Alternatives to MP Drugs

[Guest guest]

I can agree with most of your post. The following paragraph however

reflects a common misconception, and is NOT a valid reason for doc

not to prescribe the protocol:

" Since many CFIDS sufferers have low blood pressure and many doctors

have problems prescribing Benicar (a blood pressure lowering

medication) to individuals with already low blood pressure, does

anyone know of other ARB drugs that have similar anti-inflammatory

effects? "

You can look at the FDA dosing info. More benicar does not cause

blood pressure to drop further, and it states clearly that dosing

needs to be individualized. Most people find their bp stabilizes,

sometimes up, not down. I started with extremely low blood pressure

(80/50 range, sometimes 70/40) and it has not dropped with the

Benicar.

If you are interested in persuing the MP, then you can talk to

Trevor about an alternative abx that is a possibility to be used on

the protocol. But you and your doctor would need to speak to him

about this.

If you want to experiment with alternative ARBs and/or abx, you

might also want to search the archives at sarcinfo.com and read

about people's early experiences with alternate meds.

I'll definitely be interested to hear of any alternatives that

people might come up with that are effective. From personal

experience, I think it's going to be hard to beat the Benicar, but

perhaps that will differ with the individual. reported that

Quecertin, and some other supplement (I can't recall) helped him a

lot with the other inflammatory pathways, and he thinks it's why he

responded so quickly to the Benicar. You might search for that info

as well.

penny

[Guest guest]

I find this is also the case with another drug, catapres. It is taken by

millions to lower blood pressure, but for me it raises it. This an other blood

pressure medications seem to work to " regulate " blood pressure, not specifically

raise or lower.

Doris

----- Original Message -----

" Since many CFIDS sufferers have low blood pressure and many doctors

have problems prescribing Benicar (a blood pressure lowering

medication) to individuals with already low blood pressure, does

anyone know of other ARB drugs that have similar anti-inflammatory

effects? "

You can look at the FDA dosing info. More benicar does not cause

blood pressure to drop further, and it states clearly that dosing

needs to be individualized. Most people find their bp stabilizes,

sometimes up, not down. I started with extremely low blood pressure

(80/50 range, sometimes 70/40) and it has not dropped with the

Benicar.

[Guest guest]

> The theory behind the MP has merit, but if we get stuck on ONLY

ONE

> or TWO drugs we are limiting ourselves and the number of people we

> can help. The key to the MP is reducing and controlling

inflammation

> AND attacking the invaders which should help correct the immune

> system. (I believe to really get better we also need to increase

and

> maintain our levels of GSH and correct the damage to the liver

> detoxification system as well among other things.) Identifying

> supplements (thanks Frand) and other ARBs and possibly ACE

inhibitors

> that can help to reduce inflammation for those who can't obtain or

> tolerate Benicar is a fruitful avenue. Identifying other

antibiotics

> with similar properties of minocycline for people who are possibly

> allergic and/or can't tolerate it would also be fruitful.

>

> Since many CFIDS sufferers have low blood pressure and many

doctors

> have problems prescribing Benicar (a blood pressure lowering

> medication) to individuals with already low blood pressure, does

> anyone know of other ARB drugs that have similar anti-inflammatory

> effects?

>

> I had a very severe reaction to minocycline (more like an allergic

> response than a herx response) so I'd also like to find an

> alternative to minocycline.

>

> I'll spend some time exploring this and will report back and hope

> others will as well.

>

> A big thanks to for his excellent research and synthesis of

> published articles supporting the case for a TH1 shift in the

immune

> system. I still have questions about this, but it will have to

wait

> for another day.

Hi

You might be interested in the fact that twice now I have really

benefited from doing the oral Kane protocol from her Detoxx book in

conjuction with firstly Samento for 6 months and now Cats Claw tea 3

times daily plus Doxycycyline 100mg x 3 every other day protocol.

I mention that the Kane protocol has helped me twice, I got to

feeling 90% of normal for a couple of months this year but stupidly

stopped both the Kane protocol and the Samento cos I felt so well I

didn't think I needed them anymore. Within 3 weeks ALL my symptoms

were back.

Luckily I keep daily records so I could look back and see where I

had gone wrong but I found this very difficult cos I felt so sick.

The following list shows what I have had to do to greatly improve

how I am feeling and able to do -

I had to increase my thyroid meds right up (Armour from 1/2 grain up

to 3 grains) my body temperature had taken a nose dive down to 36.1

from 36.6.

I restarted Phosphotidyl choline 2 am and 2 pm

I carried on with Butyrate 2 am and 2 pm

I started Balanced Electrolytes drinks 3 times daily

(All the above supplements were from Allergy Research but bought

over the Net)

I take milk thistle 3 times daily plus loads of basic supplements

like B complex, C, E and Selenium

I ran out of Samento and researched Cats Claw and decided there was

enough evidence for plan Cats Claw bark being effective so have been

taking this as tea 3 times daily for a month now

I started Amocillin for 6 days but felt terrible on it

I started Doxycycline and have worked up to 100mg x 3 but I am using

an every other day protocol. Have had some severe aching on it but

this has improved recently and no real herxes this week.

Did develop a nasty yeast issue after 2 weeks and had to take

Diflucan which worked well and in addition I have done 10 days of

Pau D'Arco

The improvements came after 2 weeks on the above regime, temperature

back up to 36.6/36.5, loads of energy, rode my bike for 4 miles

yesterday on a very humid day when the temperature was 27 degrees

and this was on top of driving 40 miles in the morning and doing

some shopping.

Admittedly I did get dizziness in the back of the head from 5 pm

which was the neuro symptoms reminding me that I am not cured but I

had an excellent long sleep of 8 hours and today all dizziness is

gone and I am ready to do an hour of pilates and this afternoon I

will be going to visit a country house and look around the gardens.

This is twice this year I have got to really improve my quality of

life so I am positive it can be done. BTW As you probably all know

I did get rid of the poison of mercury from my body 2 years ago by

having all my fillings removed and chelating out the mercury and

last year Dr W diagnosed me with borrelia and co-infections. I have

been helping my worn out adrenals with 2.5mg Prednisolone for 20

months and still it is needed but this could be a completely

separate problem in my case going back to 1973 after loosing a

considerable amount of blood after the birth of my son. It might

not be connected to the CFS at all but it would certainly have made

it worse. However the adrenals are also much stronger now because

last year I had to take double the dose of Pred I am taking now so

there has been a definite recovery here too.

I think there should be much more emphasis on what Kane et al are

saying about improving the cell lipid structure, it doesn't have to

involve drugs either and it does make a lot of sense.

Pam

[Guest guest]

Other ARBs: Lozaar, Diovan, Avapro, Atacand, Micardis, Teveten.

Benicar has demonstrated efficacy for lowering blood pressure

compared to the others, but has a high incidence of associated

dizziness. Other side effects of ARBs but not all: headache, flu-

like symptoms, upper respitory tract infections. Some Side effects

associated with ACE inhibitors include: dry persistent cough and

angioedema. Due to these side effects, ARBs are increasingly

popular. Many studies are underway to study the effects of ARBs on

cardiovascular and renal disease, but few applying these drugs to

bacterial/viral infections. However, I did find the following

articles.

These articles gets at the reason why ARBs might be considered for

infectious conditions.

http://www.genomedics.com/investor/AT1RSARS.pdf

GenoMed, Inc. Reaffirms Potential Utility Of Sartans For SARS

ST. LOUIS, April 28 /PRNewswire-FirstCall/ -- GenoMed, Inc (OTC Pink

Sheets: GMED)( " the Company " or " GenoMed " ), a St. Louis, Missouri-

based medical genomics and Next Generation Disease Management

company, announced today that, after review of the available

literature, it has changed its idea of mechanism but retains its

conclusion that angiotensin II receptor blockers (ARBs), whose

chemical names all end in " sartan, " ought to be a valuable treatment

for SARS (severe acute respiratory syndrome). The Company is still

looking for patient and physician collaborators.

In its press release of April 25th, the Company discussed the utility

of ARBs for T cell-mediated immunity, so-called " acquired immunity. "

But review of the lung pathology of SARS patients reveals that

monocyte/macrophages, not T cells, are the primary immune cell

involved in SARS. Monocyte/macrophages are a more ancient defense

against invading viruses, and represent the body's " innate immunity. "

The picture of what happens in SARS now appears to be as follows: the

virus infects macrophages which line the gas-exchange unit of the

lung, called the alveolus. The macrophage responds by becoming

activated, which involves synthesis of angiotensin I converting

enzyme (ACE) and production of angiotensin II. Angiotensin II

generated by the activated macrophage stimulates not only the

macrophage itself, but neighboring macrophages. Activated macrophages

promptly begin synthesizing and secreting additional cytokines,

including tumor necrosis factor-alpha (TNF-alpha). TNF-alpha alone

has been shown to cause the high fever, muscle aches, and malaise

which all SARS patients experience. TNF-alpha also causes apoptosis

of lymphocytes in the bone marrow, which could explain the low

lymphocyte counts seen in SARS.

A few days later, the epithelial cells of the lung become damaged by

the SARS coronavirus. They undergo cell death, in a process also

accelerated by angiotensin II. Their ingestion by neighboring lung

macrophages further activates the macrophages, increasing the

synthesis of cytokines. More monocytes are recruited from the

bloodstream, and take up residence in the lung, explaining the

monocytic infiltrate in lung biopsy specimens.

The net effect is a clinical picture that resembles acute respiratory

distress syndrome (ARDS). In this syndrome, death of epithelial cells

results in progressive respiratory failure. Lung epithelial cells,

once they are killed by smoke inhalation, chemotherapy such as

bleomycin, radiation, or microbes, begin an often irreversible

process of lung failure.

Evidence for this hypothesis is the extremely low mortality (4%) seen

at Prince of Wales Hospital in Hong Kong, compared to the 20%

mortalities seen at another hospital in Hong Kong and in Canada. The

only difference was that the Prince of Wales hospital was aggressive

in its use of steroids. It may be that steroids have more clinical

usefulness than antiviral therapy.

Steroids do not cure all patients with ARDS, nor did they prevent

death completely at Prince of Wales hospital. GenoMed therefore

suggests the use of a " sartan, " at a dose low enough not to lower

blood pressure, for all patients suspected of SARS. As prophylaxis,

this approach should be of less risk than recommending the use of

prophylactic steroids, since not all fevers are due to the SARS

virus. Most pneumonia will still be due to other microbes, for which

appropriate antibiotics exist, and whose course may be aggravated by

steroids. The use of steroids should be reserved for patients with

progressive SARS despite earlier therapy with a " sartan. "

If the " sartan for SARS " hypothesis is confirmed, then an obvious

additional hypothesis to test will be " ARBs for ARDS. "

About GenoMed

GenoMed, Inc. is a medical genomics company whose mission is to

improve patient outcomes by identifying the molecular pathways that

cause disease. A St. Louis Business Journal article

(http://www.stlouis.bizjournals.com/stlouis/stories/2002/05/13/story8.

html ) first reported that the company has applied for patents based

on its finding that the ACE gene is associated with a large number of

common diseases. The Company has filed worldwide patent applications

on its new treatments, and is eager to license them globally.

GenoMed's research results are more fully described on its website,

www.genomedics.com

For questions, please contact GenoMed at 314-977-0110, FAX 314-977-

0042, email: dwmoskowitz@... or dpollack@... ,

or visit GenoMed at www.genomedics.com.

This press release contains forward-looking statements, including

those statements pertaining to GenoMed, Inc.'s (the Company's)

treatments and business model. The words or phrases " would

be, " " ought to, " " will allow, " " may, " or similar expressions are

intended to identify " forward-looking statements " within the meaning

of the Private Securities Litigation Reform Act of 1995. Actual

results could differ materially from those projected in the forward

looking statements as a result of a number of risks and

uncertainties, including but not limited to: (a) whether patients

with coronavirus infection and SARS respond to this treatment

approach; ( whether we will have sufficient financing to conduct

our research and development; © how competition from existing or

new competitors will impact our business, and (d) our research and

development being subject to economic, regulatory, governmental, and

technological factors. Statements made herein are as of the date of

this press release and should not be relied upon as of any subsequent

date. Unless otherwise required by applicable law, we do not

undertake, and specifically disclaim any obligation, to update any

forward-looking statements to reflect occurrences, developments,

unanticipated events or circumstances after the date of such

statement.

SOURCE GenoMed, Inc.

-0- 04/28/2003

/CONTACT: Dave Moskowitz, dwmoskowitz@..., or

Pollack, dpollack@..., both of GenoMed, +1-314-977-0110,

or fax, +1-314-977-0042/

/Web site: http://www.genomedics.com /

(GMED)

CO: GenoMed, Inc. ST: Missouri IN: OTC MTC HEA SU:

KH-KW -- FLM015 -- 8750 04/28/200311:39 EDThttp://www.prnewswire.com

*************************************************************

The differences between ACE inhibitors vs. ARBs

ARBs Do More Than Just Lower Blood Pressure

Summarized by W. Griffith, MD

May 7, 2002 (Reviewed: July 16, 2004)

Introduction

Angiotensin is substance in the blood that is necessary for the blood

vessels to constrict. One way of treating high blood pressure is to

block the formation of angiotensin, or block its action on the blood

vessels. There are two classes of drugs that make use of this

approach. The so-called angiotensin-converting enzyme (ACE)

inhibitors block an enzyme in the body that is necessary for the

formation of angiotensin, while the angiotensin receptor blockers

(ARBs) block the access of angiotensin to its point of action in the

blood vessels. It looks like ACE inhibitors and ARBs have the same

result - stopping angiotensin contracting the blood vessels - so

what, if any, are the differences between them?

Two of the earliest physicians working in the angiotensin field have

recently reviewed our knowledge of the ACE inhibitors and ARBs in the

medical journal, Lancet. This is a summary of their review, with some

additional information.

Effective medical treatment of high blood pressure has been available

for the last 50 years, and with every new class of drugs introduced

there has been a reduction in the number and severity of the side

effects that they cause. This is real progress, as antihypertensive

treatment is, usually, a lifelong undertaking; without

the 'motivation' provided by obvious disease symptoms, taking a pill

a day requires that it doesn't cause side effects.

The ACE inhibitors and the ARBs have side-effect profiles that are

almost ideal for effective medications. However, there is still a lot

to be learned about the way they work and their full effects on the

cardiovascular system.

Advantages of ACE inhibitors and ARBs

In studies where they were compared with dummy tablets (i.e. placebo-

controlled studies), ACE inhibitors were shown to reduce the risk of

illness and death from heart attack, heart failure, kidney disease,

and stroke. The newer ARBs have so far provided similar results for

kidney disease and heart failure. In the case of heart failure,

giving an ARB (valsartan) to patients already taking an ACE inhibitor

improved their outcomes still further.

The so-called LIFE study1 examined over 9,000 patients with high

blood pressure and enlargement of the left heart chamber (ventricular

hypertrophy), who were given an ARB (losartan), or another, older

class of drug, a beta-blocker (atenolol). After 4 years' treatment

there were less illness and deaths due to stroke or heart attack with

the ARB, and also a smaller number of these patients developed

diabetes for the first time, compared with the beta-blocker. In those

LIFE study patients who had diabetes from the beginning of the study,

reduction of fatal heart attacks and heart failure were greater with

the ARB than with the beta-blocker.

Importantly, measurements of heart enlargement showed that there was

a greater reduction with losartan than with atenolol. The finding was

not totally surprising, as angiotensin is considered a 'growth

factor' for heart muscle, so that blocking it's action would limit

heart muscle growth.

Differences between ACE inhibitors and ARBs

The favorable effects of ACE inhibitors and ARBs on blood pressure

are virtually the same. They also have similar effects on other

angiotensin-related conditions, like heart muscle enlargement and

kidney disease. But, how do they differ?

One of the commonest side effects of ACE inhibitors is a dry,

persistent cough. It occurs in about 1 in 10 of people taking them.

None of the ARB drugs have been found to have this effect, which is

gives them a clear advantage over the ACE inhibitors.

Other possible differences between ACE inhibitors and ARBs may be

revealed in future studies. In the meantime, we can conclude that the

benefits of both are extremely similar, their actions that go beyond

merely lowering blood pressure are also similar, but they differ in

that the ACE inhibitors have likely to cause an irritating cough in

some patients.

Source

Angiotensin blockade for hypertension: a promise fulfilled. HR.

Brunner, H. Gavras, Editorial. Lancet, 2002, vol. 359, pp. 990--991

Footnotes

1. Cardiovascular morbidity and mortality in the Losartan

Intervention For Endpoint reduction in hypertension study (LIFE): a

randomized trial against atenolol. B. Dahlof, RB. Devereux, SE.

Kjeldsen, et al., Lancet, 2002, vol. 359, pp. 995--1003