Re: Ken's Short Version of Treatment for CFIDS/FM

[Guest guest]

Hi ken

thanks for this timely reminder.

but i'm wondering why you don't do the anticoagulation therapy first not last?

would the herx be too intolerable?

tnx

>

> I ended up doing this up after a long call today, so I thought that I would

share it here also for any one that is interested. It was worked for 4 people in

this house [TREATMENT was DIFFERENT for each, because labs showed different

problems for each]

>

> Short Version of Treatment for CFIDS/FM

> (see http://lassesen.com/cfids/)

>

> Step 1: PCR Testing for the infections that can cause it:[if general testing

was done for the FAMILY, then for positive items it should be followed up for

the specific one] See http://www.lassesen.com/cfids/infections.htm. EXCLUDE

nothing -- there is the risk that you are a symptomless carrier...

> * Mycoplasma

> * Epstein Barr (EBV)

> * Q-Fever

> * Rickettsia (Lyme disease, Rocky Mountain Spotted Fever etc)

> * Helicobacter pylori

> * Cytomegalovirus / Herpes (HHV-6)

> * Chlamydia

> * Candida

> * Varicella zoster

> * Leprosy (I have met CFIDSer who came down with it ~ 2 yrs after recovering

from Leprosy)

> * Parvovirus B

> * Hepatitis

> * TB

> * XMRV

> Step 2:A

> Treat all of the above infections found until clear. Make sure that the

anti-???? is effective against the specific infection.

> * Personal preference is the use of targeted -Transfer Factor for virus. (Seen

EBV specific TF being very effective)

> ---- It's old technology (pre-antibiotics), but still effective.

> ---- Takes much longer to clear the infection than antibiotics but does it

with less risk of bad herxs and seem to help the body learn to target the

infection reducing risk of reoccurance.

> Step 2:B

> COMPLETE (and I mean COMPLETE) testing for

> * All coagulation factors -- for myself, I typically sit at thr 94%ile for

soluble fibrin monomer when in recovery. With CFIDS it was > 99%ile.

> * All inherited coagulation factors currently know

> Step 3:

> * Use of fibrinolytic enzyemes (Nattokinease, Serrapetase, Lubrokinese,

Bromelain)

> --- WARNING: they will typically cause antibiotic/antiviral tissue to

concentrations to increase 10 fold and can result in a massive herx on low

dosages of antibiotics and antivirals.

> ---- Without clearing fibrin deposits, locii (reserves) of the infections will

persist and re-occur.

> * Use of Nootropics (Piracetam) and other (conventional) treatments associated

with Stroke and head trauma.

> * Appropriate treatment for the nature of coagulation problem (some may not be

prescription -- for example, turmeric --kitchen spice)

>

> IMHO: CFIDS is a disease cause brain trauma with the brain trauma resulting

from alteration of blood flow due to coagulation or inflammation of tissue.

>

[Guest guest]

" louella m " <lmonrovia@...> wrote:

> but i'm wondering why you don't do the anticoagulation

> therapy first not last?

Ken L. writes:

> > COMPLETE (and I mean COMPLETE) testing for

> > * All coagulation factors -- for myself, I typically

> > sit at thr 94%ile for soluble fibrin monomer when

> > in recovery. With CFIDS it was > 99%ile.

> > * All inherited coagulation factors currently know

The other side of the hypercoagulation coin is: already

having blood on the thin side (which would be exacerbated,

possibly dangerously so, by blood thinners either by Rx

or various blood-thinning herbs and supplements).

23andme.com for example tests for genetic Warfarin sensitivity,

among dozens of other medical risks. Their drug reactions are

one of the best features on 23andme, a direct-to-consumer

genetics company, along with the Raw Data Browse by gene and

SNP rs# for advanced students and informal researchers.

I'm in the 12% of Euro ancestry who have a 2.5-fold increase

in Warfarin sensitivity.

Type O-neg blood has the thinnest blood of the different

blood types, all other things being equal (which they rarely

are). I'm O-neg.

Neither of these qualifies as a clotting problem, but either

tends to have thin *enough* blood where a blood thinner

is contraindicated. This would not show

up on hypercoagulation testing.

Carol W.

willis_protocols

[Guest guest]

>

> The other side of the hypercoagulation coin is: already

> having blood on the thin side (which would be exacerbated,

> possibly dangerously so, by blood thinners either by Rx

> or various blood-thinning herbs and supplements).

>

> 23andme.com for example tests for genetic Warfarin sensitivity,

> among dozens of other medical risks. Their drug reactions are

> one of the best features on 23andme, a direct-to-consumer

> genetics company, along with the Raw Data Browse by gene and

> SNP rs# for advanced students and informal researchers.

> I'm in the 12% of Euro ancestry who have a 2.5-fold increase

> in Warfarin sensitivity.

>

>

> Type O-neg blood has the thinnest blood of the different

> blood types, all other things being equal (which they rarely

> are). I'm O-neg.

>

> Neither of these qualifies as a clotting problem, but either

> tends to have thin *enough* blood where a blood thinner

> is contraindicated. This would not show

> up on hypercoagulation testing.

I'm O negative, but have very thick blood. And I got a big increase in die-off

from using various enzymes.

Generally speaking, having CFS trumps everything else, I think.

Best,

[Guest guest]

There are so many different causes of CFS and aspects of

the individual case, I don't think hypercoagulation is

a safe assumption, and needs to be tested for.

Carol W.

[Guest guest]

>

> There are so many different causes of CFS and aspects of

> the individual case, I don't think hypercoagulation is

> a safe assumption, and needs to be tested for.

>

>

> Carol W.

>

Well, part of the problem with this is the frustrating case definition.

If you look at CDC CFS, I would agree with you.

If you look at Canadian Consensus Criteria CFS, everything I've heard or seen

suggests it's quite homogenous.

So a major goal, in my opinion, is to separate out the people with CCC CFS to

recognize that their disease is discrete.

The movement seems to be to do that and call that subsegment " ME. "

It will be a challenge to make it happen though.

Best,

[Guest guest]

>

do these coag problems put us at a greater risk of heart attack and stroke?

Then add to it the fact that we can't get much exercise, are we at great risk?

[Guest guest]

The link in Step 1 (for tests) did not work for me, are the tests listed on your

website in the FWIW Protocol, Stage Two: Determine Surviving Pathogens the

correct & current tests? If so, I went to the Lab site and did not see a CFIDS

panel as indicated on your website... (to test for infections)

Can you point me in the right direction?

Thanks

>

> I ended up doing this up after a long call today, so I thought that I would

share it here also for any one that is interested. It was worked for 4 people in

this house [TREATMENT was DIFFERENT for each, because labs showed different

problems for each]

>

> Short Version of Treatment for CFIDS/FM

> (see http://lassesen.com/cfids/)

>

> Step 1: PCR Testing for the infections that can cause it:[if general testing

was done for the FAMILY, then for positive items it should be followed up for

the specific one] See http://www.lassesen.com/cfids/infections.htm. EXCLUDE

nothing -- there is the risk that you are a symptomless carrier...

> * Mycoplasma

> * Epstein Barr (EBV)

> * Q-Fever

> * Rickettsia (Lyme disease, Rocky Mountain Spotted Fever etc)

> * Helicobacter pylori

> * Cytomegalovirus / Herpes (HHV-6)

> * Chlamydia

> * Candida

> * Varicella zoster

> * Leprosy (I have met CFIDSer who came down with it ~ 2 yrs after recovering

from Leprosy)

> * Parvovirus B

> * Hepatitis

> * TB

> * XMRV

> Step 2:A

> Treat all of the above infections found until clear. Make sure that the

anti-???? is effective against the specific infection.

> * Personal preference is the use of targeted -Transfer Factor for virus. (Seen

EBV specific TF being very effective)

> ---- It's old technology (pre-antibiotics), but still effective.

> ---- Takes much longer to clear the infection than antibiotics but does it

with less risk of bad herxs and seem to help the body learn to target the

infection reducing risk of reoccurance.

> Step 2:B

> COMPLETE (and I mean COMPLETE) testing for

> * All coagulation factors -- for myself, I typically sit at thr 94%ile for

soluble fibrin monomer when in recovery. With CFIDS it was > 99%ile.

> * All inherited coagulation factors currently know

> Step 3:

> * Use of fibrinolytic enzyemes (Nattokinease, Serrapetase, Lubrokinese,

Bromelain)

> --- WARNING: they will typically cause antibiotic/antiviral tissue to

concentrations to increase 10 fold and can result in a massive herx on low

dosages of antibiotics and antivirals.

> ---- Without clearing fibrin deposits, locii (reserves) of the infections will

persist and re-occur.

> * Use of Nootropics (Piracetam) and other (conventional) treatments associated

with Stroke and head trauma.

> * Appropriate treatment for the nature of coagulation problem (some may not be

prescription -- for example, turmeric --kitchen spice)

>

> IMHO: CFIDS is a disease cause brain trauma with the brain trauma resulting

from alteration of blood flow due to coagulation or inflammation of tissue.

>