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Other symptoms

links to related articles as follows

  • anemia of chronic disease may be a protection against mycobacterial persistence
  • fatigue and lethargy may take many years on MP to resolve
  • fibrosis encases bacterial pathogens in collagen, from which they will eventually begin to break free, and is not stopped by steroids.
  • effect on pace of tissue regeneration
  • nails of fingers or toes are frequently affected in sarcoidosis
  • hypervitaminosis D
  • gray hair may not indicate normal aging

Fibrosis

When the immune system fails to deal with a pathogen it encases the diseased (infected) tissue in collagen. Angiotensin II is known to accelerate the deposition of collagen into tissue. This is part of the body's immune response. Long-term deposition of collagen leads to fibrosis (falsely called 'scar' tissue).

Deposition of collagen to encase pathogens which have escaped the immune system is one of the last lines of defense of the body.

Autoimmune damage

…..'autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body damage' does not exist, except in the minds of the scientists who study it. It would take a whole conference on the topic to get beyond that simple statement. You can look at my Bio21 lecture for a slide with a little more background on this issue.

There is currently very little known about fibrosis in Sarcoidosis. Since nobody has been healed of the disease (prior to the MP) the scientists have just been guessing at what causes the fibrotic tissue deposition.

Recovery from fibrosis

Medicine will tell you that fibrotic tissue does not remodel, but that is not what we are seeing.

Fibrosis (collagen) is thought to be permanent, but it isn't. In Rheumatoid Arthritis, collagen, especially when under mechanical stress (as it is in the lungs) will resorb, and potentially release some of the diseased tissue.

“I don't think it will be necessary to stop Benicar in order to get cartilage remodeling. I say that because of lesser remodeling of tendons on arms and legs which is occasionally reported by the cohort. I know that Angiotensin II is thought to be key in deposition of fetal cartilage, abut I am not sure that this function is not supplanted later in life. You are correct in expecting it to be at the 5+ year mark into recovery, however…” ..Trevor..

Cartilage research

Physicochemical and biomechanical stimuli in cell-based articular cartilage repair. 1)

Anti-inflammatory strategies in cartilage repair. 2)

Tissue engineering for articular cartilage repair–the state of the art. 3)

Effectiveness of chitosan scaffold in skin, bone and cartilage healing. 4)

Role of platelet-rich plasma in articular cartilage injury and disease. 5)

Role of the Subchondral Bone in Articular Cartilage Degeneration and Repair.  6)

Cartilage repair across germ layer origins. 7)

Smart Polymeric Hydrogels for Cartilage Tissue Engineering: A Review on the Chemistry and Biological Functions. 8)

Gelatin-Methacryloyl Hydrogels: Towards Biofabrication-Based Tissue Repair. 9)

Evolution of autologous chondrocyte repair and comparison to other cartilage repair techniques. 10)

Mechanism research on a bioactive resveratrol- PLA-gelatin porous nano-scaffold in promoting the repair of cartilage defect. 11)

Remodelling

Fibrosis remodelling occurs as the Vitamin D metabolites normalize, for much the same reason as arthritic joints recover during the several years of phase 3.

We have seen no sign in our cohort that the organs cannot heal to restore full function, even though deposited collagen remains in place. The lungs are really good at healing, even though they may be badly scarred from years of fibrosis.

The issue of fibrosis is complex, and we are learning more all the time. But the conventional view that the body cannot heal because of fibrotic tissue is absolutely incorrect. We have proved that. Beyond that statement, only time will tell.

As the body heals (with the MP) the fibrotic tissue will 'remodel' and be replaced by new healthy tissue. We have no data yet on what happens at this point, as nobody has ever recovered from this disease before the MP, and scar tissue was thought to be permanent. We now know that it isn't, that it remodels, but beyond that is still unchartered territory.

Liver fibrosis is reversible in humans. Everything heals on the MP, but at differing rates. For example, neuropathy is slower to respond, and fibrosis is very slow. But the body has demonstrated that it can eventually recover from just about everything caused by Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue..

We are seeing that fibrosis in kidneys, livers, and lungs slowly remodels after the patient has been returned to health. It is part of the gradual recovery which will creep up on you over many years.

Folks recovering on the MP need nothing except their returning health. The angiotensin blockade (Benicar) inhibits the formation of new fibrotic tissue. Eventually, a fully-functioning immune system (without antibiotics) will do the job perfectly well. Prof. Marshall

Assessing recovery from fibrosis

Even though you may still be feeling terrible, a CT scan might well show that the lymph nodes are steadily shrinking. Granuloma shrink too, but not those which have been calcified or turned fibrotic.

The PFTs usually improve, particularly the DLco, or gas diffusion capability.

The more fibrotic tissue a patient has accumulated, the more sensible it is for that patient to continue with the MP until all signs of the disease have disappeared.

The immune system kills CWD, not the drugs

ImmunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. (Herxheimer reaction) is to be expected and should not be interpreted as a side effect, adverse reaction or intolerance.

We know that when the immune system is effectively fighting infection, the result is cell death. But this is the road to recovery. It is a mistake to focus on the drugs. It is the immune system that is killing the intracellular bacteria.

The aim of the combined essential elements of the MP (avoiding light and vitamin D, using the MP meds etc) is to stimulate/activate the immune system.

The innate immune system can work properly when the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. is not over-stimulated, and the antibiotics are often not necessary to continue the process. The antibiotics may ensure a more even species-kill, and establish a pattern to the response.

Even in the absence of Benicar (and abx), the immune system will usually keep killing bacteria for months, until D(1,25) creeps up again.

Cell death (apotosis) must precede cessation of fibrosis

Immunupathology resulting from fibrosis remodeling

If you have significant fibrosis there is reason to expect your immune system will have ongoing low-levels of pathogens to deal with for quite some time.

Also, as the immune system becomes more competent again it has the ability to go after species which it could not deal with during earlier phases of your recovery.

As the fibrotic tissue is remodelled (by the body's own processes) there may be times when many encased pathogens are suddenly released.

As a consequence, patients with extensive pulmonary fibrosis may experience sudden bouts of severe pulmonary immunopathology (which may include extreme SOB).

At any stage along the MP the immune system may become particularly active due to remodeling of fibrosis and need more modulating than stimulating.

Regular doses of antibiotics can be modulatory and may actually reduce your immune response. The regular cycles and meds adjustments may help to make the immune response fit into a predictable pattern.

Pneumothorax

It is the sarcies who seem most at risk of sudden and/or severe immunopathology, with lots of lung fibrosis.

Those who have severe respiratory disease should be encouraged to keep the oxygen concentrator handy for a year or two into phase 3, out of an abundance of caution .

Sarcoidosis patients often have surgery on their lungs. The open lung biopsy, by thoracotomy, is a very invasive procedure that (thankfully) is not used much any longer. But even bronchoscopy can lacerate the lung tissue a little. This damaged tissue may be the source of previously resistant pathogens which cause this sudden severe immune system response.

Sarcoidosis patients who have had a lung biopsy to be particularly careful of leaks in their lungs, which may occur gradually or suddenly, causing large or small pneumothorax. I had 'an adhesion' in 1989, where the bottom of my right lung stuck to my diaphragm, an extremely painful event. This was at the point where tissue had been removed for the thoracotomy biopsy in 1978. This area has been the site of severe immunopathology.

Only when treatment is absolutely necessary

Blood transfusions should not be given unless warranted by dangerously low Hct and Hgb because they carry serious risks. Not listed is also the probable infusion of CWD bacteria with each transfusion.

Transfusion

If your Hct and Hgb are dangerously low a blood transfusion is the standard treatment.

A Canadian Critical Care Trial Group studycompared “restrictive” Hgb to “liberal” Hgb transfusion strategies. The “restrictive” strategy was as effective and superior to the “liberal” transfusion strategy among patients less than 55 and without cardiac disease. Patients had an overall greater decrease in mortality and less complications. They concluded that a transfusion threshold of 7 g/dl is safe in critically ill patients, including those with minimal cardiopulmonary disease. Recent recommendations suggest RBC transfusion only in cases with <Hgb and known clinical symptoms.

Blood transfusions should not be given unless warranted by dangerously low Hct and Hgb because they carry serious risks. Not listed is also the probable infusion of CWD bacteria with each transfusion.

Nails

Does the disease process or the MP cause hair and/or nail changes? See hair changes

Sideways lines are a recognised indication of infection.

Nails are part of the Integumentary system and can be used as described to help in diagnoses of stress and various forms of illness.

Member experiences

I have noticed that my toenails on both feet are changing. I have had diabetes for 46 years and I have deep ridges in great toes but, the ridges are disappearing and the nails are becoming smoother. I think this is SIGNIFICANT for a long time insulin dependent diabetic. Any one else notice this? I have NEVER heard of this! ~ Debbie Y

my fingernails have vertical ridges along with the horizontal ridges - growing out. ~AB

The finger nail problems you describe are very common with psoriatic arthritis. My fingernails have looked the way you describe for many years, long before I got sick. Mine aren't so angled as they are wavy. Sometimes these problems are associated with fungus and go away with rather strong medication (that would clearly not be permitted with the protocol). Sometimes people actually lose their nails–simply shed them. I lost one a year ago and to my amazement a perfect one grew back. I'm quite proud of it.Everything about it is perfect. Might be the first small physical improvement I've experienced in several years. ~Jim

I'm not exactly sure when mine appeared, but I have many, fine ridges running lengthwise on all my fingernails which are easily felt and seen. I have wondered myself whether or not they may be connected to this illness. Brad has always had some ridges but they are noticibly worse.(very rough) ~Paulette

My experience has been that my nail ridges are much less obvious now than pre-MP. Back then, I used to get inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and lots of tiny blisters behind my cuticles and then deep ridges in my nails as a result. ~Belinda

I've had those ridges in my nails for several years before I got sick. I was in my 20's so I don't think age is the reason. ~CFSgirl

I HAVE ALSO NOTICED HEAVY RIDGES OR LINES HAVE APPEARED ALONG THE LENGTH OF MY NAILS,NOT ON THE OUTER EDGES BUT TOWARD THE MIDDLE,MY NAILS SEEM STRONGER AND AT THE SAME TIME FLEXABLE,BUT THE RIDGE RIDDLE I HAVE NO ANSWER TO ~vda51

I, too, have ridges in most all of my fingernials. There appears to be no fungal problem. I can remember that I had nice smooth nails when I was younger, before roughly the time when I got bit by my first tick. My ridges developed over much time, slowly. Not really sure when they started. But they certainly showed up as my disease increased in severity. ~Dark Vader (aka, George)

I have vertical ridges on my nails that have “worsened” on the MP. Three nails that were ridge-free, are now ridged as well. I don't think it has to do much with aging, unless the aging has to do with intracellular bacteria wreaking havoc in the body. So I'm blaming the ridges on the bacteria in the meantime. Time will tell…! Alayne 2006 Just wanted to say a couple of months later that my nails continue to increasingly ridge. My thumbnails were relatively ridge-free as of my last post here 2 months ago. They've grown quite ridged and uneven since then. Pain free herx? If vertical ridges were all I had to worry about…what a world it would be! ~Alayne

Yes, my nails were always fine before I became ill with (Hashimoto's) autoimmune thyroiditis. Then suddenly they got very brittle, with deep ridges. I guess it is the lack of thyroid hormone which causes this. I suffered a lot of hair loss which has been reversed with thyroxine, but sadly my nails haven't recovered. I wonder if the MP can fix my nails too? ~Claudia

I can not remember when I had vertical lines on my nails since I always had them I though it was normal. ~Ramzi70

I don't think ridges on nails have anything to do with aging either, as I am 27 and have always seemed to have ridges on my nails. They run from the base (cuticle) to the tip of the nail, though sometimes they look slightly cross-hatched, not just straight lines. ~Lantern

I noticed this week that the nail ridges have all but disappeared from my right hand and are substantially lessened on my left hand. ~Desert Marie

Yes, I have noticed my nails are much stronger. ~Aunt Diana

I had to cut my nails recently because they were too long…that's the first time in several years. They would usually break or split. Definitely healthier. ~DNStog

I too have fine lines in my nails,, no fungus.~weepingsparrow

When I got to Phase 2 of the MP, the ridges disappeared from my fingernails. (I never got to Phase 3 because of moving and the changes from Medicare D, which eliminated my drug coverage from Medicaid, which had formerly paid for Benicar.) Since I have been off the MP for about a year, ridges have returned, worse than before. I just got back on Phase 1 and I expect the ridges will eventually disappear again. ~Lily

I too have had these since my teens on each nail; they are pearlized (like tiny little droplets making up the ridges). In my 20s, they would turn purple underneath and become very painful. (But no sign of fungus.) For years now, pre-MP my nails have chipped and broken off before I could cut them, splitting from the side and down the ridges. ~eClaire

===== Notes and comments =====

there is good MPeer commentary on nails at end now placed above except Dr Alan Cantwell, MD (dermatologist) reports that the CWD bacteria love sweat glands and hair follicles. Please see Dr. Cantwell's paper at The Eccrine Sweat Gland As A Possible Focus Of Infection With Acid-Fast Cell-Wall-Deficient Bacteria and material on diet, some of which could be used elsewhere

  • This is quite a hodge podge of symptoms. I'm not sure if it's good idea to group them together. It may end up that we need to create individuals for some or all of these. For now though, let's just collect some content and see how it goes. — Paul Albert 2008/11/25 00:39
  • Legacy content

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Anemia

My doctor says I'm anemic. What should I do?

Anemia is common in Th1 inflammation. It is not due to iron deficiency and will not be helped by iron supplements. In fact, iron supplements are counterproductive because iron will help L-formsDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. multiply.

Anemia of chronic disease Many physicians are aware of the anemia of chronic disease - or the anemia of infection and inflammation. This is one of the most common syndromes in medicine. If your physician is not aware of this, please share this information with him/her.

According to the textbook “An Introduction to Human Disease: Pathology and Pathophysiology Correlations” by Leonard V. Crowley, “Many conditions may depress bone marrow functions. Chronic diseases of all types may impair hematopoiesis and lead to mild or moderate anemia, which is called the anemia of chronic disease… The most common cause of this type of anemia is chronic infection, but other chronic diseases and some malignant tumors may also be responsible.”

See Diagnosing Anemia

GI bleeding A simple outpatient two minute check of your stool for blood would rule out your doctor's concerns pertaining to bleeding into the gut. (Hemoccult test in this country)

Anemia of chronic disease pathogenesis A number of bacterial pathogens have developed a mechanism for acquiring iron directly from the (human) host. These bacteria can actually hoard iron for their own use (instead of the human's benefit). Bacteria use several mechanisms to successfuly compete for available iron in the host, and their increased supply of iron may enhance bacterial pathogenicity.

The human body has limited defense mechanisms to limit the availability of iron to bacteria, thus blocking their growth. Once this iron-restricted erythropoiesis and the 'anemia of chronic disease' has developed, iron supplementation is not useful.

Iron transport and anemia are related to cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. that are produced in inflammatory and infectious diseases, such as Tumor Necrosis Factor alpha and Interferon Gamma. The cytokines associated with Th1 immune response are sensitive to intracellular iron concentration. The regulation of iron transport by cytokines is a key mechanism in the pathogenesis of anemia of chronic disease.

See Iron is required for growth of bacteria

In sarcoidosis, granuloma sequester Ferritin and iron, and the low assay is closely tied to the presence of inflammatory granuloma. Serum ferritin may be high in anemia of chronic disease, especially if the liver is involved.

One of the potential 'benefits' of the anemia of chronic disease is that bacteria are being starved of the iron essential for their proliferation. Once CWD bacteria are killed off, iron stores will be available for your own body once again.

Fatigue from chronic disease is a common symptom and is seen even in patients without anemia. Fatigue is not directly related to anemia. It will gradually resolve as Th1 inflammation resolves on the protocol but it it is often one of the longer-lasting symptoms.

See Bacterial iron acquisition systems

Testing Hemoglobin, hematocrit and serum ferritin are the most common ways to test for anemia but they do not differentiate between iron deficiency anemia (IDA) and anemia of chronic disease.

Normal hemoglobin results vary, but in general are:

-Male: 13.8 to 17.2 gm/dL (140-174g/l)

-Female: 12.1 to 15.1 gm/dL (123-157g/L)

Hematocrit is a blood test that measures the number of red blood cells and the size of red blood cells. It gives a percentage of red blood cells found in whole blood. Most automated cell counters measure the hemoglobin directly, but the hematocrit is calculated. Generally, therefore, it is probably more reliable to base clinical decisions on the hemoglobin concentration.

Iron supplements are usually well tolerated by patients so many doctors will not bother to definitively diagnose iron deficiency anemia. They will use iron supplements as a therapeutic probeA brief trial of the Marshall Protocol to see if it will generate an immunopathological response. The "gold standard" for testing whether a patient is a good candidate for the MP. and retest Hgb and Hct to see it they are effective. Before you agree to taking an iron supplement, talk with your doctor about further testing to determine if you have anemia of chronic disease.

To identify iron deficiency anemia, hemoglobin must be measured together with more selective measurements of iron status. This articlelists the other tests done when a differential diagnosis is needed. Ask your doctor to test:

-serum ferritin.

-serum iron

-total iron binding capacity (TIBC; an indirect reflection of the transferrin level)

-percent transferrin saturation (calculated from the serum iron and the TIBC)

-soluble transferrin receptor (sTfR)

All of these tests reflect slightly different aspects of internal iron metabolism and give the most complete picture of the iron status of the patient.

Serum (soluble) transferrin receptor A new test called serum transferrin receptor (sTfR) is a good way to verify anemia of chronic desease because it is not affected by inflammation. Serum ferritin may be high in anemia of chronic disease, especially if the liver is involved. The normal range for serum transferrin receptor is 3-9 mg/l.

The sTfR test should be considered for anemic patients whose differential diagnosis includes iron deficiency and anemia of inflammatory disease. Transferrin receptor values are elevated in iron deficiency anemia (IDA), and in chronic hemolytic anemias.

Source: https://www.med.yale.edu/labmed/labnews/jan1999c1.jpg

According to this reference:

Anemia of chronic disease and iron deficiency anemia, the most common forms of anemia, are differentiated primarily by estimates of iron status. Standard measures of iron status, such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease. In contrast, soluble transferrin receptor (sTfR) is elevated in iron deficiency but is not appreciably affected by chronic disease.

In summary Anemia of chronic disease equals:

-ferritin normal or high

-iron low

-normal to low soluble transferrin receptor (sTfR)

-normal to low total iron-binding capacity (TIBC)

Anemia may excerbate due to immunopathology The antibiotics on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. will treat the underlying disease (bacterial pathogens) and the cytokines associated with infection and inflammation to resolve this anemia. During treatment, however, it is expected that anemia might temporarily worsen during the immune system reaction to antibiotic therapy.

It is suggested (male or female) that if your Hgb falls to 11 and/or your Hct falls to 28, you should slow down your immune response by managing all aspects of the MP. Please see My immune system reaction is too strong. What should I do? If you need help with this, please ask a moderator for assistance in your progress report on the website.

Recheck your Hgb/Hct in a few weeks to make sure they are going back up. It may take 24-36 months for anemia blood markers to return to normal range. See How long does the MP take?

Hgb and Hct are effective tests to monitor anemia of chronic disease. It is not necessary to test Hgb and Hct often. Your doctor will use his/her judgement re the frequency of testing to monitor your anemia.

“You are assuming that anemia is a condition whose seriousness is comparable to your Th1 immune disease. It is not. The Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens. will kill you. You and Doc need to balance which is the more important issue to focus upon.” ~Dr. Marshall

There are four different types of tests that measure the body's iron levels and storage.They are called iron level tests, total iron-binding capacity (TIBC) tests, ferritin tests, and transferrin tests.

Iron Iron is associated with Th1 immune activity. Macrophages, the Th1 phagocyte, accrete ferritin. Ferrodoxin is also oxidized and reduced when 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. is converted to 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.. So iron is closely associated with Th1.

The iron level test measures the amount of iron in the blood serum that is being carried by a protein (transferrin) in the blood plasma.

Serum iron (60-170 mcg/dl) on its own provides no useful information. Serum iron has a diurnal variation that can be as much as 30% within a single individual, it is sensitive to the day's dietary iron intake and is affected by all the confounding diseases listed above. A low serum iron picked up as an incidental finding has a very low specificity for iron deficiency.

Serum ferritin The ferritin test measures the level of a protein in the blood that stores iron for later use by the body.

Serum ferritin represents the iron stores in the body. Serum ferritin is also an acute phase reactant and will rise rapidly in the face of inflammation. Iron depletion (low serum ferritin) does not prove iron deficiency anemia.

We do not know how low is too low for iron stores to go. Your doctor may not be happy until your iron is within the normal range. If you decide to supplement we suggest that you retest frequently to maintain the level at the bottom of the normal range.

Male: 12-300 ng/mL

Female: 12-150 ng/mL

Total Iron Binding Capacity (TIBC) Total iron binding capacity (TIBC) is a blood test that shows if there is too much or too little iron in the blood. This test helps measure the ability of a protein called transferrin to carry iron in the blood. Normal range 240-450 mcg/dl.

TIBC is typically measured along with serum iron to evaluate people suspected of having either iron deficiency or iron overload. The iron concentration divided by TIBC gives the transferrin saturation, which is a more useful indicator of iron status than iron or TIBC alone.

The TIBC test measures the amount of iron that the blood would carry if the transferrin were fully saturated. Since transferrin is produced by the liver, the TIBC can be used to monitor liver function and nutrition.

Transferrin The transferrin test is a direct measurement of transferrin–which is also called siderophilin–levels in the blood. Some laboratories prefer this measurement to the TIBC. The saturation level of the transferrin can be calculated by dividing the serum iron level by the TIBC.

It is customary to test for transferrin (instead of TIBC) when evaluating a patient's nutritional status or liver function. Because it is made in the liver, transferrin will be low with liver disease. Transferrin levels also drop when there is not enough protein in the diet, so this test can be used to monitor nutrition.

Iron supplements Do not take iron supplements in an effort to increase hemoglobin and and hematocrit. Iron will only help the CWD bacteria multiply. Increasing iron in your diet would also be counterproductive. This article from the CDC's Emerging and Infectious Diseases explains how microbes sequester iron from the host: “Iron Loading and Disease Surveillance” https://www.cdc.gov/ncidod/EID/vol5no3/weinberg.htm

Transferrin saturation Transferring saturation (normal 20-50%). As an index of iron transport rather than storage, this measure (calculated from serum iron and TIBC) is an alternative to serum ferritin. However, as it is affected by the same confounding factors it will not add much additional information in iron deficiency if a serum ferritin has already been ordered. A serum transferrin saturation of >55% can be a very useful indication of possible iron overload. On the other hand, if serum ferritin is elevated but transferrin saturation is low, the patient is unlikely to have iron overload.

Mean corpuscular volume (MCV) MCV measures the size of the red blood cells.Larger or smaller than normal red blood cells may indicate anemia. Ref. Range 80 - 97

Mean corpuscular volume is decreasedin anemia of chronic disease.

Tracking immunopathology with lab tests -Transient decrease in Hgb and hematocrit are common in the early phases of the MP. My use of lab tests is to help determine pace of therapy…… ~Greg Blaney, MD

When palliation treatment is necessary Blood transfusions

If your Hct and Hgb are dangerously low a blood transfusion asap is the standard treatment.

A Canadian Critical Care Trial Group studycompared “restrictive” Hgb<7) to “liberal” (Hgb <10) transfusion strategies. The “restrictive” strategy was as effective and superior to the “liberal” transfusion strategy among patients less than 55 and without cardiac disease. Patients had an overall greater decrease in mortality and less complications. They concluded that a transfusion threshold of 7 g/dl is safe in critically ill patients, including those with minimal cardiopulmonary disease. Recent recommendations suggest RBC transfusion only in cases with <Hgb and known clinical symptoms.

Blood transfusions should not be given unless warranted by dangerously low Hct and Hgb because they carry serious risks. Not listed is also the probable infusion of CWD bacteria with each transfusion.

Erythropoiesis-stimulating agents

Although they are not without risk and we do not recommend them, Erythropoiesis-Stimulating Agents ((Aranesp, (Epogen and Procrit) may be necessary if Hct and Hgb are extremely low and do not respond quickly to measures to reduce your immune system reaction. ESAs (Procrit and Epogen) do increase red blood cells but they also have serious side effects and we don't know how they might affect the immune system. The decision to treat is based on risk/benefit.

Doctors using these drugs are advised “to maintain the lowest hemoglobin level consistent with avoiding the need for transfusions.” It isn't necessary to maintain a normal Hgb and Hct while you are recovering on the MP.

Members' experiences -My red blood count has risen into the normal range without any kind of iron or vitamin supplemenation. ~NorCalJim in phase 3

You can find personal stories in the topic Anemia and Th1 Disease.

Pernicious anemia

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Low carbohydrate eating on a budget lowcarbbudgetlink

Low Carb For Life Reprint Low Carb on a Budget

By Dana Carpendar

(edited to omit foods high in Vitamin D)

Now that the holidays are over, while our VISA cards are still smoking in our wallets, it seems an opportune moment to tackle a common complaint regarding a low carb diet: “It's so expensive!”

At first glance, this seems true. If you've been basing your meals on potatoes, rice, pasta, and generic white bread, you've been getting away with a lower cost-per-serving than, say, steak. However, I have several thoughts on this matter.

First, and most important, is this: Any food that makes you fat, tired, sick, and hungry would not be cheap even if they were giving it away. If you are carbohydrate intolerant, if you have the illnesses that have been identified as being related to high insulin levels - diabetes, hypertension, high triglycerides, polycystic ovarian syndrome, and the like - “cheap” carbs are a luxury you can't afford. You'll pay for them in the form of doctor visits, medicines, sick days, dental bills, and new clothes in bigger sizes.

Second, remember that many carb-y foods are not even cheap to buy. I've long suspected that cold cereal is a conspiracy to get us to pay three and a half bucks for fifteen cents worth of grain. Bulk potatoes may be cheap, but Pringles are expensive. Frozen dinners, canned biscuits, boxed potatoes, and other prepared foods are not budget items, and most of them are loaded with junk carbs and bad fats. Cut all of this rubbish out of your food budget, and you'll find a bit more room for protein and vegetables.

That being said, real, good, nutritious food does cost more per pound than the cheapest carb-y junk. How to deal with this?

*Not one of those expensive low carb specialty foods is essential to your success. When I went low carb they didn't exist. Going low carb meant eating unprocessed real foods, and I suspect that some of the health benefits stemmed from this simple fact. You'll save big money eating real food instead of low carb macaroni-and-cheese mix.

*Your body does not care if you get your protein from steak, and boneless, skinless chicken breast, or from hamburger, and chicken leg-and-thigh quarters. Hereabouts those boneless, skinless breasts often run $4.99 a pound, while leg-and-thigh quarters often go on sale for 69c a pound or less. Big difference.

*Buy in bulk When hamburger, butter, canned broth, natural peanut butter, or the like goes on sale, stock up. A freezer lets you take advantage of meat specials. I bought my deep freezed used for $225 and it has paid for itself many times over.

* We love rib eye steaks, which run $8.99 a pound. So I wait till whole rib eyes go on sale for $4.99 a pound, and have the nice meat guys slice one into steaks for me. No charge for this service, and I get steaks for several months for the price of one dinner at Outback. I also buy leg of lamb on deep discount, and have it cut into steaks - much cheaper than lamb chops.

* Eat what's in season. Asparagus, lettuce, berries, and melon, all great low carb foods, are sky-high this time of year. Cabbage, broccoli, brussels sprouts, and cauliflower are all in season, and are cheaper - I just bought cabbage for 39c/pound. This makes coleslaw, steamed broccoli, and cauliflower “fauxtatoes” better choices than salad. Turnips and rutabaga (I adore rutabaga!), spaghetti squash, and celery are other winter vegetables that work well for us. Grapefruit is abundant, wonderful and cheap in the winter, and has only about 10 grams of usable carb per half.

* Bagged salad, pre-cut veggies, skinless chicken, pre-made hamburgers are all expensive. The more food preparation you do yourself, the more money you will save. Spend an hour on the weekend prepping stuff yourself, and stash it in the fridge for busy days.

* Nuts are low carb, but so are pumpkin seeds, and they're far cheaper. More minerals, too!

* Drink homemade iced tea instead of diet soda.

* One of the lowest carb-and-calorie desserts is also one of the cheapest - store brand sugar-free gelatin.

* Cut way back on eating out. The same food is always far cheaper at home.

* Bag lunches are a great way to use up leftovers - who wants to pay for food to turn green in the fridge?

_ All contents Copyright (C) 2006, Hold The Toast Press. Lowcarbezine mailing list Lowcarbezine@holdthetoast.com https://www.ericschmitz.com/mailman/listinfo/lowcarbezine __ Nothing contained in this site is or should be considered, or used as a substitute for, medical advice, diagnosis or treatment by your physician.

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Fibrosis

Folks recovering on the MP need nothing except their returning health. The angiotensin blockade (Benicar) inhibits the formation of new fibrotic tissue. Eventually, a fully-functioning immune system (without antibiotics) will do the job perfectly well.

Dr. Marshall

The innate immune system can work properly when the VDR is not over-stimulated, and the antibiotics are often not necessary to continue the process. The antibiotics do ensure a more even species-kill, and establish a pattern to the response.

Even in the absence of Benicar (and abx), the immune system will often keep killing the bacteria for months.

See Cell death (apotosis) must precede cessation of fibrosis.

See What should I know about respiratory immunopathologyA temporary exacerbation in symptoms of the lungs due to bacterial death. Requires careful management by physicians.?

Patients experiences

E, when we met you were on a very high oxygen flow and I suspect that probably means you may have had some degree of pneumothorax for some time. Especially as you reported that you were able to manage with 2 L/min again yesterday. I suspect that once your lungs are reinflated you are going to have many more 'flashes of improvement' showing just how much disease the MP has chased away.

..Trevor..

Guss Wilkinson (pulmonary sarcoidosis involvement) wrote a good summary of his healing on the MP.

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Tissue regeneration

Tissue regeneration

Dr Marshall wrote:

I can assure you that the brain regenerates , that most systemic soft tissue regenerates, and the nerves regenerate, with only fibrotic damage being slow to change. My eyeglass prescription has remained the same, but the decrease in light sensitivity would tend to imply that the eye retinal tissue is regenerating, too.

Eventually the immune system will get rid of all pathogens, and most immunoglobulin activity will cease. That will take a few years, though. They say it takes 5 years to clear TB out of a body, which is a similar persistent intracellular pathogen.

Will defective genes return to normal?

“Some will go back quickly, some will take a while for the body's DNA repair mechanisms to work. All the expression changes occur pretty rapidly, it is only the mutations that will repair slowly.

Some mutations may not repair at all, but this is unlikely.”

..Trevor..

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Does the disease process or the MP cause hair and/or nail changes?

Dr Alan Cantwell, MD (dermatologist) reports that the CWD bacteria love sweat glands and hair follicles. Please see Dr. Cantwell's paper at The Eccrine Sweat Gland As A Possible Focus Of Infection With Acid-Fast Cell-Wall-Deficient Bacteria

Your hair and 1,25-D are closely coupled:

Hairless suppresses vitamin D receptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. transactivation in human keratinocytes.

Hair growth is closely related to the VDR and 1,25-D.

https://mend.endojournals.org/cgi/content/abstract/me.2004-0415v1

This article makes a close connection between alopecia and psoriasis, which the MP has been determined to resolve.

See Changes resulting from changes in 1,25D-hydroxyvitamin-D

Members' experiences

My hair stopped falling out and going grey! The new regrowth is my childhood colour !!!!!!!! ~Grazyna My hair grows much faster now. I always wanted it to grow grow grow and it just sort of sat there, now it grows super fast. ~Natalie17 Yes, hair and the lack of it where I want it (top front of my head) has been a big favorite with me and my disease. Cosmetics and hair pieces or a wig can help you feel better about your self image while on the MP, a good hat works too. ~jrfoutin Okay, I hadn't thought of this until a neighbor of mine starting losing clumps of hair in the shower and went to the doctor. She now takes Zoloft for too much stress which is 'supposedly' causing the hair loss. This person, too, has a lot of sinus trouble and has some back pain. Probably a th1 inflammation sufferer just like the rest of us. Behold!! I also have been losing hair in the shower for years. I have plenty of hair to go around, but it doesn't mean I want to lose it all to this disease. I'm thinking th1 inflammation is the cause. I do not lose clumps, but a small circle of hair, about half the size of my palm. Every day this happens when I wash my hair. ~Mindy One of the “moments of healing” for me was one morning in 2002 when I woke up and couldn't feel my hair anymore. Prior to this Liz had to cut my hair, as I was too jumpy at the barber's shop, and couldn't handle the transient pain. But one morning I woke up and realized that I couldn't feel my hair anymore. Well, I could feel it, but it didn't hurt in any way to run my fingers through it, or bend, shape, and mangle it. After being assured that was 'normal,' I settled back to enjoy another of the pleasures I had been missing all my life ..Trevor.. My hair is still coming out a little more than usual. My scalp feels tender and, though it's not particularly hot, it feels like heat is radiating from it. ~TickTock I have been trying to define what this hair pain and head pain actually feel like. Just barely touching the hair gives the same sensation as a blow to the head.. so it is shocking and disconcerting.. scalp has some itch as well, so the touching is more careful now. ~Aussie Barb I seem to be growing hair on my head WHERE NONE HAS EXISTED FOR QUITE SOME TIME … HAIR ON MY HEAD STILL GROWING ,THE WAY IT IS GOING I WOULD NOT BE SURPRISED IF I END UP WITH A FULL HEAD OF HAIR. ~vda51 -I am watching my (thyroid) antibody count drop as I progress on the MP. I've been on the MP for almost a year now. My Thyroid itself has been herxing…… as I have noted at the start of each phase: my TSH jumped. That went along with pain and swelling in my throat and hair-loss , which was a hypo-thyroid symptom. Then it levelled out as my body progressed through the phases. The hair-loss is something I've come to expect and it grows back each time - giving an interesting natural “layered” effect! HaHaHa ~Claudia

-I've noticed in the past few months that my hair hardly falls out at all - not even the normal everyday fallout you're supposed to have. Pre-MP, I had episodes of losing handfuls a day (generally with bouts of MCS). But even on “good” days, there was always a goodly amount left in the brush or shower. Now? Barely anything falls out, even when brushed hard. Hair is getting thicker as a result and also seems to be growing more quickly than it used to.~Alayne

-My hairdresser and I have noted that since I've been on the MP, my hair is thicker. I used to lose it in little clumps due to papulonodular scalp lesions.~Meg

-I have also seemed to lose hair in fluctuating cycles. Well…actually I haven't lost it. Its in my brush. I have noticed that there have been periods when my brush takes a lot, and other times much less. I just assumed this was due to fluctuating metabolism and hormones due to the Th1, and changes brought about by the MP. I think my hair may have initially thinned on the MP, but like Meg, it now seems to be thickening up again. ~DaveW

-I am happy to report that I no longer feel “hair pain” as I call it. That sensation really irritated me - it didn't really hurt so bad as it was just such an annoying pain. But a few months ago, it stopped. ~FeatherRiver

-Mobile home hairdresser also came: had to trim the small amount of longer hair that was left after the hair loss. my hair is growing back “soft like baby's hair” says hairdresser. is very short, but strong. ~AB

Hair Color KenC: Is anyone else loosing their gray hair?

Jigsaw in phase 1 Have others had white hair go dark?

-Interview of Sue Andorn: “I have very little grey hair and the new hair that is growing in is black rather than grey.”

You may also want to read posts by Carole, wytnez and JudyBeauty in MARSHALL PROTOCOL SUCCESS STORIES because they talk about their hair loss when ill and how this aspect changed in their recovery.

-Also, have a “symptom” to take off my list, which I never had put on the list since I thought it was normal. Last month when it was time to do the roots of my hair to cover grey, I couldn't see any grey. I thought I was losing my ability to see color. Great. So, I finally had someone else look at it for me, and they could not see any grey either! Also, the non-grey roots which had become increasingly dark the past few years, were close to my normal blonde color, they were a dirty blonde, I could barely tell the difference from them and the color I've been using. I am keeping my eyes open for the next time around, need to double check and see if it happens again! ~CFSgirl

Nails

Longitudinal lines in the nails may be due to aging, psoriasis or a fungal nail infection. It's a good idea to observe the nails because they can provide clues to systemic disease, as discussed in this article from the American Family Physician.

The Mayo Clinic offers information about nail ridges - and a photo - at this link.

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