hpu and detox protocol

[learner2life]

Hey all,
I came across an interesting video from Dr. Klinghart talking about the hpu illness that often times is associated with lyme disease and autism. It really sounds like something that we should test for. Please watch all of the seminar. It is packed with incredible insights and different treatment ideas from beginning to end. I am really interested in trying some of his detox programs that he describes. Please watch.
The video is at the bottom of the page.

http://planetthrive.com/2010/04/hpukpu-protocol-for-lyme-and-autism/

What do you think?
David

 

[Cindi]

I have most of the symptoms of Pyroluria and have tried main supplements from time to time. I could not concentrate on the issue as i am quite ill.. There is a yahoo group called Pyrroluria. You might wish to check.Best wishes.

 

[kday]

My chest pain went away, and my anxiety greatly decreased after taking his Core supplement for Pyroluria. I had chest pain for two years before this supplement (especially severe in the morning).

I'm beginning to think that many of us could have "rare" porphyrias and pyroluria that leads to Cytochrome P450 metabolism and methylation problems, B12 deficieny, food sensitivities, environmental illness, mold illness, EMF illness, etc. Up to 20% may be carriers of porphyria and an infectious or toxic insult could cause secondary porphyria. Unfortunately it can be difficult to test for.

I started using binders that are supposed to bind porphorins, and my liver congestion (as tested by percussion dullness) and urine frequency is better.

 

[aprilk1869]

This is something I've been thinking about for a while but the thought of taking large amounts of minerals scares me.

My mum has MS (symptoms fatigue and declining cognition) and is on Freddd's protocol.

Seemingly HPU can be caused by stress. My mum got ill 3 years after her dad died. She was very stressed and upset about it and would grind her teeth. Apparently teeth grinding is a sign of HPU. It can also cause mercury from fillings to be released (she ended up with a lot of dental problems).

Add all this to the fact that she was on a low b12/fat diet and would exercise excessively. I wonder if some sort of infection then came along and it was the straw that broke the camel's back.

I've also read that many people with MS and ME have very low ESR levels. It's thought that this is because of pathogens produce fibrin causing hypercoagulation. Anything less than 4 is considered very low and my Mum's ESR came back recently as 1.5.

Lets put this in plain English. When a pathogen(s) gains a foothold, especially in the endothelial cells in the blood vessels (as well as other cells), the bug(s) can be protected by the coagulation mechanism of fibrin deposition on top of the infected cells. Half of the patients form fibrin very fast, becoming fibrin(oid) deposition. Half of the patients have an inability to clean up the fibrin, and therefore continue to have oxygen and nutrient starvation of tissues for a long time. For example, if the fibrin deposition occurs in a muscle, it says ouch, and you have a tender point as in Fibromyalgia. If it is in the placenta, the placenta is compromised by fibrin deposition and the baby aborts. As blood viscosity increases and blood flow is reduced throughout the body, the patient becomes hypo-this and hypo-that, such as hypothyroid, hypo-HPAaxis, hypo-estrogen, etc. The use of low dose heparin restores blood flow throughout the body and hormones from the endocrine system tend to normalize. Thus, the blood flow issue becomes one of the most important issues of chronic illnesses. Unfortunately there is no easy test to measure blood flow, only the effects of blood flow.
http://www.springboard4health.com/notebook/health_hypercoagulation_ill.html

HPU can be caused by various pathogens and various pathogens can cause low ESR. So could low ESR be an indicator of HPU?

Another thing about HPU and the deficiencies it causes, I came across this study about MS:-

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.

Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 microg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.
http://www.ncbi.nlm.nih.gov/pubmed/10985916

High levels of NO have also been linked to fibrin/low ESR.

When she first got ill she was basically told "you have MS, there's nothing that can be done, go home and forget about it." So she got Judy Graham's book and started taking Evening Primrose Oil. It's difficult to say whether it helped or not but this is one kind of oil that's suggested as part of the HPU protocol.

We're in the process of getting a hair analysis so it will be interesting to see what comes up.

 

[liquid sky]

My chest pain went away, and my anxiety greatly decreased after taking his Core supplement for Pyroluria. I had chest pain for two years before this supplement (especially severe in the morning).

I'm beginning to think that many of us could have "rare" porphyrias and pyroluria that leads to Cytochrome P450 metabolism and methylation problems, B12 deficieny, food sensitivities, environmental illness, mold illness, EMF illness, etc. Up to 20% may be carriers of porphyria and an infectious or toxic insult could cause secondary porphyria. Unfortunately it can be difficult to test for.

I started using binders that are supposed to bind porphorins, and my liver congestion (as tested by percussion dullness) and urine frequency is better.

Hi Kday, may I ask what binders you used to bind porphorins? Having similar liver problems. Thanks.

 

[kday]

I've been taking activated charcoal (about 5 grams twice a day which I think is quite a lot) and I have been taking Chlorella. I am not sure how much the Chlorella does.

If you don't do well with activated charcoal, Another option for binding porphorins is cholestyramine.

I got most of tratment info here:
http://www.cpnhelp.org/secondaryporphyria

Some abstracts here about activated charcoal/cholestyramine and porphoria:
http://www.cpnhelp.org/book/export/html/3755

If you take activated charcoal, it is important to take 2 hours away from food and supplements. I took a Vicodin the other night without thinking about an hour after ingesting the activated charcoal and it had no effect.

 

[liquid sky]

Hey kday, I meant to come back and thank you for the links, but forgot. I looked up about porphyria. I would like to take charcoal, but am really afraid it will interfere with my meds. unfortunately, I take a lot of medication throughout the day and night.Thanks again.

 

[Dufresne]

Hey all,
I came across an interesting video from Dr. Klinghart talking about the hpu illness that often times is associated with lyme disease and autism. It really sounds like something that we should test for. Please watch all of the seminar. It is packed with incredible insights and different treatment ideas from beginning to end. I am really interested in trying some of his detox programs that he describes. Please watch.
The video is at the bottom of the page.

http://planetthrive.com/2010/04/hpukpu-protocol-for-lyme-and-autism/

What do you think?
David

It seems Klinghardt is less excited about his HPU protocol these days. He was talking about it as if it was the missing link a couple years ago. Now he states that if MMP-9 is elevated, as it is with many if not most of us, the protocol will actually make things worse. The reason for this is MMP-9 is zinc dependent, and what the enzyme does is "...makes it easier for the bugs to eat you."

Although I value Klinghardt's insights, I believe it's wise to take his ideas and enthusiasm with a grain of salt; try them but listen to your body, which is hard to do in this instance as the HPU protocol is no walk in the park. All that said, I admire when a researcher or clinician is able to change direction.

Seemingly HPU can be caused by stress. My mum got ill 3 years after her dad died. She was very stressed and upset about it and would grind her teeth. Apparently teeth grinding is a sign of HPU. It can also cause mercury from fillings to be released (she ended up with a lot of dental problems).

According to Klinghardt, grinding the teeth can also be indicative of parasites.

 

[Dufresne]

If you take activated charcoal, it is important to take 2 hours away from food and supplements. I took a Vicodin the other night without thinking about an hour after ingesting the activated charcoal and it had no effect.

Concerning dosing with CSM and other sequestrants, the following seems to make sense: (from http://www.ei-resource.org/articles...es/neurotoxins--treatment-information-sheet/)

1- Take your thyroid as soon as you wake (leave it at your bedside with a glass of water). A half-hour later take your Daily Energy Enfusion vitamin powder, lipoic acid 300 mg and nystatin (and Cortef if prescribed). You can also take any other medications that are needed for other problems at this time. Take the Questran one hour later (1 scoop mixed in eight ounces of apple juice or distilled water followed by 12 ounces of distilled water). Exactly one-half hour after taking Questran, eat something that has at least a teaspoon of healthy fat (e.g. -- one egg or a pat of butter). Eating makes your body pour the neurotoxin containing bile into your gut. Eating hour after the Questran puts the medicine right where it needs to be (like a catchers mitt) to soak up and bind the neurotoxins.
2- Also take the next 2 doses of Questran (each day) as close to a half hour before lunch and dinner as you can. Take your last (4th) daily dose one-half hour before bedtime and eat some turkey or an egg right at bedtime. Take your sleep medications/herbals an hour before the nighttime Questran.

 

[aquariusgirl]

A word of caution about questran/cholestyramine. I believe it binds B12 & fats.
I have had the most hellacious experiences taking this product & other PWCs have said the same thing.
Some folks can tolerate it.
IF you get a bad reaction, I would supplement some fatty acids & B12 double quick.
Personally, I know I cannot tolerate it.

 

[aquariusgirl]

Dufresne: where did you get the latest info about Klinghardt KPU & MMP9? Thanks.

 

[aprilk1869]

I found a lot of good info about the latest feelings about HPU at this link: http://betterhealthguy.com/joomla/blog/242-a-deep-look-beyond-lyme

 

[Dufresne]

A word of caution about questran/cholestyramine. I believe it binds B12 & fats.
I have had the most hellacious experiences taking this product & other PWCs have said the same thing.
Some folks can tolerate it.
IF you get a bad reaction, I would supplement some fatty acids & B12 double quick.
Personally, I know I cannot tolerate it.

Shoemaker has said he suspects most people who have this reaction to cholestyramine have Lyme. That the exacerbation of symptoms is the result of mobilizing toxins.

The above link from thebetterhealthguy is great but there are also the following sets of notes from the same conference.

http://lymebytes.blogspot.com/2011/05/highlights-from-deep-look-beyond-lyme.html

http://webcache.googleusercontent.c...es+(fms-like+or+not)&cd=1&hl=en&ct=clnk&gl=ca

 

[aprilk1869]

Klinghardt refers to MMP-9 and says we should get that down before going on HPU protocol. I wanted to see if there was a connection between MMP-9 and the methylation cycle. It seems that there is. Those who have high levels of homocysteine also have higher levels of MMP9 than controls.

Impaired Inhibitory Effect of Interleukin-10 on the Balance Between Matrix Metalloproteinase-9 and Its Inhibitor in Mononuclear Cells From Hyperhomocysteinemic Subjects


Background and PurposeHomocysteine has been linked to increased risk of ischemic stroke and other cardiovascular events, but the mechanism by which elevated plasma levels of homocysteine promotes atherogenesis remains unclear. Matrix degradation, partly regulated by the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), plays an important role in atherogenesis and plaque destabilization, and we hypothesized an imbalance between MMPs and TIMPs in hyperhomocysteinemia.

MethodsSerum MMP-9 and TIMP-1 was measured in 12 hyperhomocysteinemic and 12 control subjects. The release of MMP-9 and TIMP-1, with and without interleukin-10 (IL-10), and the effect of IL-10 on signal transducer and activator of transcription 3 (STAT3) phosphorylation were measured in peripheral blood mononuclear cells (PBMCs) from hyperhomocysteinemic and control subjects.

ResultsOur main findings were: (1) hyperhomocysteinemic subjects had raised serum levels of MMP-9 and MMP-9/TIMP-1 ratio comparing healthy controls; (2) although IL-10 markedly suppressed MMP-9 release from PBMCs in controls, no or only minor effect was seen in hyperhomocysteinemic subjects; (3) although IL-10 enhanced TIMP-1 levels in PBMCs from both hyperhomocysteinemic and control subjects, the increase was more prominent in controls, resulting in a marked difference in IL-10 induced changes in MMP-9/TIMP-1 ratio between these 2 groups; and (4) comparing PBMCs from controls, cells from hyperhomocysteinemic individuals had impaired IL-10 induced STAT3 phosphorylation.

ConclusionsOur findings suggest an attenuated inhibitory response to IL-10 on MMP-9 activity in hyperhomocysteinemic subjects, potentially promoting atherogenesis and plaque instability, representing a novel explanation for increased risk for atherosclerotic disease in these individuals.

stroke.ahajournals.org/content/37/7/1731.full.pdf

I also came across info relating to ALA and MMP-9

Alpha lipoic acid and multiple sclerosis Lipoic acid in multiple sclerosis: a pilot study.
Multiple Sclerosis. 2005

The purpose of this study was to determine the pharmacokinetics, tolerability and effects on matrix metalloproteinase-9 (MMP-9) and soluble intercellular adhesion molecule-1 (sICAMP-1) of oral Alpha Lipoic acid in patients with multiple sclerosis. Thirty-seven multiple sclerosis subjects were randomly assigned to one of four groups: placebo, Alpha Lipoic acid 600 mg twice a day, Alpha Lipoic acid 1200 mg once a day and Alpha Lipoic acid 1200 mg twice a day. Subjects took study capsules for 14 days. We found that subjects taking 1200 mg had substantially higher peak serum Alpha Lipoic acid levels than those taking 600 mg and that peak levels varied considerably among subjects. We also found a significant negative correlation between peak serum Alpha Lipoic acid levels and mean changes in serum MMP-9 levels. There was a significant dose response relationship between Alpha Lipoic acid and mean change in serum sICAM-1 levels. We conclude that oral Alpha Lipoic acid is generally well tolerated and appears capable of reducing serum MMP-9 and sICAM-1 levels. Alpha Lipoic acid may prove useful in treating multiple sclerosis by inhibiting MMP-9 activity and interfering with T-cell migration into the CNS.

Caution: High dosages of may cause heart rhythm problems. Use less than 50 mg of R alpha lipoic acid. I'm fascinated by the possibilities of nutritional substances in altering the course of chronic medical conditions for which modern medicine does not have good options. Although this study in no way says ALA will be a cure or long term benefit for those with multiple sclerosis, it does open the door for further exploration. I think the dose of 1200 mg is extremely high, and I would not recommend more than 50 mg a day of R-Alpha Lipoic Acid for long term use.

Alpha lipoic acid inhibits human T-cell migration: implications for multiple sclerosis.
J Neurosci Res. 2004
We have demonstrated previously the ability of the antioxidant alpha lipoic acid (ALA) to suppress and treat a model of multiple sclerosis, relapsing experimental autoimmune encephalomyelitis (EAE). We describe the effects of ALA and its reduced form, dihydrolipoic acid (DHLA), on the transmigration of human Jurkat T cells across a fibronectin barrier in a transwell system. ALA and DHLA inhibited migration of Jurkat cells in a dose-dependent fashion by 16-75%. ALA and DHLA reduced matrix metalloproteinase-9 (MMP-9) activity by 18-90% in Jurkat cell supernatants. These data, coupled with its ability to treat relapsing EAE, suggest that ALA warrants investigation as a therapy for multiple sclerosis.

http://www.raysahelian.com/multiplesclerosis.html

There also seems to be a connection with glutathione.

Alterations of glutathione S-transferase and matrix metalloproteinase-9 expressions are early events in esophageal carcinogenesis.

CONCLUSION:

Decreased GST and increased expression of MMP-9 in Barrett's metaplasia-dysplasia-adenocarcinoma sequence as compared to normal tissue suggest their association with esophageal tumorigenesis. Loss of GST and gain of MMP-9 in Barrett with dysplasia compared to non-dysplastic metaplasia indicate that these alterations may be early events in carcinogenesis. Quantification of these parameters in Barrett's esophagus might be useful to identify patients at higher risk for progression to cancer.

http://www.ncbi.nlm.nih.gov/pubmed/17278189

The incidence of allele variants of glutathione-S transferase M1 xenobiotic detoxification gene and matrix metalloproteinase 9 gene was analyzed in patients with chronic obstructive pulmonary disease. A strict gene-gene interaction between these two genes in the formation of hereditary predisposition to this disease was first demonstrated. The combination of glutathione-S transferase M1 genotype 0/0 and matrix metalloproteinase 9 mutant allele (-15621) is a risk factor for chronic obstructive pulmonary disease
http://www.springerlink.com/content/w42271675t1021u6/