Does the diabetes epidemic have a bacterial cause ?

Does the diabetes epidemic have a bacterial cause?

If you are suffering from diabetes, you have probably been told that it is due to your life-style destroying the Beta- cells in your pancreas. This is an urban myth. Isolate the duodenum and these useless Beta-cells suddenly, as if by magic, start working again. You are probably dying slowly as a result of ignorance and a general belief in a piece of unscientific folk law. They tell you it is all your fault in the first place and your fault when the treatment fails. This used to happen with ulcers until they discovered Helicobacter pylori and started using antibiotic treatment. I have found a bacterium that is capable of producing the symptoms of diabetes and caused remission of my diabetes with antibacterial treatments alone.

Symptoms of C. novyi infection Mechanism for causing symptoms.
Hyperglycaemia (too much sugar in blood.)
Hyperinsulinaemia (too much insulin)
Discovering the cause
Methodology and results of testing
Sedating the duodenum
Finding the bug
Treating the bug
Clostridium novyi 

Symptoms of C. novyi infection; Mechanism for causing symptoms; Hyperglycaemia; too much sugar in blood; Hyperinsulinaemia; (too much insulin; Discovering the cause Methodology ; Sedating the duodenum; Finding the insulin bug; Treating the insulin bug; Clostridium novyi


Does the diabetes epidemic have a bacterial cause

What you and your doctor should know.

There are at least four biochemical mechanisms leading to hyperglycaemia.

1.          Hypoinsulinaemia (not enough insulin), the only mechanism known to most clinical practitioners.

2.          Hyperinsulinaemia (too much insulin), rats used as a model for human diabetes have been genetically engineered to produce excess insulin, leading to fasting hyperglycaemia (too much sugar.)

3.          Reduced activity of the alpha-1 gamma-aminobutyric acid (GABA) receptor on the alpha-cells. GABA switches off glucagon production by the alpha-cells. Without inhibition the alpha-cells continue to promote the liver to release glucose, and will continue to do so until they die.

4.          Excessive stimulation of the alpha-1 adrenaline receptor on the alpha-cells, leading to excess glucagon production.

Have any of these been tested for, or was number 1 assumed?

The bacteria is Clostridium novyi type A, which is unknown to most clinicians but is well known to vets. Table 1 is a summary of its symptoms and the mechanisms that cause them. Most are caused by the Alpha-toxin, which destroys the actin cytoskeleton (skeleton of cells) causing them to loose shape and leave holes in tissues that should not have holes. It also disrupts the biochemical pathways involving glucose detection and the production of hormones such as insulin and hormones regulating hunger.

Supporters of the life-style theory will point to research showing the growth of diabetes with increased use of western diets in places like Japan. This does not disprove the C. novyi theory. In fact this and the fact that we are now eating more factory farmed meat may confirm the theory. Animals kept in overcrowded conditions suffer high rates of infection. This causes loss to the farmer in reduced food conversion but the loss is less than the cost of the vaccine. The economic option is to only vaccinate costly breeding stock. The ones you and I eat are often infected animals. Although cooking will kill the bacterium it will not kill the spores which are indestructible by all means except incineration. The life-style factor is increased ingestion of C. novyi spores leading to higher infection rates.

The rest of this Post is not an easy read. It began life as an article for a medical journal, but I thought it was more important to get the information out than wait until I had time to rewrite it. Bear with me, I will be making it more user-friendly.

This is an anecdote of my personal struggle for survival, backed by clinical observation, biochemical measurements, and an extensive search of the peer reviewed literature The fact that isolation of the duodenum from the lumen using bypass surgery or an impervious lining causes remission of type II diabetes [4] requires a causal mechanism. This case study indicates that Clostridium novyi infection may be the cause of some type II diabetes and provides a mechanism for the observed remissions. Reduction of serum glucose by sedation of the duodenum with mebeverine hydrochloride and remission of diabetes and its complications by antibiotic treatment have been observed. A physiological age of 46 was measured by a body scanner when my chronological age was 61. I am not qualified to give medical advice. Anyone taking any action, whatsoever, based on the information and opinions expressed here, does so of their own volition and is responsible, as I was, for their own actions.

The motivation for this study is one of personal survival. The Standard NHS (UK National Health Service) protocol reduced me to a pitiful state, my hair was turning white and falling out, my teeth were loosening and falling out, and my finger nails stopped growing resulting in trench in each nail when growth resumed.

The view that diabetes is caused by deficiency of the pancreatic beta-cells and/or insulin resistance is so well established that no other view may be considered clinically. When patients fail to respond to standard treatments they are classed as uncooperative. However, in my experience, clinicians, when pressed to provide an explanation as to what factors have caused my supposed beta-cells malfunction, resort to what physicists refer to as "hand waving explanations" involving lifestyle. I am not obese, so I have been treated to such gems as; over indulgence in pies and ale (not part of my regular diet) or my failure to eat baked potatoes! In physics such behaviour is considered a sign of general ignorance while trying to present a front of knowledge, hence the derogatory description.


1.1 Problems with the standard model

Leaving aside the foibles of human nature, there are serious problems with the standard paradigm. Firstly, there are at least four mechanisms leading to hyperglycaemia.


1.          Hypoinsulinaemia, the only mechanism known to most clinical practitioners.

2.          Hyperinsulinaemia, rats used as a model for human diabetes have been genetically engineered to produce excess insulin, leading to fasting hyperglycaemia.

3.          Reduced activity of the alpha-1 gamma-aminobutyric acid (GABA) receptor on the alpha-cells. GABA switches off glucagon production by the alpha-cells. Without inhibition the alpha-cells continue to promote the liver to release glucose, and will continue to do so until they die.

4.          Excessive stimulation of the alpha-1 adrenaline receptor on the alpha-cells, leading to excess glucagon production.


Here in the UK, little if any testing is done before starting treatment for the first mechanism and if the glucose tolerance test proves negative for hypoinsulinaemia then the results are ignored. Clinicians know that diabetes is a progressive incurable disease, so are blind to clinical evidence that may give clues to a cure.

There are many other problems with the standard paradigm. To provide a coherent narrative I use the device of raising numbered questions to be answered later.


Question 1 Duodenal bypass surgery and the GI Dynamics EndoBarrier cause remission of type II diabetes. 

Studies on rats indicate that nutrient restriction is not the cause. If the beta-islets lacked the functional capability of sustaining life without intervention, there is no plausible mechanism whereby insertion of an inert tube into the duodenum could re-stablish adequate functionality.

Question 2 Many diabetics fail to achieve control of serum glucose using standard methods. In my case I was unable to establish any parameters that I may have been able to vary to achieve control.

Question 3 A large proportion of diabetics who do achieve control, nevertheless, still go on to develop the complications associated with high serum glucose.


This case study is the result of detailed observation of prescribed and self-medication by a scientifically trained observer backed by an extensive search of peer reviewed literature. I make no apologies for its anecdotal nature. It would be unethical to use anyone else as a subject, so personal anecdote is all I have.

I used to have a reputation as having a "cast iron gut" until I came into contact with some luggage which had been contaminated with raw sewage in a flood in Brazil. Since that time, I have suffered with intestinal dysfunction of varying severity for 35 years. Since no specific cause or treatment was found I learned to live a reduced quality of life.


2.1 Testing the treatment of Diabetes Bacteria

 2.1 Testing the treatment of Diabetes Bacteria

17 years ago hyperglycaemia was discovered and, in spite of no beta-islet deficiency being found by the glucose tolerance test, I was treated as a diabetic, first with glyclazide, then with metformin and insulin. The first insulin trial showed no statistically significant negative correlation between increasing insulin dosage and serum glucose (Spearman rank order correlation +0.21 with 0.67 probability, student algorithm.) Whereas, multivitamin tablets, taken in place of insulin as a control, showed a correlation of -0.68 with a probability of 0.98. This result led me to try the US Pharmacist Magazine's recommended protocol of chromium picolinate and biotin [1]. This did not work.


After another year of metformin with no results, I was persuaded to try aggressive treatment with the maximum dose of metformin and resumption of insulin. The metformin caused painful muscle swelling and destabilized my serum glucose into range 20 to 30 mM/l. The muscle swelling I put down to carbohydrate loading due to concurrent high serum glucose and insulin intensified by the effect of metformin. Carbohydrate loading is a term used by body builders who starve themselves before a show then gorge on pasta resulting rapid carbohydrate uptake leading to osmotic swelling.

The first insulin dose resulted in a severe nocturnal hypoglycaemic event with sweating and loss of consciousness. My general health deteriorated rapidly involving hair whitening and loss, teeth loosening and falling out, my nails stopped growing leaving trenches when growth resumed, and general lassitude and debility. At this stage I decided I needed to find out things for myself.


3 Discovering the cause of Diabetes Bacteria

 3 Discovering the cause of Diabetes Bacteria

3.1 Methodology and results of testing


Starting with a blank sheet of paper and a paradigm free environment, my first step, as a physical scientist, was to obtain a signal to analyse, using high resolution monitoring (every 15 minutes during waking hours) of serum glucose. This signal showed no periodicity, nor 1/f or 1/fnoise. This eliminated CNS involvement since brain activity and music are both 1/fnoise. The only correlation with external events was that steep falls in serum glucose caused feelings of hunger, with or without duodenal spasm, resulting in a steep rise. This pattern was familiar to me from more subjective observations over the years. When I have attempted to present these observations to various clinicians I have been treated with incredulity, derision, or outright hostility. The observations may be summarised as, when I start to cook my meal serum glucose rises, when I eat the meal it goes down. Use of a continuous monitor showed this to be true about 30% of the time but generally there is no correlation between alimentary glucose and serum glucose which is idiopathic (not controlled by external factors.)


Question 4 What causes these very steep falls in serum glucose (12 to 19mM/l/hour compared to the healthy young man on a glucose tolerance test of 2.3mM/l/h)?


The signal is ultimately due to electromagnetic forces between molecules so stochastic (random) processes are ruled out. This leaves only one explanation of the signal, deterministic chaos, in particular a driven dissipative system. From the point of view of physical science, it would be remarkable if the glucose homeostasis system were not chaotic, consisting as it does of two feedback loops and two time scales, milliseconds for enervation and seconds for hormone mediated inputs. Indeed, Somogyi has shown that chaotic behaviour may be induced in healthy young men by insulin induced hypoglycaemia [10]. Somogyi did not have the concepts of deterministic chaos available to him in 1951. 

Given a chaotic system we must examine closely the concept of normality. For the simplistic standard paradigm, normal means active control around 6mM/l. For a driven dissipative chaotic system (DDCS) 6mM/l is only one strange attractor (unstable quasi periodic orbit) among many. The fact that it appears to be usual is only because the system is not usually perturbed by driving impulses so being dissipative settles into its lowest energy state. Normal for a DDCS is that given a single impulse it will evolve through a series of unstable quasi periodic orbits punctuated by chaotic variation until the lowest energy state is reached. If you want to observe this in a mechanical model, set up a simple pendulum on a springy support. The gravitation forces represent one feedback loop and elastic forces represent the other feedback loop of the homoeostatic system. Release the pendulum at a large angle to the vertical and watch the motion evolve through a series of unstable quasi periodic orbits punctuated by wild chaotic motion. Given repeated impulses, the system never returns to its lowest energy state thus is diagnosed as diabetes and abnormality concluded when the system is behaving normally for the type of system it is. This is the most important discovery of this investigation, so I will repeat it in big letters. In diabetics, the glucose control is normal for a driven dissapative system. Only the driving impulses are abnormal. This partially answers question 1. There was nothing wrong with the beta-cells, only the signals they were responding to.


 These mathematical considerations are not without clinical significance. The standard paradigm leads to clinical practice being


Hyperglycaemia = beta-cell dysfunction/insulin resistance = metformin and or insulin.


Hyperglycaemia = impulses = find and eliminate impulses so letting the system return to lowest energy state.


(Note that this not preclude beta-cell deficiency which may be an impulse to be suspected after all the other possible impulses have been removed. Unless the other impulses have been eliminated then assumed beta-cell deficiency may be an artefact of other causes.)


3.2 Sedating the duodenum of Diabetes Bacteria


Taking the later view and considering the effects of duodenal isolation, I set out to eliminate impulses originating in the duodenum. A search of online information led me to sedate the duodenum with mebeverine hydrochloride, 135mg every 6 hours achieved continuous sedation. This failed to tame the wild fluctuations in serum glucose but the baseline for these fluctuations stepped down through various levels (strange attractors) until it became 6mM/l, fig 1.


During part of this process I was on a continuous monitor (red bars on fig 1) This showed broad agreement with my blood tests except for transient rapid falls. Blood test results were lower than the readings of the continuous monitor (time averaging errors) at these events, which had physiological consequences promoting me to test and seek food, since there is a very much higher than chance coincidence between testing and transient falls. It is a matter of concern that the time averaging errors on the monitor make the existence and full extent of these transients invisible to clinical practice. The final monitored transient hypoglycaemia was off the scale resulting an a calibration error termination of monitor function. Measurements from the continuous monitor trace show that I was able remove serum glucose at the rates up to 19mM/l/h. This hyperinsulinaemia is probably responsible for the spontaneous transient hypoglycaemic events.

My success was short lived, my duodenum suffered extreme oedema, painfully distending the abdominal wall. Serum glucose began to rise.


Question 5 Why did this swelling of the duodenum occur when serum glucose was reduced?


3.3 Finding the bug of Diabetes Bacteria


This state of affairs continued for several months combined with spontaneous hypoglycaemia causing me to loose consciousness at work on two occasions. At one stage there was dorsal swelling in the region of the pancreas, but this released suddenly so was probably only a blocked duct. I was prescribed a PPI but this only made the situation worse so was discontinued and I was referred for endoscopy.


Proton Pump Inhibitors or other antacids are not a good idea with Clostridium infections since they allow the bacteria to migrate into the stomach.


In desperation I drank TCP [a propriety topical antiseptic consisting of phenol and trichlorophenol] (50ml at 30% dilution morning and night for three days.) The results were dramatic. The duodenum deflated overnight. I concluded that the cause was a bacteria infection of a topical nature in the duodenum. This did not eradicate the organism because there were relapses on a 7 to 14 day cycle which were treated at the first sign of symptoms with the same TCP protocol. As a result of this treatment I experienced increased vigour and my hair colour began to return indicating production of sufficient stem cells to produce new melanocytes. This stem cell production has had a general rejuvenating effect, even one big toe that was developing a bunion has straightened out. The receding hairline began to advance. Subcutaneous adipose tissue, which had been absent, began to regenerate in a bizarrely patchy manner but the patches soon joined on the torso and advanced down the limbs. This may be due to reduced inflamation,

"When the researchers suppressed the inflammatory response, either byreducing NF-kappaB protein levels or by using pharmacologic agents that activate SIRT1 (and, thus, inactivate NF-kappaB), they found that adipose cells have improved insulin signaling and improved insulin-stimulated glucose uptake. These results put SIRT1 in the center of a pathway connecting insulin resistanceand inflammation. Based on their anti-inflammatory effect, activators of SIRT1 may turn out to be a useful therapeutic intervention for improving insulin sensitivity as a means of treating type 2 diabetes.

I began a relapse two days before endoscopy but left it untreated. The endoscopy result was that the duodenum was oedematous with patchy erythema and nodality in the first part.

I carry a bacterium which occasionally affects my oral cavity. It is characterized by rapid onset of extreme oedema. It starts in crevices or the salivary duct i.e. relatively anaerobic conditions. I usually treat it by sluicing with TCP but sometimes it is inaccessible and antibiotics are required. It responds rapidly to penicillin (but has a poor response to amoxil). It is, therefore, Gram positive. Persistence in inactive form for a period of years indicates it is spore forming. Taking penicillin for an outbreak in my salivary gland caused complete deflation of the duodenum to the extent that I could no longer feel it through my abdominal wall even when full. Vigour considerably increased and hair colour return accelerated. I experienced two severe hypoglycaemic events with painful muscle swelling but these events moderated as I adjusted to a new level of normality of duodenal signalling. I conclude that it is the same gram positive organism in both duodenum and oral cavity. These characteristics, especially the extreme oedema with rapid onset, identify the organism as Clostridium novyi type A. [11]


3.4 Treating the bug of Diabetes Bacteria


Treatment with doxycycline accelerated the elimination of the organism and also led to remission of diabetic complications. Renal function in terms of the ability to concentrate urine markedly improved. Mild oedema, with small blood vessels visible, in feet and ankles completely disappeared together with dilated veins on lower leg. Erectile function returned.


However, by day 5 of the treatment the organism had developed resistance and in the nine days before I was able to get back to my GP, severe reinfection occurred. This infection was mainly in my colon since this was beyond the reach of the TCP which I deployed until I was able to secure a further supply of penicillin. In these nine days, my peristalsis ceased, my abdomen became distended, my blood became a pinkish colour and failed to clot (C. novyi gamma toxin.) I felt severely ill, somnolent and feverish, but there was no increase in temperature, indicating no immune reaction. These were reminiscent of the symptoms of the original infection 30 years ago.


The first effects of penicillin were deflation of abdomen without deflation of the colon. This was accompanied by frequent high volume urination. I conclude the peritoneal cavity was fluid filled (dirty dish water found post mortem in the peritoneal cavity of cattle with black disease (severe C novyi infection)) The rectum was blocked with an impacted stool only part of which I was able to pass. As the colon deflated and peristalsis returned, I found the descending colon entirely blocked. Aggressive treatment with glycerine suppositories and magnesium sulphate cleared this blockage in liquid form. However, part of the original impacted stool remained but gradually eroded and I was able to pass wet faeces with the use of a laxative. This precluded the use of mebeverine hydrochloride to reduce serum glucose. Prolonged exercise caused increased oedema in the neck and a return of symptoms. I conclude increased toxin production with reduced serum glucose. Serum glucose had become very high (20 to 30 mM/l) during the reinfection period and unstable from day to day. This eventually began to settle into the range 9 to 15mM/l but there were idiopathic rises correlating with constipation. I conclude that C. novyi was hiding from the penicillin in the immobile matter in the colon.


Six weeks into the penicillin treatment, the last of the impacted stools was expelled as an egg-sized fibrous mass. Four hours after this toxin factory was voided there was a period of frequent high volume urination with a marked reduction in abdominal volume. This was accompanied by a marked reduction in serum glucose to a preprandial value of 7.9mM/l with a two hour postprandial value of 6.6mM/l. There was an extreme sensation of hunger when serum glucose was less than 9mM/l. This was countered by a resumption of duodenal sedation with mebeverine hydrochloride. Long periods of lower serum glucose associated with prolonged exercise resulted in increased toxin production as evidenced by swelling and soreness in the salivary gland, resulting in increased serum glucose later in the day or the following morning. Although food intake was reduced there was still an increase in adipose tissue on the lower abdomen. By week ten of the penicillin treatment a preprandial serum glucose of 5.7mM/l was achieved.

In week 11, the organism acquired a beta-lactamase gene and stopped responding to penicillin, resulting in serum glucose of 13.4mM/l, which remained steady irrespective of alimentary glucose. There was severe oedema in the neck accompanied by somnolence. The antibiotic was changed to erythomycin 250mg 4TD resulting in a marked reduction in oedema and lowering serum glucose. During the second week of erythomycin treatment I acquired a rrhino virus following which the C novyi infection reduced to the point where I was able to suspend antibiotic treatment. What I believe has happened is akin to viral interference. Under the combined influence of rrhino virus and clostridial fragments the immune system was primed to act against C novyi, thus effectively vaccinating me. Indeed reinfection, as evidenced by renewed swelling in the neck, went into rapid remission. However, when the immune system was compromised, as evidenced by cold sores, reinfection from spores was not prevented and antibiotic support was required.


I began a war of attrition where there is persistent mild reinfection followed by spontaneous remission. It is anticipated that it may take a number of years to completely remove the residual spores accumulated over a period of decades. I keep a stock of erythomycin so that I may may act quickly if the immune system becomes unable to prevent reinfection.

Ten months into this protocol, there was another coincidence of rrhino virus and antibiotic use. This resulted in a very active immune response especially in my kidneys, resulting in swelling and inflammation, during and after which, I regained normal renal function. This has remained stable.

I had another rhinovirus infection during which I took erythomycin. I had inflammation of the gut followed by another marked reduction in the volume of the abdomen accompanied by increased urination. Most of the abdominal organs regained the size they were when I used to do mountain running. The exceptions being the appendix and the liver which were visible as swellings.

I discovered a new tick to train the immune system. Since the insulin levels are no longer dangerously high, I can induce hypoglycaemia by not eating until I am shaking. This promotes the C. novyi to produce toxins which, in turn provokes an immune response. This makes me feel ill for a few days but by this means I have reducedthe swelling of the liver and appendix. I shall be trying this on a seven day cycle to keep mopping up the germinating spores.

It appears that this adjuvant action on the immune system of rhinovirus and clostridium fragments, released by the action of the antibiotic, is real and is cumulative. I was unable to obtain samples of rhinovirus to test the hypothesis, but wild strains are common enough. Considering the implications for the treatment of other intractable Clostridium infections, it should be thoroughly investigated.

After reviewing the evidence that co-enzyme Q10 reduces fasting insulin levels by 25%, I began taking Q10 (100mg 2TD). I reasoned that there may be deficiency, due to liver damage caused by C. novyi. (aero chocolate liver in pigs.) This appears to have been beneficial. I have lost the strung out driven feeling associated with hyperinsulinaemia. However, in the resulting sense of peace and happiness, I am finding it difficult to motivate myself.

I am still waiting to get advice from a specialist in Clostridium eradication. However, this may now be redundant since I am symptom free, full of energy, and have regained the physique I had in my 20s.


4 Clostridium novyi of Diabetes Bacteria


Clostridium novyi (oedematiens), in spite of being ubiquitous, found in soil, the intestinal tract, and faeces, and being well known in veterinary practice, is virtually unknown in clinical practice. Part of the reason for this is the natural prejudice in favour of the familiar. Despite the fact that clostridial infections are rarely singular, many authors report testing for C. perfringens (welchii) only and if found are satisfied that they have fully characterised the infection. The literature contains an increasing number of first time identifications of Clostridiaceae in gas gangrene infections. The three main species found in gas gangrene are C. perfringens, C. novyi, and C. sordellii. Clinical practice and much research also appears to be blind to the fact of symbiotic relations between clostridia. In many media clostridia only produce toxins at points of cross streaking. [13]


Another reason is the difficulty of isolating and culturing this extreme anaerobe which is also fastidious, requiring the presence of thiols as reducing agents in order to grow at all. [8]  s presented by McLauchlin [9] and Brazier [12] in relation to deaths of injecting heroin users (presumably from a common cause) show a false negative rate of 40% in ideal conditions. Only positive results are reliable. It is strongly advised that, in the UK, advice be sought from the Anaerobe Reference Library, Cardiff. Commercial kits may be inadequate. [12]


We now have a possible answer for question 1. The remission of type II diabetes when the duodenum is isolated from the lumen is readily explained by the fastidiousness of the organism. Thiols are not a normal component of human cell secretions but are common in food (e.g. methanethiol from nuts and cheese) Isolation of the duodenum results in an environment substantially free from thiols, thus C novyi can not flourish leading to remission of this duodenum mediated disease. Agresive prophylactic antibiotic treatment associated with intestinal surgery may also be a factor. The duodenum shows a particular sensitivity to the alpha-toxin of C novyi. When injected, the alpha-toxin causes extreme oedema of the submucosal layers of the duodenum while not affecting the stomach. [6] Little, if any, biochemical research into the causes of this phenomena has been undertaken. One suspects that enhansed expression of the gene for O-linked-N-acetylglucoseaminetransferase, OGT, as in the pancreatic beta cells, will be found. My experience shows that an oedematous duodenum, especially if it responds to penicillin, should lead to a suspicion of C novyi.


The above is consistent with the general lowering of serum glucose by sedation of the duodenum with mebeverine hydrochloride. The mechanism being that irritation of the duodenum, resulting in an adrenalin cascade stimulating the androgenic alpha-1 receptors on the alpha-islets leading to excessive glucose release, may be the cause of type II diabetes when beta-islet deficiency is absent. However this can not be the whole story since the variability of the serum glucose signal is still not accounted for.


The phylogenetic data [14] show that while its close relatives have undergone recent specieation, C. novyi type A is not evolving in this manner. This implies that it has found a niche into which it is evolving. It is posited here that the niche is maintaining a glucose rich environment within its host to facilitate its own spore production. The principle adaptation being the fact that the substrate for the action of the C. novyi type A alpha-toxin is a UDP-N-acetylglucoseamine [15] rather than UDP-glucose as used by other clostridia. The most visible effect of this toxin is found in its action on the signalling proteins responsible for the maintenance of the actin cyctoskeleton resulting in morphological changes in the affected cells. The cells become spherical and the conections are reduced to thin strings. [11] All cell types are affected. [18]


The effect on the microvascular system is to cause leakage, resulting in haemorrhages and oedema. Indeed injection of the alpha-toxin into the eye produces lesions similar to the flame haemorrhages found in diabetic retinopathy. [6] The Sparrow equation tells us that the lower extremities are most likely to suffer oedema. The same morphological changes to cells comprising the nephrons would compromise the ability of the kidneys to concentrate urine. We now have an answer to question 3. These complications can not be caused simply by excess serum glucose. Using the mathematical method of disproof by counter example, one example of a well controlled diabetic developing complications would be sufficient to dispel this notion. I have seen one estimate of 40% of well controlled diabetics developing complications. Any attempts to circumvent this logic must be considered as hand waving. C. novyi type A infection in all classes of diabetics developing complications is a more simple explanation. (It is also to be noted that once sufficiently anaerobic conditions can be established in the lower extremities, a gangrene producing organism is already in place to begin consuming the host tissue.) This is also consistent with my observation of the remission of complications under antibiotic treatment. It is suggested that the associated angiopathy is an over-enthusiastic attempt by the body to repair alpha-toxin damage. The action of the alpha-toxin may also explain the increased serum cholesterol found in diabetics. Porosity of the gut epithelium allowing secreted cholesterol to be reabsorbed.

The growth pattern of C. novyi in vitro is, an incubation period where no toxin is produced, once growing vigorously toxins are produced, toxin production then declines as C. novyi switches to spore formation. It is suggested here that when glucose levels drop and energy for spore formation is reduced, C. novyi switches back to toxin production. This needs to be tested in vitro. However, the infection in my salivary gland does give a visible indicator of toxin production. [18] After prolonged exercise, when serum glucose is expected to be lower, there is a marked increase in oedema below my jaw. This answers question 5.


Glucose detection at the cellular level is the synthesis of UDP-N-acetylglucoseamine from glucose and glutamate in a pathway with the rate limiting step being glutamate:fructose-phosphate-amidotranferase, GFAT, which is inhibited by UDP-N-acetylglucoseamine. [16] The first stage in both insulin production and sensitivity is the action of OGT on signalling proteins. [16] OGT is site specific not target specific. The site is determined by the start position on the codon, [16] OGT is highly conserved in eukaryotes, where it is involved in the assembly of the nuclear pore. OGT expression is enhanced in the pancreatic beta-cells. Mice genetically modified to over-express GFAT serve as an animal model for diabetes exhibiting hyperinsulinaemia leading to fasting hyperglycaemia. [16] This suggests an explanation of my observed hyperinsulinaemia in the relative kinematics of reactions involving UDP-N-acetylglucoseamine. If the following relation holds between the absolute values of the rate constants, K, with repect to UDP-N-acetylglucoseamine

then uncontrolled insulin production and utilisation resulting in excessive serum glucose reduction and muscle swelling when glucose is also high is readily explainable by alpha-intoxication. Insulin production begins but competition between GFAT inhibition and the alpha-toxin results in a delayed switch-off leading to runaway insulin production. A further refinement to the alpha-toxin's action in this regard is the inhibition of the pancreatic alpha-cells by GABA [19] produced by the beta-cells in conjunction with insulin. GABA receptors are critically dependent on an intact actin cytoskeleton for their function. [17] The alpha-toxin in the alpha-cells prevents GABA inhibition, so effectively decouples the the two parts of the glucose homeostasis system, allowing simultaneous production of insulin and glucagon, leading to wild fluctuations. The prevention of alpha cell inhibition is sufficient to account for the initial symptom of diabetes, elevated serum glucose. The predicted reduction of hyperinsulinemia with reduced toxin levels was observed by monitoring serum glucose, at 15 minute intervals, on days 15 and 22 of the second penicillin treatment. On these days, increased hyperinsulinaema (although at reduced levels than pre-antibiotic treatment) was also observed concurrent with increased oedema in the salivary gland. This short term variability precludes the alternate explanation of hyperinsulinaemia by beta-cell proliferation or over-expression of genes caused by the action of gastric inhibitory peptide or glucagon-like peptide-1. [4] This answers question 4.


The production of ghrelin, which is OGT mediated, may also be affected by the same mechanism. This may explain the observed correlation between hyperglycaemia and subjective hunger.


The answer to question 2 is more multifactoral. Before labelling the patient as uncooperative, one should consider that serum glucose may not, in fact, be controllable by the standard protocols, as this case study demonstrates. One should consider the feel-bad factor of increased toxin load when serum glucose is reduced, and the inhibition of alpha-1 GABA receptors in the brain leading to anxiety and risk avoidance behaviour. 

4.1 Progress of infection of Diabetes Bacteria

 My experience shows C. novyi infection, when well established and affecting serum glucose, proceeds through four stages.


1. Low levels of toxin irritate the duodenum generally raising serum glucose but the correlation with alimentary glucose is maintained; take the normal serum glucose - time graph and add a constant to the glucose data set.


2. Moderate levels of toxin affect the GABA receptors on the pancreatic alpha-cells leading to idiopathic rises in serum glucose and a breakdown of correlation between serum glucose and alimentary glucose.


3. High levels of toxin affect the glucose sensing mechanism in the pancreatic beta-cells leading to hyperinsulinaemia and fully developed chaos in the serum glucose signal.


4. Very high levels of toxin lead to serious illness with destruction of erythocytes by the gamma-toxin, somnolence, and feverishness without a rise in body temperature. This phase is to some extent self-limiting in that the switch to spore production eventually reduces toxin levels.


Long term complications are dependant on the outcome of the body's struggle to repair the general cell damage caused by the alpha toxin.


The reduced serum protein levels found in diabetics may be the result of the zeta-toxin which destroys proteins.


5 Discussion of Diabetes Bacteria 

Published data plus two common sense assumptions, which are testable in vitro, show that C novyi is capable of causing all the observed symptoms of diabetes and its complications. The two parts, high base line and chaotic variability, of the serum glucose signal are controllable by treatments predicated on the assumption of C novyi infection. The overall level of serum glucose may be reduced by sedation of the duodenum with mebeverine hydrochloride. The variability about this level may be reduced by reduction in the toxin load with antibiotic treatment. Remission of readily observeable complications by the use of antibiotics has been demonstrated. A cure has not yet been demonstrated; elimination of C novyi is likely to be a prolonged process. The prognosis is that a cure may be effected, whereas the standard protocols can only offer symptomatic relief with a prognosis of deterioration due to an incureable and progressive illness. There is a caveat. Changes to the signalling regeim caused by the suggested treatment may result in severe hypoglycaemic and hyperglycaemic events until the body adjusts to more normal signalling. I am certainly experiencing an improved quality of life, increased vigour, and remission of the symptoms of ageing due to the treatments advocated in this paper. There is indirect supporting evidence for a bacterial cause :-


1. Longo-Mbenza[20] has successfully treated insulin resistance using antibiotics. Although he was treating for H. pylori, the treatment would also have killed C. novyi.


2 Treatment for priodontal disease, presumably antibacterials, improved glycaemic control for at least 3 months[21]


3 Chinese herbal medicines, presumably with antibiotic properties, delayed the onset of diabetes and improved glycaemic control in pre diabetics.[22]


Concluding remarks of Diabetes Bacteria 

The above is anecdotal and controversial. However, it is logically consistent and in accord with the literature and observation. As an hypothesis it warrants proper investigation. If proven correct the consequences of a cure for, or even a vaccine against diabetes would be significant, in addition to savings of health care costs. There are animal vaccines but they appear to be only effective for about two years. In the absence of a human vaccine, clinical trails of the empirically derived protocol of erythomycin plus infection with a strain of rrhino virus with a strong viral interference ability, with or without mebeverine hydrochloride would be cheap and relatively risk free if applied to patients with recently diagnosed diabetes. The prescription of insulin or insulin enhancing drugs in the absence of direct evidence of beta-islet deficiency, or even in spite of direct evidence to the contrary, may be detrimental to patients who may be producing excess insulin resulting in hyperglycaemia by Somogyi rebound. Without such direct evidence one is only acting on a belief in a commonly held view. I fully endorse the comments made by McLaughlin et al [9] concerning the need for intensive microbiological investigation (including strict anaerobic culture) for patients with unexplained morbidity.


Conflict of interest statement

The author has no financial or personal links with any organisation or institution and the only bias was a desperate wish to survive in the face of adverse effects of standard protocols. This study was entirely funded by the author.


Frequently asked questions of Diabetes Bacteria


My serum glucose readings are all over the place, does that mean I am chaotic?

No. The signature of chaos is active control about some level other than 6mM/l. The only was to see this is high resolution testing, say every 15 minutes.  This means one sore finger. You may see large changes punctuated by shorter periods where the readings hover around some value before performing further large changes. I have recorded active control about 24mM/l for one hour. I have also seen very stable control about 11mM/l for up to 16 hours. During one of these episodes, I tried to disrupt the control by giving myself a glucose tolerance test. I did not even get a blip. This means control is being driven by something other than alimentary glucose.


Before going to bed my glucose is about 7mM/l I take my insulin but in the morning my glucose is very high. This is confusing.

This is fasting hyperglycaemia, sometimes called the dawn effect because overnight is the longest fasting period. It is caused by too much insulin being produced, leading to hypoglycaemia resulting in a rebound to hypergylcaemia. What is unknown to many clinicians is that hypos are relative as well as absolute. That is a sudden fall in serum glucose, even if it bottoms out at a high level produces the same physiological effects as a very low level. In the review article on this[citation to be added] there is a horror story of an elderly lady, taken to A&E in a confused mental state. Her serum glucose was high, so they gave her long term insulin. Her mental state did not improve so she was admitted to a geriatric ward and kept on long term insulin. It was several weeks before an alert doctor rescued her.  These  events are examples of Somogyi rebound. These transient hyperinsulinaemia events are destabilising.[10] Healthy young men can be turned into temporary diabetics and stable diabetics destabilised for 6 weeks. Taking glucose readings every 15 minutes and drawing the graph may give you a picture of what is happening. In any case you should make sure your doctor knows these facts and ask him to review the use of long term insulin.

 Does the diabetes epidemic have a bacterial cause?


[1] Singer G.M., Geohas J. Diabetes Technol. Ther. 2006 Dec;8:636-43

[2] Rubino F., Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg 01 Jan 2004:239(1): 1-11

[3] Pachedo D. et al. The Effects of duodenal-jejunal exclusion on hormonal regulation of glucosemetabolism in Goto-Kakizaki rats. The American journal of surgery. 2007, vol 194, no2 pp 221-224

[4] Ashrafian H. le Roux C.W. Metabolic surgery and gut hormones - A review of bariatric entero-humoral modulation. Physiology & Behavior 97 (2009) 620-631

[5] Finn S.P. et al. Autopsy findings in an outbreak of severe systemic illness in heroin uses following injection site inflammation: an effect of Clostridium novyi exotoxin. Archives of pathology and laboratory medicine. vol 127, No. 11, pp 1465-1470

[6] Aub J.C. ey al. Physologic action of Clostridium oedematiens (novyi) in dogs. J Clin Inest 1947 May; 26(3): 404-410

[7] Busch C. et al. Characterization of the catalytic domain of Clostridium novyi alpha-toxin. Infect Immun. 2000 November 68(11): 6378-6383

[8] Moore W.B. Solidified media suitable for the cultivation of Clostridium novyi type B. J. gen. Microbiol. (1968), 53, 415-423

[9] McLauchlin J. Amplified fragment length polymorphism (AFLP) analysis of Clostridium novyi, C perfringens and Bacillus cereus isolated from injecting drug users during 2000. J. Med. Microbiol. - vol 51 (2002), 990-1000

[10] Somogyi M. EFFECT OF INSULIN HYPOGLYCEMIA ON ALIMENTARY HYPERGLYCEMIA. Journal of Biological Chemistry, Baltimore, 1951 193: 859-863

[11] Ball D. W. et al. Purification and Characterization of Alpha-Toxin Produced by Clostridium novyi Type A. Infection and Immunity July 1993 2912-2918

[12] Brazier J. S. et al. Isolation and identification of Clostridium spp. fom infections associated with the injection of drugs: experiences of a microbiological investigation team. J Med. Microbiol. 51 (2002) 985-989

[13] Roth G. D. Myers H. I. Egg Yolk Reactions By Organisms From the Oral Cavity of Man. J DENT. RES. 1957; 36; 104

[14] Sasaki Y. Phylogenetic positions of Clostridium novyi and Clostridium haemolyticum based on 16S rDNA sequences. International Journal of Systematic and Evolutionary Microbiology (2001), 51, 901-904

[15] Selzer J. et al Clostridium novyi alpha-toxin-catalyzed incorporation of GlcNAc into Rho subfamily proteins. J Biol Chem. 1996;4:375-382

[16] Love D. C. Hanover J. A. The Hexamine Signaling Pathway: Deciphering the "O-GlcNAc code." Sci. STKE 29 November 2005 Issue 312, p. re13


[17] Meyer D. K. et al. Regulation of Somatodentric GABA alpha Receptor Channels in Rat Hippocampal Neurons: Evidence for the Small GTPase Rac1. The Jounal of Neuroscience 2000) 20(18):6743-6751



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