What about CIRS and Obesity or Induced Type II Diabetes?
In Dr. Ritchie Shoemaker's book "Lose the Weight You Hate" he documented how the chronic inflammation of CIRS causes obesity and induces Type II Diabetes.
He explains it this way:
"Many of these patients gained the weight 'overnight' and didn’t respond to even the strictest of diets…
Of course, the problem of neurotoxin-induced obesity is also growing daily in this country, even as the doctors continue to misdiagnose it… What are the sure signs that the overweight patient must actually be suffering from an environmentally acquired disorder?
· The patient doesn’t lose weight successfully, no matter how carefully he or she observes the diet
· Look for some of the symptoms on the long list of complaints that are linked to neurotoxin-mediated illness
· Take the VCS test and learn in five minutes whether or not you’ve got the telltale deficit of the ability to distinguish black from grey from white
…The mechanism responsible for new onset of persistent insulin resistance probably does its destructive work by activating the endogenous manufacture of inappropriate amounts of pro-inflammatory cytokine called “tumor necrosis factor alpha” or TFN.
In order to understand how the process works, let’s start by remembering that the receptor-insulin – glucose interaction on the outer cell membrane is actually quite complex.
Step 1: In most cases, a molecule of insulin must link up with a second, similar molecule – thus creating a two-piece hormonal entity know as a 'dimer' (pronounced diemer.) The dimer’s job is to turn on the receptor.
Step 2: Now the receptor activates an enzyme, tyrosine kinase, which proceeds to drop a phosphate group on a specific amino acid – threonine – contained in the insulin.
Step 3: Now an additional reaction kicks in, stimulating the receptor to pinch off a bit of membrane around the dimer-glucose-receptor complex.
Step 4: Time now for a key maneuver: the shifting of the pinched-off membrane (in the form of a covered bubble, or endosome) to be moved into the cell.
Step 5: A positively charged hydrogen ion is pumped into the endosome which now opens up (de-granulates) and thus releases the glucose. The latter is then added to glycogen –if space permits – or else is burned for fuel.
Step 6: The insulin receptor is recycled to the membrane, and the insulin is sent back in the bloodstream as a single unit (monomer) in search of more glucose and insulin receptors.
…when TNF is tremendously over-produced in fat cells (and especially in the over-weight) as a result of exposure to neurotoxins, essentially the TNF disrupts the normal initiation of the receptor activity by forcing the tyrosine kinase to drop the phosphate group on a different amino acid (serine), located directly adjacent to threonine. The phosphate groups are huge on a molecular scale and completely alter the normal size/shape relationship of one molecule to the next in three dimensions.
The bottom line on all of this is that when the bulky phosphate group 'gets in the way,' the 'lock and key' system of insulin attachment doesn’t work, and the sugar never makes it into the cell. After that, the body responds by either creating fatty acids from the sugar (and thus making you fat) or by allowing the sugar molecules to pile up in the blood stream and tissues (and thus leaving you with diabetes.)"
So what Dr. Shoemaker explains is that "Step 2" (above) of the process to unlock fat fails because of too many inflammatory cytokines. No fat to burn means no energy and that your body has to burn protein stores just to survive. Most dieticians warn us about diets that cause "protein wasting." For those of us with CIRS all diets will cause protein wasting unless we get our inflammation levels down first!
Dr. Shoemaker also explains that this induced Type II Diabetes is curable:
"The answer came from a study that focused on 15 Type II diabetics who did not have a family history of the illness. I did symptom lists and VCS testing in all the patients who had a strong family history of diabetes.
The findings showed a marked difference in the number of symptoms and VCS deficits between the non-family history group and the others. The bottom line was that the subjects without the family history were actually suffering from neurotoxin-mediated illnesses. They didn’t have Type II diabetes at all!...
As the numbers of successfully, family history-negative diabetic patients grew, it became clear that the concept of environmentally acquired obesity and diabetes were well supported by clinical results…
The best study results were that the 'acquired' diabetics rarely needed to take any diabetes medications once the neurotoxins were cleared from their body…
And indeed, after treatment for neuro-toxic illness, both the VCS deficit and the blood sugar problems resolved. These patients had displayed the same A-1-C hemoglobin levels and the same elevated random sugar and insulin levels found in normal diabetics, but after neurotoxin treatment, the A-1-C hemoglobin, sugar and insulin levels returned to equal those of the control, non-diabetic patients.
The first-ever description and assessment of the neurotoxic symptoms in patients with neurotoxic illness was contained in the recently published paper (co-authors, Shoemaker and Dr. Hudnell) in the NIH/NIEHS journal, Environmental Health Perspectives, back in May 2001…"
This is why you have to treat CIRS before you can resolve obesity or biotoxin-induced Type II Diabetes.
He explains it this way:
"Many of these patients gained the weight 'overnight' and didn’t respond to even the strictest of diets…
Of course, the problem of neurotoxin-induced obesity is also growing daily in this country, even as the doctors continue to misdiagnose it… What are the sure signs that the overweight patient must actually be suffering from an environmentally acquired disorder?
· The patient doesn’t lose weight successfully, no matter how carefully he or she observes the diet
· Look for some of the symptoms on the long list of complaints that are linked to neurotoxin-mediated illness
· Take the VCS test and learn in five minutes whether or not you’ve got the telltale deficit of the ability to distinguish black from grey from white
…The mechanism responsible for new onset of persistent insulin resistance probably does its destructive work by activating the endogenous manufacture of inappropriate amounts of pro-inflammatory cytokine called “tumor necrosis factor alpha” or TFN.
In order to understand how the process works, let’s start by remembering that the receptor-insulin – glucose interaction on the outer cell membrane is actually quite complex.
Step 1: In most cases, a molecule of insulin must link up with a second, similar molecule – thus creating a two-piece hormonal entity know as a 'dimer' (pronounced diemer.) The dimer’s job is to turn on the receptor.
Step 2: Now the receptor activates an enzyme, tyrosine kinase, which proceeds to drop a phosphate group on a specific amino acid – threonine – contained in the insulin.
Step 3: Now an additional reaction kicks in, stimulating the receptor to pinch off a bit of membrane around the dimer-glucose-receptor complex.
Step 4: Time now for a key maneuver: the shifting of the pinched-off membrane (in the form of a covered bubble, or endosome) to be moved into the cell.
Step 5: A positively charged hydrogen ion is pumped into the endosome which now opens up (de-granulates) and thus releases the glucose. The latter is then added to glycogen –if space permits – or else is burned for fuel.
Step 6: The insulin receptor is recycled to the membrane, and the insulin is sent back in the bloodstream as a single unit (monomer) in search of more glucose and insulin receptors.
…when TNF is tremendously over-produced in fat cells (and especially in the over-weight) as a result of exposure to neurotoxins, essentially the TNF disrupts the normal initiation of the receptor activity by forcing the tyrosine kinase to drop the phosphate group on a different amino acid (serine), located directly adjacent to threonine. The phosphate groups are huge on a molecular scale and completely alter the normal size/shape relationship of one molecule to the next in three dimensions.
The bottom line on all of this is that when the bulky phosphate group 'gets in the way,' the 'lock and key' system of insulin attachment doesn’t work, and the sugar never makes it into the cell. After that, the body responds by either creating fatty acids from the sugar (and thus making you fat) or by allowing the sugar molecules to pile up in the blood stream and tissues (and thus leaving you with diabetes.)"
So what Dr. Shoemaker explains is that "Step 2" (above) of the process to unlock fat fails because of too many inflammatory cytokines. No fat to burn means no energy and that your body has to burn protein stores just to survive. Most dieticians warn us about diets that cause "protein wasting." For those of us with CIRS all diets will cause protein wasting unless we get our inflammation levels down first!
Dr. Shoemaker also explains that this induced Type II Diabetes is curable:
"The answer came from a study that focused on 15 Type II diabetics who did not have a family history of the illness. I did symptom lists and VCS testing in all the patients who had a strong family history of diabetes.
The findings showed a marked difference in the number of symptoms and VCS deficits between the non-family history group and the others. The bottom line was that the subjects without the family history were actually suffering from neurotoxin-mediated illnesses. They didn’t have Type II diabetes at all!...
As the numbers of successfully, family history-negative diabetic patients grew, it became clear that the concept of environmentally acquired obesity and diabetes were well supported by clinical results…
The best study results were that the 'acquired' diabetics rarely needed to take any diabetes medications once the neurotoxins were cleared from their body…
And indeed, after treatment for neuro-toxic illness, both the VCS deficit and the blood sugar problems resolved. These patients had displayed the same A-1-C hemoglobin levels and the same elevated random sugar and insulin levels found in normal diabetics, but after neurotoxin treatment, the A-1-C hemoglobin, sugar and insulin levels returned to equal those of the control, non-diabetic patients.
The first-ever description and assessment of the neurotoxic symptoms in patients with neurotoxic illness was contained in the recently published paper (co-authors, Shoemaker and Dr. Hudnell) in the NIH/NIEHS journal, Environmental Health Perspectives, back in May 2001…"
This is why you have to treat CIRS before you can resolve obesity or biotoxin-induced Type II Diabetes.
