and lifestyle. This shows that even though individuals ma have the necessary gene(s), the disease will occur only in response to certain dietary and/or environmental circumstances.
Disease trends over time show the same thing. The worldwide prevalence of Type 1 diabetes is increasing at an alarming rate of 3% per year. This increase is occurring for different populations even though there may be substantial differences in disease rates. This relatively rapid increase cannot be due to genetic susceptibility. The frequency of any one gene in a large population is relatively stable over time, unless there are changing environmental pressures that allow one group to reproduce more successfully that another group. For example, if all families with Type 1 diabetic relatives had a dozen babies and all the families without Type 1 diabetic relatives died off, then the gene or genes that may be responsible for Type 1 diabetes would become much more common in the population. This, of course, is not what is happening, and the fact that Type 1 diabetes is increasing 3% every year is very strong evidence that genes are not solely responsible for this disease.
It seems to me that we now have impressive evidence showing that cow’s milk is likely to be an important cause of Type 1 diabetes. When the results of these studies are combined (both genetically susceptible and not susceptible), we find that children weaned too early and fed cow’s milk have, on average, a 50-60% higher risk of Type 1 diabetes (1.5-1.6 times increased risk).
…Two of the better known of these studies have been underway in Finland, one starting in the late 1980’s and the other in the mid 1990’s. One has shown that cow’s milk consumption increases the risk of Type 1 diabetes five- to sixfold, while the second tells us that cow’s milk increases the development of at least another three to four antibodies in addition to those presented previously. In a separate study, antibodies to beta-casein, another cow’s milk protein, were significantly elevated in bottle-fed infants compared to breast-fed infants; children with Type 1 diabetes also had higher levels of these antibodies. In short, of the studies that have reported results, the findings strongly confirm the danger of cow’s milk, especially for genetically susceptible children.

Imagine looking at the front page of the newspaper and finding the following headline: “Cow’s Milk The Likely Cause of Lethal Type 1 Diabetes.” Because the reaction would be so strong, and the economic impact monumental, this headline won’t be written anytime soon, regardless of the scientific evidence. Stifling this headline is accomplished under the powerful and label of “controversy”. With so much at stake, and so much information understood by so few people, it is easy to generate and sustain controversy. Controversies are a natural part of science. Too often, however, controversy is not the result of legitimate scientific debate, but instead reflects the perceived need to delay and distort research results. For example, if I say cigarettes are bad for you and provide a mountain of evidence to support my contention, the tobacco companies might come along and pick out one unsolved detail and then claim that the whole idea of cigarettes being unhealthy is mired in controversy, thereby nullifying all my conclusions. This is easy to do, because there will always be unsolved details; this is the nature of science. Some groups use controversy to stifle certain ideas, impede constructive research, confuse the public and turn public policy into babble rather than substance. Sustaining controversy as a means of discrediting finding that cause economic or social discomfort is one of the greatest sins in science.
…Take a recent scientific review of the cow’s milk -Type 1 diabetes association. In ten human studies (all case-control) summarized in a paper published as part of a “controversial topic series”, the authors concluded that five of the ten studies showed a statistically significant positive association between cow’s milk and Type 1 diabetes and five did not. Obviously, this at first seems to demonstrate considerable uncertainty, going a long way to discredit the hypothesis.
However, the five studies that were counted as “negative” did not show that cow’s milk decreased Type 1 diabetes. These five studies showed no statistically significant effect either way. In contrast, there are a total of five statistically significant studies and all five showed the same result: early cow’s milk consumption is associated with increased risk of Type 1 diabetes. There is only one chance in sixty-four that this was a random or chance result.
There are many, many reasons, some seen and some unseen, why an experiment would find no statistically significant relationship between two factors, even when a relationship really exists. Perhaps the study didn’t include enough people, and statistical certainty was unattainable. Perhaps most of the subjects had very similar feeding practices, limiting detection of the relationship you might otherwise see. Maybe trying to measure infant feeding practices from years ago was inaccurate enough that it obscured the relationship that does exist. Perhaps the researchers were studying the wrong period of time in an infant’s life.
The point is, if five of the ten studies did find a statistically significant relationship, and all five showed that cow’s milk consumption is linked to increasing Type 1 diabetes, and none show that cow’s milk consumption is linked to decreasing Type 1 diabetes, I could hardly justify saying, as the authors of this review did, that the hypothesis “has become quite murky with inconsistencies in the literature.”
In this same review, the authors summarized additional studies that indirectly compared breast-feeding practices associated with cow’s milk consumption and Type 1 diabetes. this compilation involved fifty-two possible comparisons, twenty of which were statistically significant. Of these twenty significant findings, nineteen favored an association of cow’s milk with disease, and only one did not. Again, the odds heavily favored the hypothesized association, something that the authors failed to note.
I cite this example not only to support the evidence showing a cow’s milk effect on Type 1 diabetes, but also to illustrate one tactic that is often used to make something controversial when it is not. This practice is more common that it should be and is a source of unnecessary confusion. When researchers do this-even if they do it unintentionally-they often have a serious prejudice against the hypothesis in the first place. Indeed, shortly after I wrote this, I heard a brief National Public Radio interview on the Type 1 diabetes problem with the senior author of this review paper. Suffice it to say, the author did not acknowledge the evidence of the cow’s milk hypothesis.
Because this issue has mammoth financial implications for American agriculture, and because so many people have such intense personal biases against it, it is unlikely that this diabetes research will reach the American media anytime soon. However, the depth and breadth of evidence now implicating cow’s milk as a cause of Type 1 diabetes is overwhelming, even though the very complex mechanistic details are not yet fully understood. We not only have considerable evidence showing that the association between diabetes and cow’s milk is biologically plausible. Human breast milk is the perfect food for an infant, and one of the most dangerous things a mother can do is to substitute the milk of a cow for her own.

…First, by definition, each of these diseases involves an immune system that has gone awry in such a way that it attacks “self” proteins that look the same as foreign proteins.
Second, all the autoimmune diseases that have been studied have been found to be more common at the higher geographic latitudes where there is less constant sunshine.
Third, some of these diseases have a tendency to afflict the same people. MS and Type 1 diabetes, for example, have been shown to coexist in the same individuals . Parkinson’s disease, a non-autoimmune disease with autoimmune characteristics, is often found with MS, bother within the same geographic regions and within the same individuals. MS also has been associated-either geographically or within the same individuals-with other autoimmune diseases like lupus, myasthenia gravis, Grave’s disease and eosinophilic vasculitis. Juvenile rheumatoid arthritis, another autoimmune disease, has been shown to have an unusually strong association with Hashimoto thyroiditis.
Fourth, of those diseases studied in relation to nutrition, the consumption of animal-based food-especially cow’s milk-is associated with greater disease risk.
Fifth, there is evidence that a virus (or viruses) may trigger the onset of several of these diseases.
A sixth and most important characteristic binding together these diseases is the evidence that their “mechanisms of action” have much in common-jargon used to describe the “how to” of disease formation. As we consider common mechanisms of action, we might with sunlight exposure, because this somehow seems linked to the autoimmune diseases. Sunlight exposure, which decreases with increasing latitude, could be important-but clearly there are other factors. The consumption of animal-based foods, especially cow’s milk, also increases with distance from the equator. In fact, in one of the more extensive studies, cow’s milk was found to be as good of a predictor of MS as latitude (i.e., sunshine). In Dr. Swank’s studies in Norway, MS was less common near the coastal areas of the country where fish intake was more common. This gave rise to the idea that the omega-3 fats common to fish might have a protective effect. What is almost never mentioned however, is that dairy consumption (and saturated fat) was much lower in the fish-eating areas. It is possible that cow’s milk and lack of sunshine are having a similar effect on MS and other autoimmune disease because they operate through a similar mechanism? This could be very interesting, if true.
…The first step in the vitamin D process occurs when you go outside on a sunny day. When the sunshine hits your exposed skin, the skin produces vitamin D. The vitamin D then must be activated in the kidney in order to produce a form that helps repress the development of autoimmune diseases. As we’ve seen before, this critically important activation step can be inhibited by foods that are high in calcium and by acid-producing animal proteins like cow’s milk (some grain’s also produce excess acid). Under experimental conditions, the activated vitamin D operates in two ways: it inhibits the development of certain T-cells and their production of active agents (called cytokines) that initiate the autoimmune response, and/or it encourages the production of other T-cells that oppose this effect. This mechanism of action appears to be a strong commonality between all autoimmune disease so far studied.
Knowing the strength of the evidence against animal foods, cow’s milk in particular, for both MS and Type 1 diabetes, and knowing how much in common all of the autoimmune diseases have, it is reasonable to begin thinking about food and its relationship to am much broader group of autoimmune diseases. Obviously, caution is called for; more research is needed to make conclusive statements about cross-autoimmune disease similarities. But the evidence we have now is already striking.

(End text)

One theory I would like to posit is that the autoimmune response may be provoked in response to pasteurized milk. Of course, this might be splitting hairs but, if BSA has a similar protein conformation to the beta cells of the pancreas, then perhaps the presence of BSA that has been denatured through pasteurization might be what trips the autoimmune response. It could be that the denatured proteins in cow’s milk are regarded by the immune system as damaged or improperly differentiated and, hence, potentially pre-cancerous, or, perhaps even cancerous beta cells and therefore elicits a movement by the immune system towards elimination of these aberrant cells.

Here is an interesting video courtesy of Dr. John McDougall which explores the links between milk, isolated soy protein and IGF-1 (insulin growth factor 1) which he suggests promotes cancer cell growth.

Also of note is this article in wikipedia which discusses the similarities in structure between casein and gluten.

I find this to be a very interesting development in terms of discovering the answer to what provokes Type 1 diabetes. It is important to note that in “The China Study” the authors make a point of noting that the proteins are incompletely digested. This would bolster the suggestion that the leaky gut syndrome is a necessary precondition for the development of Type 1 diabetes. However, if this is what provokes the immune response against the beta cells, why is it sustained, even after the complete elimination of cow’s milk from the diet?

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An encouraging video for Type 2 diabetics

I would be remiss in overlooking Type 2 diabetes in this blog. Admittedly, I will be devoting 99% of my efforts to tackling Type 1 diabetes but, I happened upon this video and realized I owe it to everyone to at least post it. We leave in an information age and this took no effort. After all, Type 2 diabetes is much more pervasive and is becoming a pandemic in North America.

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Suspected Causes of Type 1 diabetes: The Leaky Gut

The ‘leaky gut’ has repeatedly cropped up in my search for explanations as to the origins of Type 1 diabetes. I had come across the term repeatedly but did not fully comprehend what it meant. In essence, it is increased permeability of the absorptive surface of the intestine arising from irritation of the superficial tissue.

Here are a couple links to information on ‘leaky gut syndrome’. It is interesting to note that in the ‘wikipedia’ entry leaky gut is postulated as a cause of Type 1 diabetes. I am also including an interesting video detailing ‘leaky gut’ and ways to assist in healing this. Here is another short video also on the causes of the ‘leaky gut syndrome’.

Now, the internet is replete with information from a lot of different sources, each of them of differing credibility. So, I figured I would search ‘pubmed’, which is a very reputable resource when it comes to scientific research pertaining to medicine. Finding a good abstract that bolsters the hypothesis that leaky gut is a major factor is one thing but, I managed to luck out as the authors saw fit to provide the entire article for anyone to read. Here is another abstract from pubmed that also implicates a leaky gut as a cause of multiple diseases/disorders including Type 1 diabetes.

I am beginning with ‘leaky gut’ because I firmly believe it is likely to be an integral part of the development of Type 1 diabetes. And, when reflecting on my own situation, the idea of leaky gut as part of the initial conditions giving rise to diabetes makes a lot of sense. I believe this for several reasons:

1) I was treated with antibiotics as a young kid. I had recurrent tonsil and ear infections between the age of 2-3. I was given amoxicillin to treat them. I suspect that this contributed to the destruction of good intestinal flora, likely contributing to the initial conditions necessary for the development of ‘leaky gut syndrome’.

2) I received vaccinations at a young age. The issue of vaccination possibly causing a number of diseases, syndromes, etc. has become a highly contentious one. I will entertain it here, though. Much of the controversy surrounds the inclusion of the preservative ‘thiomersal’, which is a mercury based preservative. Mercury will tend to displace zinc, limiting its bio-availability. (It should be noted that the vaccines are injected and not ingested, meaning that the way the gut tissues are exposed to mercury is different than had it been ingested.) Zinc is important to many functions in the body including both digestion and immune function. Among the problems arising from a lack of zinc is hypochlorhydria. Zinc is also involved in insulin production. In this abstract it is suggested that zinc deficiency might exacerbate the effects of the autoimmune attack on the beta cells. (It also provides links to other abstracts and articles on the subject.) This abstract offers some insight to the effects of zinc on insulin absorption.

3) I was weaned using cow’s milk. Milk also factored in my diet very prominently for many, many years. (Milk will be addressed in a separate post.)

4) My diet and eating habits from young age all the way to a few years ago: 0 green vegetables or fruits (for almost 2 decades.) Wheat, corn, additives, preservatives, etc. were mostly what I subsisted on. (This is also significant because I have recently discovered that I am sensitive to wheat.) I also required antibiotics periodically for the treatment of illnesses, which could have compounded the situation.

5) Despite a hearty appetite, I was a meager child.

6) Decreased lymph flow: I have sought treatment from a couple different holistic medicine practitioners, including a Naturopath and have found that all have noted that my lymphatic system is congested. I have also been treated for parasitic, fungal, and bacterial infections which usually signify diminished lymphatic function and/or a lack of good flora in the gut.

7) NODULES: I have a number of nodules/cysts on my body. Most are in areas of Chapman’s reflexes (for the small and large intestine especially). Each organ has an association with different muscles in the body. The small intestine corresponds with the abdominal muscles and the quadriceps. The large intestine corresponds with the the TFL (tensor facia lata), the quadratus lumborum, and the hamstrings. The top left image displays two nodules on the side of my left thigh, which corresponds to neurolymphatic reflex for the gallbladder muscles (anterior deltoid and popliteus). The nodules on my arms might be explained by the fact that I have had numerous IVs. I would speculate that proteins and lipids, able to pass through the intestinal wall in an undigested/semi-digested state, have accumulated in these areas because of the increased permeability of the vasculature in response to inflammatory processes in the local vicinity. It is also possible that the proteins and lipids actually leached out into the adjacent interstitial space from the vein because of the actual perforation of the vessel from the IV. I do wonder as well about the possibility of sub-acute inflammation around the IV sites arising from excess bad fats in the diet, hormonal imbalance, excessive inflammatory process due to the ingesting of allergens, parasitic infestation causing an increase in inflammatory chemicals, and hypothetically, ongoing emotional states which might contribute to the prolongation of inflammatory process. (My association with IVs is not the best. My first encounter was traumatic. I still have a subtle response when blood is drawn or I have an IV line started).

Perhaps the ‘nodules’ are lymphatic nodes that are congested with lipids, proteins and glycoproteins from things like cow’s milk, wheat, gluten, etc. and, because of their presence, the immune system reaction is being sustained. So, if the lymphatic system can be mobilized so as to excrete these lipids, proteins and glycoproteins and the foods can be avoided, perhaps the autoimmune impetus to destroy the beta cells can be relieved?

I am curious as to the complex interplay of conditions that lead to Type 1 diabetes. Assuming that the leaky gut is a key factor in the development of diabetes, does it persist in all cases? Does it (leaky gut) resolve with time? If yes, what perpetuates the immune response? Since an estimated 50-75% of the immune system resides in the gut, if the resolution of the leaky gut is not sufficient to induce a cessation of immune mediated destruction of the beta cells, what is the missing piece of the puzzle?

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