Candida Yeast & CF

I have long said that the role candida plays in a CF'ers health is critical and, I believe, long overlooked. Here is an article that seems to point to the fact I may not be 'that far out there' after all.


Medical Mycology:
http://epubs.rcsi.ie/cgi/viewcontent.cgi?article=1036&context=medart

Patients with CF are at an increased risk of acquiring Candida due to use of inhaled steroids,
diabetes mellitus and lifelong antibiotic treatment however despite its frequent isolation from
sputum, oral and vaginal swabs, it remains unclear what such culture actually means in
practical terms for CF clinicians

Candida as the second most frequent fungal growth to Aspergillus in the CF airway and such
growth has been associated with more severe CF where patients receive prolonged treatment
with antibiotics, glucocorticoids and probiotics (9-12). I

whilst invasive airway infection is a rare event, extent
of airway damage from hypersensitivity phenomena remain unknown ............{{This airway sensitization is what I experience as I have never cultured it in my airways but, due to chronic colonization of the gut I believe it increased my overall inflammatory levels in my body and causes reactive airways as well as increased allergies and chemical sensitivities}}

((risk factors for orally recovery include))....
include poor dentition, older age, diabetes mellitus, use of inhaled or systemic steroids,
smoking, malignancy and frequent antibiotic use. Oral thrush usually presents as discomfort
associated with a dry mouth and associated dysphagia. In some cases, altered taste is
experienced. The diagnosis is usually straightforward and by direct observation of white
membraneous plaques on the buccal mucosa or soft palate.

. In our own institution’s experience, we encounter regular instances of oral
candidiasis annually following courses of antibiotics but which resolve after a short burst of
anti-fungal treatment (Fluconazole). We recommend microbiological confirmation by
scrapings in all cases unless white plaques are directly observed on oral examination. This is
because some of the symptoms described are not specific to oral thrush but can be found in
associated vitamin deficiencies (B6, B12) or by simple blistering. We recommend that CF
patients attending routine clinic be screened for risk factors and questioned at three-monthly
intervals with regard to the symptoms of oral thrush including frequency of sore or dry
mouth, crusting lips, dysphagia, dysphonia or hoarseness and difficulties with taste.

Despite this clear lack of available
literature, we strongly recommend screening questions for infection at all CF clinic visits anddepending on clinical findings, anti-fungal treatment prescribed either empirically or
following microbiological confirmation.

((HAVE YOU HAD TROUBLE WITH A PORT OR BLOOD INFECTION????))))

A more commonly encountered systemic infection associated with Candida involves the
presence of a “port”. Candida species in this setting are
recognized as the most common infecting organism associated with a port resullting in
septicaemia

CANDIDA....CHICKEN OR THE EGG
, a view of many clinicians and it may be
that the organism acts as nothing more than a microbiological marker of disease severity in
CF. To challenge this paradigm, we are currently prospectively evaluating whether airway
colonization by Candida albicans may act pathogenically by affecting clinical outcomes in
CF including FEV1, BMI, hospitalizations for infective exacerbations and sputum
colonization with Pseudomonas or Aspergillus species. Notably, a previous cross sectional
analysis of a European CF registry did show that Candida albicans colonization was
associated with 5-10% predicted decrease in pulmonary function

SO THE QUESTION IS DO WE GET SICKER BECAUSE OF CANDIDA OR DOES CANDIDA SIMPLY GET A FOOT HOLD ONCE WE ARE ALREADY SICKER? MY OPINION IS CANDIDA IS OVERLOOKED IN ITS ROLE IN OUR DETERIORATION!

Bacteria and fungi are found together in a variety of
environments but particularly in biofilms, where adherent species interact through diverse
signaling mechanisms. In the host C. albicans can often be found growing with bacteria in
polymicrobial biofilms and interspecies interactions occur that can impact on the transition of
C. albicans between virulent and nonvirulent states (27). Under conditions of immune
dysfunction, such as in the CF lung, colonising C. albicans can become an opportunistic

Bacteria and fungi are found together in a variety of 

environments but particularly in biofilms, where adherent species interact through diverse 

signaling mechanisms. In the host C. albicans can often be found growing with bacteria in 

polymicrobial biofilms and interspecies interactions occur that can impact on the transition of 

C. albicans between virulent and nonvirulent states (27). Under conditions of immune 

dysfunction, such as in the CF lung, colonising C. albicans can become an opportunistic 

...............BASICALLY THE PRESENCE OF YEAST/CANDIDA ALLOWS THE BACTERIA TO BE MORE RESISTANT AND CREATE MORE DESTRUCTIVE BIOFILMS IN OUR LUNGS....IE THEY TEAM UP

N=1 Kalydeco Trial

I was accepted in December to one of the clinical trials to try and extend the use of Kalydeco, I started a blog specifically for that, check it out here:

http://www.bignewbreath.blogspot.com/

Microlife Peak Flow

So I found the microlife peak flow online running for 65% off, must be the model/brand is outdated now. I want to start tracking my values and get a baseline that way when I try something new I can see the affect it has on me (or not).

Tonight is the first night I received it, it really was easy to use and set up. It recommends you do a few readings at a time and then it saves the best one between when you turn it on and when you are done and turn it off.

I have NO idea what my normal liters run since I always look at and track % predicated FEV1. I also don't know how this home device compares to the clinic. That being said I'm happy to see a peak flow of 600 and 3.31 liters. Using the CDC calculator for my age/weight/height it said my FEV1% predicated is 3.06 liters which would put me at 108% (3.31/3.06*100).

2 weeks ago my lungs were in very inflamed bad state but I started cayston and did 3 days of 10mg prednisone and then today took 5mg. I have been doing aLOT better and getting stuff up now but I'm still not buying the 108% so we'll have to monitor it for a while and then see how it compares to the clinic.

Looking forward to seeing how the numbers track over time and using the software....yes I am just that geeky.

Supplements- Ginseng

I needed a refill on a number of supplements so I decided to review my regimen and see what I'd like to modify and give a try. 


My main problem seems to be inflammation over infection so I'm going to go after that aspect and try to get better at regularly taking my items that don't go in my pill box. I'm great at taking my am/pm meds and have that routine established but it's things that should be taken at meal times, that need kept in the fridge etc I am bad about. 


Going to try ginseng so here is some info on that, thanks to my friend Tara for recommending it and getting me interested in reading. 

Active constituents found in most ginseng species include ginsenosides, polysaccharides, peptides, polyacetylenic alcohols, fatty acids and trace elements. It is generally believed that ginsenosides and their metabolites are the most important components determining the pharmacological effects of ginseng.

Ginsenosides are the thing that has the most potent affect. In an effort to standardize  and measure how much was in the different supplements they came up with a way to measure how much ginsenosides were present in these different supplements which is G115 which is what some of the studies utilized. Essentially the G115 is a standard composition that is required to have 4%ginsenosides so that you know what you are getting.

The particular study I have listed 1^st below here they used G115 so if you aren’t going to use ginsana G115 name brand supplement here is the breakdown:

They used 4% @ 500mg 2x/day so……

500mg x2=1000mg * 4% = 40mg of ginsenosides

So for me I use wonder laboratories so I am going to try this Panax Ginseng http://www.wonderlabs.com/itemleft.php?itemnum=1929

500mg capsule standardized to 5% = 25mg ginsenosides x2=50mg

Ginsana used in study: http://www.ginsana.com/ingredients_ginsana.htm

Links to Studies:

medline plus information: http://www.nlm.nih.gov/medlineplus/druginfo/natural/1000.html

enhances bacterial clearance and decreases lung pathology in athymic rats with chronic P. aeruginosa pneumonia http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1997.tb00591.x/abstract

• reduces bacterial load and lung pathology in chronic Pseudomonas aeruginosa pneumonia in rats
  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC163833/
  
  

  Effects of ginseng on Pseudomonas aeruginosa motility and biofilm formation.

  http://www.ncbi.nlm.nih.gov/pubmed/21303421

  
  
  
  

'CFTR-opathies': disease phenotypes associated with cystic fibrosis transmembrane regulator gene mutations

*Note from Nicole: My post with my take on all of this to come but for a bit I am going to be posting articles related to 'atypical' or 'mild' CF.

CFTR-opathies': disease phenotypes associated with cystic fibrosis transmembrane regulator gene mutations

Peadar G Noone 1 and Michael R Knowles1

Abstract
Cystic fibrosis is a genetic disease that is associated with abnormal sweat electrolytes, sino-pulmonary disease, exocrine pancreatic insufficiency, and male infertility. Insights into genotype/phenotype relations have recently been gained in this disorder. The strongest relationship exists between 'severe' mutations in the gene that encodes the cystic fibrosis transmembrane regulator (CFTR) and pancreatic insufficiency. The relationship between 'mild' mutations, associated with residual CFTR function, and expression of disease is less precise. Atypical 'mild' mutations in the CFTR gene have been linked to late-onset pulmonary disease, congenital bilateral absence of the vas deferens, and idiopathic pancreatitis. Less commonly, sinusitis, allergic bronchopulmonary aspergillosis, and possibly even asthma may also be associated with mutations in the CFTR gene, but those syndromes predominantly reflect non-CFTR gene modifiers and environmental influences.

Introduction
Cystic fibrosis (CF) is a recessive genetic disease that is caused by mutations on both CFTR alleles, resulting in abnormal sweat electrolytes, sino-pulmonary disease, male infertility, and pancreatic exocrine insufficiency in 95% of patients [1,2]. In its classic form, the disease is easily diagnosed early in life, through a combination of clinical evaluation and laboratory testing (including sweat testing, and CFTR mutation analysis) [3]. Depending on the ethnic background of the populations tested, common genetic mutations are identified in the majority of cases of CF. In the USA, two-thirds of patients carry at least one copy of the ΔF508 mutation, with approximately 50% of CF patients being homozygous for this mutation [4].

A wide spectrum of molecular abnormalities may occur in the CFTR gene, and uncommon mutations that result in partial (residual) CFTR function may be associated with nonclassic presentations of disease. Overall, 7% of CF patients are not diagnosed until age 10 years, with a proportion not diagnosed until after age 15 years; some of these patients present a considerable challenge in establishing a diagnosis of CF. Moreover, the phenotype in these patients may vary widely [5,6]. The focus of the present review is on nonclassic phenotypes associated with mutations in the CFTR gene, which may manifest as male infertility (congenital bilateral absence of the vas deferens [CBAVD]), mild pulmonary disease and idiopathic chronic pancreatitis (ICP). These phenotypes are included within the definition of 'atypical CF'.

Cystic fibrosis transmembrane regulator: the relationship between gene mutations and function

CFTR is a transmembrane spanning protein with multiple activities that are related to normal epithelial cell function [2]. Mutations in CFTR result in abnormalities in epithelial ion and water transport, which are associated with derangements in airway mucociliary clearance and other cellular functions related to normal cell biology [7]. Depending on the molecular abnormality, the defect in CFTR may be the equivalent of that associated with a 'null' mutation, or may be 'mild', with partial/residual function [4]. At one end of the spectrum of severity, 'null' or 'severe' mutations reflect nonsense, frame-shift or splice mutations; these result in absence of production of functional CFTR, which correlates strongly with pancreatic exocrine insufficiency, but less strongly with severity of lung disease. At the other end of the spectrum, 'mild' mutations may result in some production of functional CFTR protein at the apical membrane, with partial CFTR channel function, and are generally associated with pancreatic sufficiency and milder pulmonary disease.

The molecular basis for the severity of mutations may derive from the extent to which normal mRNA transcription or protein synthesis takes place; for example, splice mutations may influence the efficiency of normal/abnormal CFTR mRNA transcription to varying degrees. In turn, the severity of the abnormality in CFTR may relate directly to the phenotypic expression of disease, with absent function causing more severe disease, whereas some residual function may modulate the severity of disease in different organ systems. Clinically, this may be reflected in normal or borderline sweat chloride values in patients with atypical CF.
Other factors, including non-CFTR gene modifiers and environmental influences, are probably also associated with the severity of disease. Given this background, it is not surprising that disease expression is complex and that nonclassic CF phenotypes exist.

Phenotypes associated with atypical cystic fibrosis

Table 1 provides a schema of how mutations on one or both alleles of the CFTR gene might relate to nonclassic phenotypic expression of disease. 'Atypical CF' includes those clinical phenotypes that have the strongest associations with mutations in the CFTR gene: CBAVD in males, mild pulmonary disease and ICP.

Table 1
Hierarchy of associations with mutations in the cystic fibrosis transmembrane regulator gene


Congenital bilateral absence of the vas deferens
Although not all males with CBAVD have mutations in the CFTR gene, approximately 50% have abnormal CFTR alleles [8]. Generally, one 'severe' allele is combined with one 'mild' allele, such that the 'mild' allele appears to dominate and cause the milder phenotype (e.g. ΔF508 in combination with R117H). Routine screening for common mutations that does not take into account milder or rarer mutations may miss many of the mild mutations associated with this particular clinical expression of disease [8]. This combination of mutations may occur in other forms of atypical CF (see below).

One particular abnormality deserves a special mention – the various alleles of the polythymidine tract in the intron 8 (IVS8) of the CFTR gene [9]. Of the three alleles that have been identified in IVS8 (5T, 7T and 9T), the 9T allele is associated with the most efficient usage of the intron 8 splice acceptor site. This efficiency decreases with shorter polythymidine tracts (5T and 7T), which results in a lower than normal level of full-length CFTR mRNA and presumably in a decrease in mature, functional CFTR protein. For example, the mild CFTR mutation R117H is influenced by the polythymidine tract sequence, such that an R117H-bearing allele in cis with a 7T allele may result in CBAVD, whereas when R117H is associated with the 5T allele the phenotypic expression may be associated with atypical CF. R117H with a 9T allele may exhibit a normal phenotype. The 5T allele under the influence of other sequence variants in the CFTR gene may also be associated with atypical CF [10].

Although males with CBAVD may present to urology clinics, with no discernable lung or other organ presentation of disease, a careful work-up should be carried out to determine whether subtle lung disease is present. Evidence of CFTR dysfunction may be found on laboratory testing, with abnormal or borderline sweat chloride levels and/or abnormal CFTR-mediated chloride conductance in nasal epithelia [11,12]. Whether lung disease may develop later in life in these generally young males remains to be determined, but they should at least be counseled regarding lung health and cigarette smoking.

Mild pulmonary disease
Older patients with mild pulmonary disease, including bronchiectasis, may not present with symptoms until later in life, but are found to have atypical CF when appropriate investigations are carried out, including normal or borderline sweat chlorides and pancreatic sufficiency [10]. Thus, as with CBAVD, a careful work-up is mandatory. This should include not only a standard diagnostic work-up, including a sweat chloride and radiologic screening for subtle lung disease, but also nasal potential difference measures in order to evaluate CFTR at a physiologic level, and screening for mild and rare CFTR mutations [10]. A 'severe' mutation may be found on one allele, with a 'mild' mutation, such as the 5T abnormality (with or without other abnormalities in the CFTR gene), on the other allele. The level of expression of full-length mature CFTR may be less than that in CBAVD, with adverse consequences for the lung, albeit with a later presentation [10]. Although the pulmonary disease is milder than that with classic CF, these patients generally exhibit phenotypic similarities to CF; for example, the distribution of radiographic changes often involve the upper lobe, and mucoid Pseudomonas aeruginosa may be present in the lower airway.

Idiopathic bronchiectasis (IB) could loosely be defined as bronchiectasis in which no clear cause has been found, and in which the clinical pattern differs from CF and other known causes of bronchiectasis. Two studies [13,14] suggested that IB may be linked to mutated CFTR. In one study [13], five out of 16 patients with IB harbored the 5T allele in the CFTR gene. Of those, two were 5T/5T homozygotes. Insufficient data were supplied regarding the clinical phenotype in the five patients harboring the 5T allele to draw any firm conclusions as to whether they would otherwise fulfill rigorous diagnostic criteria for CF [3]. In the second study [14], from France, 13 mutations were found in 16 CFTR alleles in 32 patients with idiopathic bronchiectasis. Only six of the 13 mutations were confirmed to be CF-causing mutations, with the remainder hypothesized as being 'potentially' CF causing. Four patients were compound heterozygotes, and all 11 of the patients who harbored mutations had abnormal sweat chloride levels (>60 mmol/l), with apparently no clear-cut evidence of CF otherwise ('isolated bronchiectasis'). Girodon et al. [14] speculated that IB might be related, at least in part, to mutated CFTR, with possible other factors at play. In any such population, atypical or variant CF is likely to be present in a proportion of patients studied in detail.

Idiopathic chronic pancreatitis
Recent reports [5,6,15,16] suggest that patients with an ICP phenotype have an increased incidence of mutations in CFTR. Such patients generally present with symptoms of pancreatitis at an older age than those patients with classic CF. Because CF carriers represent 3–4% of the general population, it is important to know whether one or two mutations predispose to ICP. Although the data initially appeared to suggest that patients with one mutation in CFTR were at risk, subsequent studies have borne out the observation of a link between mutated CFTR on both alleles and ICP.

A rigorous search was conducted for other mutations in patients with one CFTR mutation, and CFTR function in nasal epithelia was assessed in vivo in patients with ICP [17]. Sequencing of the CFTR gene indicated that nine out of 41 patients with ICP had two abnormal CFTR alleles; again the combination of 'severe' and 'mild', and having two mutations increased the risk for ICP 40-fold. ICP patients with two abnormal CFTR alleles had reduced CFTR-mediated chloride conductance in nasal epithelia as compared with ICP control individuals. The number of CFTR heterozygotes with ICP was no higher than is expected in the general population. These data strongly suggest that abnormalities on both alleles are required for expression of 'CF-related ICP', perhaps with some added influence from mutations in pancreatic inhibitor genes (PRSS1, PSTI) [18].

Other phenotypes associated with mutations in the cystic fibrosis transmembrane regulator gene
Other sino-pulmonary syndromes have been studied to test for a link to mutated CFTR; sinusitis, allergic bronchopulmonary aspergillosis, and asthma. However, the likelihood is that they predominantly reflect non-CFTR gene modifiers and environmental influences.

Sinusitis
In a recent study [19], DNA from 147 patients with chronic rhino-sinusitis was screened for 16 CFTR mutations, including the 5T sequence, and patients with a mutation had their DNA screened over the entire coding region. Eleven patients had a mutation in CFTR (all severe mutations, and one patient eventually developed CF), as compared with two out of 123 control individuals, whereas there was no difference in the incidence of the 5T allele between controls and study subjects. There was also a higher frequency of the M470V polymorphism on the opposite allele to that containing a severe mutation as compared with control individuals. Physiologic testing in the sinusitis patients showed normal indices of nasal epithelial sodium transport, with a slight reduction in CFTR-mediated chloride conductance. The authors of that report concluded that the combination of a severe mutation on one allele with a sequence variant that is not normally associated with CF on the opposite allele may be responsible. An analogy is again drawn with the other non-classic phenotypes, with enough residual CFTR function to protect against early, classic sino-pulmonary disease and a pancreatic phenotype, but clearly other non-CFTR factors may also be at play (Table 1).

Allergic bronchopulmonary aspergillosis
Although Aspergillus fumigatus is ubiquitous in nature, allergic bronchopulmonary aspergillosis (ABPA) occurs in only a small number of patients with asthma and CF; thus, genetic factors may play a role in the pathogenesis of ABPA in some patients. A study from several years ago [20] showed that, in a small number of patients who met criteria for ABPA, there was a higher frequency of abnormal CFTR alleles than expected. The authors of that report speculated that mutations in CFTR may play a role in the pathogenesis of ABPA, either as a result of heterozygosity alone (and 50% CFTR function), or heterozygosity plus other genetic factors that were not detected by the methods used in the study. The situation is probably similar to that in asthma, with genetic factors outside of CFTR, together with environmental influences, playing major roles.

Asthma
There are conflicting data as to whether mutations in the CFTR gene are over-represented in patients with asthma [21,22,23]. In Denmark, a questionnaire study was carried out in a cohort of carriers of the ΔF508 mutation in CFTR [24]. Of 250 adults studied, it appeared that 9% reported symptoms of asthma, as compared with 6% of control non-carriers, with airways obstruction being present in those carriers with symptoms of asthma. However, there are clear limitations in a study of this kind, relying solely on a questionnaire for diagnosis. A second study investigated 144 patients with documented asthma [22], and identified 15 missense mutations in the CFTR gene of 15 patients, compared with none in a small control group. When tests were carried out in a larger control group, however, the differences lost significance. In contrast, several other studies failed to show a link between mutations in CFTR and asthma, and if anything show a protective effect [23]. Thus, there is little evidence to support a link between asthma and abnormalities in CFTR, such that, if there is a link, then it plays a small role in the overall pathogenesis of disease, with a much larger role played both by genetic factors outside of CFTR and by environmental influences (Table 1).

Conclusion
Mutated CFTR may be associated with an atypical CF phenotype in the sino-pulmonary tract, pancreas, and male genital tract, with reduced CFTR epithelial function. Although abnormalities in the CFTR gene may play a minor role in the pathogenesis of asthma, sinusitis, and ABPA in subsets of patients, these diseases predominantly result from genetic (non-CFTR) and nongenetic environmental influences.

Abbreviations
ABPA = allergic bronchopulmonary aspergillosis; CBAVD = congenital bilateral absence of the vas deferens; CF = cystic fibrosis; CFTR = cystic fibrosis transmembrane regulator; IB = idiopathic bronchiectasis; ICP = idiopathic chronic pancreatitis.

Keywords: asthma, cystic fibrosis (CF), cystic fibrosis transmembrane regulator (CFTR), mutations, pancreatitis, phenotype

Keeping Healthy, Getting Healthier

In the past I've done a new years review and goal for my health. I was thinking that I should pick a few realistic goals this year. I am admittedly having a hard time keeping on top of everything I feel I need to do to maintain optimal health but my standards are also super high so..... I feel torn most times.

#1 is my weight, it is too high, need to trim down to prevent diabetes issues and less food will most likely improve my issues with candida as well

#2 stop skipping night time treatments, I used to be almost 100%, need to get back there

#3 add back cardio, need at least 3, preferably 5 days of getting my HR up and clearing my lungs a bit of toning would be a good idea too

#4 rinse my sinuses...daily! Even though I dont feel I have enough goo to justify it I do feel better when I do it and it will help flush out cold/flu bugs this time of year

#5 take my probiotics, lauricidin, and NAC each day....I am so good about my 'pills' but so hit or miss on these

This seems reasonable, may need ot make myself a checklist or something to get back on track.

White Tea

So I have been drinking tea for a long time but since I didn't use to drink caffeine it was mostly herbal tea packets and nothing special. Last year I started stopping by a tea shop specializing in an amazing array of loose leaf teas and brewing cups and systems. I decided it was fun to have a cup with an individual strainer in it for work.

I had only tried limited herbal and green tea varieties so imagine my surprise when a friend suggested drinking white tea helped loosen her mucous and helped her feel better. I thought she was a bit crazy to be honest. I have tried it myself and I have to say that not only do I like white tea more than green (it's smoother or more bland with less grassy/earthy taste) but that I also noticed that I got up a lot of gunk and felt good when drinking it. The other nice thing, for me, is that I can drink a lot more of it throughout the day without getting 'buzzed' on too much caffeine since it has the lowest caffeine content of all the teas.

I decided to look into the white tea phenomenon a bit since it does truly seem to help me and I found that what we've noticed is what the Chinese have known for eons......tea has a TON great stuff in it for you. White tea is also the highest in polyphenols, antioxidants, etc since it is the youngest and least processed......it also, unfortunately means its the priciest. 


Speaking of caffeine, a common website that does nothing but compare amount of caffeine in beverages had the values listed below as common for varying beverages, I thought it was interesting to see some common beverages for comparison. 

                        mg/oz (Note this is PER ounce not cup)
Decaf Coffee    0.9
white tea           1.9
green tea           3.1
Common Pop    4.5
Iced Tea           5.9
Coffee               13
Espresso           51


Tea is noted to vary widely in the levels of caffeine based on type, variety, brewing etc. The Department of Nutritional Services provide the following ranges for loose leaf tea:

                      mg/oz (Note this is PER ounce not cup)
Black Tea: 2.8-13.8
Oolong Tea: 1.5 - 6.9
Green Tea: 1 - 4.5
White Tea: .8 – 3.1

If you are sensitive to caffeine or avoid it altogether here is a handy hint. About 80% of the caffeine will be extracted within 30 seconds of steeping, you can easily remove most of the caffeine in any tea by steeping for 30 seconds in a 'throw away' cup of hot water then transfer the pre-brewed tea leaves to your cup.

I've only just begun experimenting but I'm impressed. Let me know if any of you give it a try.

Here are some links to sites with cool general info on health benefits of tea: 


http://www.whiteteaguide.com/whiteteahealthbenefits.htm

http://www.whitetea.com/benefits-of-white-tea.php

tea vs superbug & increasing effectiveness of antibiotics
http://www.sciencedaily.com/releases/2008/03/080330200640.htm

tea increases anti-inflammatory properties in body and decreases pro-inflammatory factor in body
http://www.biomedcentral.com/1476-9255/4/1

What I'm Reading

I am still loving my kindle though finding the time to read can be tough. Even though the voice on the kindle is android I have found I enjoy plugging in some earphones and listening to the books while driving.

Reading:
Bonhoeffer: Pastor, Martyr, Prophet, Spy
Weigh Down Diet
I'm Chocolate, You're Vanilla: Raising Healthy Black and Biracial Children in a Race-Conscious World


Read:
A Swiftly Tilting Planet (Madeleine L'Engle's Time Quintet)
A Wind in the Door (Madeleine L'Engle's Time Quintet)
A Wrinkle in Time (Madeleine L'Engle's Time Quintet)
Growing Up in the Care of Strangers: The Experiences, Insights and Recommendations of Eleven Former Foster Kids
Nairobi Heat (Melville International Crime)
Heaven is for Real
Unbroken: A WWII Story
Secrets in the Cellar
Damaged: The heartbreaking True Story of a forgotten Child
My Dad's a Policeman
A wrinkle in time
Tough as nails: One Woman's Journey Through West Point
Ape House: A Novel
Climbing the broken stairs
Call It What It Is
Empty Chairs
Abused--a daughter's story
Pregnant women on drugs: combatting stereotypes
Oliver Twist
Hiding Place -Corrie Ten Boom
Band of Brothers: E Company, 506th Regiment, 101st Airborne from Normandy to.....
Bondage Breaker
Lamb
Green For Life
Smoothie Revolution
Citizen Soldiers: The U.S. Army form the Normandy Beaches to the Bulge to the Surrender
Harriete Tubman: Conductor on the Underground Railroad
Taming the Nueces Strip - Durham
The War Journal of Major Damon "Rocky" Gause-Ambrose
5 Love Languages - Gray
Power Praying Wife - Omartin
Dare to Discipline - Dobson
123 Magic
When Bad Things happen to Good People - Kuhner
Scientist in the Crib--Science meets how babies brains work--this just interests me
Happiest Toddler on the Block
Millionaire Next Door - Stanley
Love Dare
Home Safe Home (alternatives to toxic laden household products)


'One of these days'
Skinny Bitch in the Kitchen (wholistic eating)
Omnivore's Dilemma
Power Spoken Word
Power Spoken Tongue
Sacred Marriage
Butekyo Breathing Shut your Mouth
The surrendered Wife-Neumans
"Better' - Atu Guande
Woman Power - Schlessinger
Priceless - Ramsey
Proper Care and Feeding Marriage - Schlessinger
QBQ - Miller
Raising Girls - Dobson
DNA of relationships-
The Greatest Words Ever Spoken
Power Praying Wife
Purpose Driven Life - Warren

cups, treatments & nebs, oh my

http://www.cff.org/UploadedFiles/LivingWithCF/StayingHealthy/LungHealth/WhichNebulizer/WhichNebulizerForWhichDrug.pdf

I was getting confused on which nebulizer cups to use with my mobilaire and my pari and for which drugs, this is helpful.

Tracking FEV1

Wow, what a slacker I am, I haven't been here in forever. I'd love to say I'm going to get better but the truth is life is pretty busy and while I think about good posts in my head they rarely make them to my fingertips. That being said I saved my pulmonary report from last week and wanted to get it recorded before I lost it.

Considering it's October, I just got over a cold, and a few other factors not in my favor I'm doing pretty well but my numbers are lower than I'd like. Need to hop on the compliance and work out bandwagon aLOT harder.

Oddly, after all my sensitivity issues and then reacting to antibiotics this most recent culture came back astoundingly sensitive, so much so I think it's a fluke. It showed only pseudomonas, no achromabacter and it was sensitive to everything except chloramphenicol which isn't even used in my clinic. I told the doctor I didn't buy it, I've worked in a lab long enough to see a HUGE outlier and we're taking bets on if the culture from this week shows up the same way or not.

Also, to note that my fantastic results of last april are highly atypical, I have not since achieved such results, of course, to be fair, I am no longer doing the candida diet and treatment, may be time to start that again. I have been running FEV1 in the 90's all year.

19Oct2011 FVC 95  FEV1-90  FEV25/75-84
Clinic Notes: One week post nasty cold, rainy, no morning breathing treatments. Mucous production still above baseline but cough back to almost baseline. Sinuses problematic lately. Some pleural tightness but not sick.


23Apr2010 FVC 127 FEV1 114 (up 14% WOW) FEV25-75 102 (up 12% WOW)
Notes: this is especially fantastic given my allergies are running wild and I have seen a drop in my peak flow the past few days from it. I normally write down my PEF (peak flow) but he pointed out that mine was off the chart this time, my Peak flow was 11.82 which equates to 150 L/min higher than two months ago i.e. the little plastic things we use measures in L/min.

Clinic Notes: Discussed recent treatment for candida. Fatigue, chronic pain, pleural pain, all gone. Lung functions are the best on record and it is after no drugs or steroids where as the 108% last year was after serious steroids.

18Feb2010 FVC 110 FEV1 100  FEV25-75 90
Clinic Notes: This was post IV's (stopped Christmas Eve) and 2 rounds prednisone totaling 5 weeks (1st round stopped New Years day and 2nd round was 3 weeks in January). Infection is gone but still having chronic pain on left side when breathing, especially deep breathing, still intermitten pleurisy, still fatigued and not feeling right, feel like I do right before I get a bleed. Discussed potentially entering chronic pain phase of CF (I do not accept this).  Also started drinking mucomyst N-acetylcysteine since last visit so reported good results in gastro area from this, no large effect noted on the lungs. Discussed going to CA to consult with Dr.Moss on inflammation and also discussed pursuing testing for candida with family doctor.

3May2009 FVC 118 FEV1 104 (down 4%) FEV25-75% 88 (up 1%)
Clinic Notes: re-check post steroids and pre-pregnancy (attempt). Everything looks great, feeling good, allergies are problematic and doc did say that my theory on my allergic reactions having residual inflammatory effect on my lungs (which I did another week steroids for) was very possible. His pregnancy recommendations are to be vigilent with physiotherapy especially hit it hard in 2nd tri' to get ready for 3rd when lungs are most compromised and there is the biggest risk.

March2009: FVC FEV1 108 FEV25-75% 87
Clinic Notes: Recheck after end of steroids, feeling good. Best FEV1 ever!

29Feb2009 FVC 111 FEV1 100 (down 3%) FEV25-75% 88 (down 14%)
Clinic Notes: feel inflammatory in nature start 2 weeks steroids 40mg taper. Still got streaking in day 2 steroids.

15Dec2008 FEV1 103 FEV25-75 102%
Clinic Notes: summer steroids early winter cold w 3 weeks cipro)

21Feb2008: FVC 105.3 FEV1 99.3 FEV25-75% 89.1 BP 114/68 HR 59 Wt152
Clinic Notes: was getting huge variability and felt something 'stuck'

25Jun2007: FVC 105 FEV1 97 FEV25-75% 82

4Dec2007: FVC 99 FEV1 91 FEV25-75% 77

update on me

  

A couple weeks ago I had a pretty nasty cold it was also right after we found out the Elliott had MRSA. I took that week, two weeks ago, off work thinking if I rested up from the cold which was kicking my butt and did the right things it would be 'just' a cold. I also figured that would give me the time to find E a new home and get our house decontaminated from MRSA which was an undertaking, the washing of stuff at the Laundromat alone cost almost $50.

I went to the doctor that week for my lungs as well which was a normally scheduled visit. My lung function was down a bit but at that point it was still just a cold and we agreed to watch and wait. I started to feel better on Sunday and was more than a bit tired of ‘taking it easy’ so I decided to be busy and productive, tell my body to get over it and all was pretty good; I was looking forward to returning to work on Monday. My body had other plans I woke up about midnight with severe lung pain on both sides, after some ibuprofen failed to work I woke Jared and asked for a vicodin that I have for lung pain then I decided to go to the ER as the vicodin wasn’t working either.

The ER was a futile trip spent in pain during all the hours of waiting while listening to the drug addict next door yell about he was in fact sober and they should let go of him and let him get back to the mission…fun times, I’d never been so glad for my kindle. Everyone seemed to think either I was having chest pain or back pain, no one seemed to accept that I was having pain from my lungs radiating down part of my back and into my chest….try explaining that when you can’t take a real breathe. I have to admit hours later when the doctor finally came in and told me it was a virus that just needed to run it’s course and I should just continue doing all my normal treatments I completely lost my cool and chewed him out telling him if I could breathe enough to do a breathing treatment I wouldn’t be here in the first place. In the end I said I’d follow up with my doctors and wanted to leave and apologized for being short. He said that he would give me something for the pain and send me home with instructions I could take two vicodin next time and then had the nurse give me so much dilaudid I was loopey the good thing was it stopped my coughing which also served to reduce the pain; I could tell as soon as it took effect as I could draw a breathe without pain.

The next day once I woke up I called my doctors who decided to start me on IV’s which arrived the next day. I was to do on inhaled antibiotic and IV zosyn which I have been on many times over the past about 5 years. The drugs in my lungs are pretty resistant to many antibiotics and zosyn seems to be the one stronghold that really works. I started my IV that night so it did one IV then and one during the night while I was sleeping and then I slept through while it was infusing my early morning one, 3 doses in total. Imagine my surprise when I woke covered in blotchy hives. Zosyn is a member of the cephalosporin family and it looks like I’ve developed a sensitivity to them. This was obviously a big blow to me since I had to stop the antibiotics and then they weren’t really sure on what they wanted to do since it appears that most of the drugs the bugs in my lungs are not resistant to also just happen to be part of the cephalosporin family. It took a day or so and then I started levaquin which is a strong oral antibiotic, initially I protested because it doesn’t normally work for me and the doctor had already passed over it in favor of IVs. I have what they call “intermediate” to that drug meaning basically it works but not as well as it should. Since our options were limited my normal doctor confirmed that was the best course but at a higher dosase and in continuance with the twice as strong inhaled antibiotics I was still doing.

The good news is that this combo seems to be working. Honestly I believe it is the inhaled antibiotic doing a good portion of the work since it started improving before the levaquin but with the type of bugs we CF’ers have in our lungs you never want to treat with only one antibiotic since that allows them to more easily build a resistance.

What one drug reaction wasn’t enough? Ok number two has intensified over the past week or so on the oral antibiotics and I am not scheduled to finish until Friday. I have previously been told I have plantar fasciitis in my right foot now it has intensified greatly and the left foot has started in. The bottoms of both feet have a swollen red nodule present just past my heel that persists despite icing and ibuprofen popping. According to Dr. Google it seems I may have really aggravated the fasciitis or partially torn it…fun. Levaquin has a black box warning from the FDA about tendonitis and tendon rupture but I am pretty certain it is responsible for this recent turn of events. I’m going to give my foot doctor a call on Monday to see if he can get me in. Unfortunately the tendon on my left wrist and foot are also hurting, I’ve had a bad bought tendinitis in my wrist before so I’m pulling out the wrist guards for sleeping to hopefully keep it from getting worse.

So let’s see, cold, MRSA scare, lung infection, hives, and now I’m hobbling like an old woman….ah these are the times of CF.

The good thing is that even if I have to stop the levaquin my lungs don’t feel in too bad of shape. I may be able to stop orals and start a second inhaled antibiotic, that will make for a lot of nebulizer times but if it lets me walk again and breathe easy it will be worth it. Better news is that the MRSA scare was just that, so far, a scare I have not tested positive for MRSA in my nose or my lungs *claps*. Also awesome news is that E is doing wonderfully as the only child in a first time foster family who are thrilled to have him are supporting reunification but also hoping to adopt some day. 

Long Overdue, Update & Candida

Seems I am long overdue for a post or an update. I have been neglecting posting things I've been thinking about but I *have* been thinking about the blog a lot. I've been wondering if I should combine this with my personal blog, it seems I have so many 'special interests' CF, IVF, budgeting/Dave Ramsey, and now being a foster parent and hopefully soon adopting and I can't start a blog for all of them LOL! I considered starting a blog for our fostering/adopting and then I thought 3 blogs, really? no way! I think there are some things on here that are just 'too much' for some in my family readership but I'm torn. What say you.........combine or compartmentalize?

Anyway I just finished a 2 week course of zosyn and tobramycin yesterday. SO thankful that is over. I know some of you are hardcore and handle IVs like a rock star and while I like to think I have a pretty high tolerance for some things IVs are NOT one of them, especially zosyn. The good thing is that it makes me take the time to rest and allow my body to heal. The bad thing is...well, I feel awful, get migraines, extreme fatigue, and nausea.

I started 40mg of prednisone yesterday. I have found the past 2 times I have done IV which for me is zosyn I get very clear, very dry, but also inf lammed. The first time they did a bronch and all sorts of stuff which I've previously talked about to confirm it was "just" inflammation. This time the inflammation is not as bad (I've got my theories on this..in a few) but I decided to ask for a short burst to get everything in tip top shape. this is a risk since I think 1/2 my town is sick right now so I'm staying away from people as best I can aside from picking kiddo up at daycare and that involves hand sanitizer galore! Right now we just got over stomach flu which is going around, I have a 1.5 you nephew who just had surgery for a sinus infection that went abscessed due to MRSA, a 3yo niece with pneumonia, and a 6 week old niece with RSV! Whew. No seeing family for a while either.

So, my 'tip top shape' plan includes drinking the NAC (for me 20% USP grade acetylcysteine) 3x/day @ 1500mg, taking a probiotic that is formulated to eat candida yeast, a probiotic blend that is highly rated, doing the 5 days of steroids, diflucan each day to kill off the overgrowth of candida, loading myself up on HTS treatments to moisten/loosen anything that got dried out and stuck during IV's (my normal pattern is to get clear/dry after a week on IVs then get nothing up then a few days after IVs I get some of the 'stuck' stuff up which I think is stuck due to the inflammation the IVs cause). I also am trying to do some light form of excercise each day but I have to work back into that since I've been out of it for a while.

The inflammatory cause, as I mentioned I have my suspects. I have been treating myself for candida overgrowth of the gut for almost a year now. I don't have it 'beat' by any means but its better and I think that is why my inflammation is better this time around. Candida for me causes a lot of inflammation. So, in addition to the regimen above I am also doing the MEVY diet again, I really should have been doing it while I was on IV's and I did, some days, or parts of some days. I am so miserable on IVs and when I first start MEVY my body was revolting and I was too weak to do both (weak as far as resolve not physically). MEVY stands for meat, eggs, veggies, yogurt which is all you are supposed to eat. I am including some nuts and a few blueberries blended into my plain no sugar yogurt to make it more palatable but other than that it's boring. I am a big fruit lover and true sugar addict so its hard. Having candida actually makes you crave sugar even more because if they aren't being fed ie carbs/sugar they aren't happy. The goal of MEVY is not to provide them with the sugar/carb sources they need to live, effectively starving them out.

If you haven't heard me talk about candida before you can look here to start but you can also look for 'candida' in my tag section and they will all come uphttp://cftoo.blogspot.com/2010/03/my-take-on-candida-in-cf-community.html

Essentially your gut has a balance of good bacteria and yeast however when your body balance is off and favors the candida yeast it can 'take over' killing off much of the good bacteria (in my case they could only find 1 of the 3 kids that are supposed to be there) which is beneficial, this then allows the candida to thrive with no one to keep their numbers in check. Excess of Candida can cause a myriad of factors, check here:   http://cftoo.blogspot.com/2010/03/candida-what-are-symptoms.html http://cftoo.blogspot.com/2010/02/candida.html One way I have heard it described is that it attacks people where they are weakest. For me it causes inflammation, my allergies got much worse, fatigue, and fuzzy thinking/irritability when it was bad.

What are some of the things that offset your bodies balance to favor yeast over beneficial bacteria? Well it seems much of what us CF'ers need to stay healthy in our lungs is hurting the balance of our body and I believe candida is MUCH more common than we know, since it mimicks and or exacerbates our symptoms of cf.

Hormone treatments including birth control and fertility treatments
Repeated antibiotic use
Steroid use
oh and stress....we never have any of that while managing a chronic disease huh?

Topical yeast, fungus, Candida Wash

I have zero idea if this will work but it *should* as long as it is not too irritating for your skin. I have had a couple people mention having topical yeast issues, of course there is some feet issues but some people seem to have it on their skin and I have read in some instances it can cause breakouts. I recently bought a 'refreshing' foot spray with peppermint oil, when I looked at it closer it said it will cure foot odor and when I looked at the ingredients I realized I could totally make it myself. 


Here is my attempt at coming up with a natural, cheap, wash for someone dealing with fungus or candida issues. I would definitely do a 'spot' test since tea tree oil can be pretty strong. 

   

http://hmbeautyrecipes.homestead.com/SKINcleansers.html

Tea Tree Oil This oil readily penetrates the skin and is useful for treating burns, scrapes, bites, stings, and various skin irritations. It may also help to prevent or treat yeast infections. Very effective fungicide, antibacterial and antiseptic. 

Rejuvenating Cleanser Recipe

Ingredients

6 tablespoon Flax Seed Oil

6 Tablespoons Olive Oil

12 tablespoons castor oil

30 drop essential oils of your choice

Instructions:

Add carrier oils to a clean, dark glass bottle. Add essential oils. Gently shake to blend before each use. Store in a dark, glass bottle in a cool place or fridge. Apply a small amount to face and massage to cleanse. Rinse with warm water and a wash cloth. Skin will feel super smooth and silky! Perfect anti-aging cleanser!

Yuck and Ugh

Well I've been meaning to post just a normal post but of course it's easy to forget when you are feeling pretty good. That's come to a crashing halt.

Last week I took off thursday since it was my 31st birthday. Wouldn't you know wednesday night I could tell I was getting sick and for my birthday I spent the day on the couch with Lillian or in my bed. I tried not to let it damper my day so when Jared got home from work he took Lillian out, picked up dinner and we ate dinner in bed with my bed heater on which I love and I opened my present from him and from Lillian and we watched a show. Friday however I was worse, I ended up with a wretched flu that is still hanging on. I started  inhaled cayston and colistin on monday and start cipro tonight (wed) a full WEEK after getting sick. Yuck! My peak flow has went from 560-570 to 420-440.

Wouldn't you know I called my new doctors office on monday and was put into a voicemail and never got a call back. Come to find out she doesnt HAVE voicemail so who knows where it ended up but its why I didnt get a call back.

I'm going to give this a try and I have a clinic appointment next week.

pH

Just realized I posted this on my family blog on accident, oops, double oops because I haven't gotten the book yet either!

So I got some test strips that measure pH from 5-10 in increments of 0.5 and my husband and daughters pH registered 7 while mine registered 6 and once 5.5 Now I just tested this randomly and there are 'ideal' times to test so I plan to do some more tests. So far my very brief research indicates that a pH of 7.3-7.4 seems to be what the majority of websites are citing.

I plan to read the book Alkalize or Die by Dr. Theodore A. Baroody

 Bodily Responses That Fight To Maintain pH

this is from here: http://www.relfe.com/health_natural/pH_human_body_balance_health_level_1.html

All metabolic processes, including immunity, depend on a delicately balanced pH, which harmonizes electromagnetic energies. The body constantly fights to maintain a blood pH at around 7.35 -7.45 much like our internal thermostat that tries to maintain a 98.6-degree body temperature. There are seven homeostatic adaptation responses that fight to maintain this pH balance.

1) Using high pH bodily fluids such as water as a solvent to neutralize acid residues.

2) Pulling bicarbonate from the pancreas into the blood (an alkalizing agent). Bicarbonate ions are generated into the blood cells from carbon dioxide and diffuse into the plasma.

3) Protein buffers of glutathione, methionine, cystine, taurine, just to name a few, act as buffers intra-cellularly to bind or neutralize acids during cellular disorganization.

4.) Electrolyte buffers of sodium, calcium and potassium work in the blood, lymph, and extra-cellular and in­tracellular fluids to bind acids, which are then removed through the urine.

5.) Pulling stored calcium and magnesium from skeletal bones and teeth to neutralize blood acids.

6.) Filtration and elimination of acidic residues through the skin, urinary tract and respiration.

7.) Pushing blood acid residues and accumulated toxins into outer extremities as a storage bin away from vital organs. The wrist, joints, fingers, toes and skin are the major target areas to keep the toxins from saturating internal vital organs like the heart and lungs.

When all seven-protection phases are over­whelmed, the end result is accumulated acid residues at the cellular level, which drown out oxygen. With this acidic, low oxygen terrain, the microzyma’s (small ferments) trigger morbid microbe infiltration of fungus, molds and parasites, cancer cells, etc., where they seek the diseased acid terrain as food. (Editor's note: The term "microzyma" was created by Antoine Bechamp. These are small living components of cells and are described more fully later in this article ).

As these organisms feed, they produce waste just like you do. Their urine and feces are called mycotoxins, which are very poisonous to humans. Being acids themselves, mycotoxins greatly worsen the acidity caused by an acidic diet and toxic acid emotions. They are spilled into the blood as well as inside cells, where they cause free radical damage to the genetic material of the cell eventually causing cell death. The dead necrotic cells also spill out acid wastes. The blood poisoning results in more cell and tissue poisoning furthering the disturbance of the microzyma triggering morbid forms of yeast, molds and viruses, which disrupts body chemistry causing disease to the systems. So it’s a vicious cycle. One acid condition creates anothet Acidic diet coupled with toxic acid emotions creates an acid pH to the cells. This causes low oxygen levels (hypoxia), which is necessary for keeping back destructive anaerobic microbes and immuno-suppression is the result. Then medical doctors come in and treat the acid condidon with another acid (pharmaceuticals).

http://www.ionizers.org/ph-balance.html

Thus the saliva pH parallels the extra cellular fluid ... pH paper test using saliva represents the most consistent and most definitive physical sign of the ionic calcium deficiency syndrome ... The saliva pH of the non-deficient and healthy person is in the 7.5 to 7.1 slightly alkaline range. The range from 6.5 which is weakly acidic to 4.5 which is strongly acidic represents states from mildly deficient to strongly deficient, respectively.

Most children are 7.5. Over half of adults are 6.5 or lower, reflecting the calcium deficiency of aging and lifestyle defects. Cancer patients are usually a bright yellow, a pH of 4.5, especially when terminal."

I'm applying for mystery diagnosis!

I'm sure it wont pan out but hoping it can raise some awareness and help others!

_______________________________________________________________________________

As an infant I had unusual bowel movements but gained weight and looked healthy.

As a young child I developed painful stomach problems that at the age of 2-3 would leave me writhing in pain and continually crying. My mother was told that as an only child I was spoiled and I needed to be locked in my room until I stopped. These stomach problems happened periodically throughout my childhood and the cause was never determined despite multiple tests and doctors, by the time I was 7 I had learned breathing and distraction techniques taught in labor classes.

My mother recalls that I had colds and flus more common that some kids and my cough would last longer after the cold was resolved. About middle school it started getting much more pronounced and I was diagnosed with asthma and re-occurring bronchitis. My stomach problems continued intermittently, about once a year.

In high school I started getting sick a lot and ended up with pneumonia, mono,  sinus infections, strep throat; you name it and I had it. I also had my first bought of pleurisy but it was after a skiing accident and was attributed to that.  My first year of college I got sick a lot, I was living in dorm and I caught everything that went around. I had had a chronic cough for years but in college it began taking on a life of its own, I would cough so much throughout the night security would wake me up at night trying to see if I was ok.

The 1^st semester of my 2^nd year  I was  seeing the campus doctors, I got sick enough that the campus doctors wrote me a note to take incompletes while they were trying to figure out what was wrong.  During 2^nd semester I dropped to a minimal course load and  quit going to 2 of my 4 classes, I couldn't keep up with classes or my job as an RA; having always been an excellent student this was very hard.  I could barely make it to my 4th floor dorm room (no elevator) and the uncontrollable cough  made sitting through classes nearly impossible. I tried to bide my time until the semester was out, when I left that summer I knew I wasn’t going to be able to come back.

Once I was home I read articles on how to talk to your doctor, I made lists and went in prepared to be an educated patient. I was told that she only did 10 minute appointments and if I had more than 1-2 items to talk about I’d have to make multiple appointments. I did multiple appointments, nothing worked even when I told her I thought I had cystic fibrosis based on my reading and reminded her that I had 4 inconclusive sweats tests performed in middle school by another doctor. During the time I was under her care I was told:  to get my asthma under control, that I had to loose weight, that I was too stressed, finally at my pushing she diagnosed me with fibromyalgia for my pain and COPD for my lungs. I was referred for a cat scan for the headaches, when that came back clear I received a referral to a psychiatrist in the mail……it was the last straw. I later my medical records and found the terms ‘drug seeking’,  ‘hypochondriac’, that I and my mother had a ‘vested interest in my health but were misguided”. I had never even received a nebulizer!

At this point I was sleeping with a trash can next to my bed for the massive amount of mucous that felt as if they were suffocating me during the night. I was suffering from chronic fatigue, my entire body was sore all the time, I had migraines, anxiety, pleurisy that at times prevented me from moving, chronically swollen lymph nodes, my anxiety was out of control because I feared that I would die in my sleep before I would be believed.

I moved to a physician’s assistant that was freshly out of school and listened to me. I was disappointed when she explained that she had to treat me by a normal protocol and then take it from there. I had been through all of this before but she had listened and I really had no other choice so I agreed and was prescribed a nebulizer and a more aggressive antibiotic. Not surprisingly none of my symptoms cleared up but surprisingly for the first time someone believed there was a real problem and she promised to follow this through! She referred me to an allergist (they said I had allergies but not to an extent to explain my symptoms),  followed by an infectious disease specialist (nothing found),  followed by an internist (nothing found), followed by a pulmonologist. All of this took a very long time and I was really struggling and I had high hopes for this doctor.

The pulmonologist saw me and prescribed me a stronger oral antibiotic and did some testing,  I never felt I was getting any answers from him despite the fact I had started coughing up blood intermittently.  Much to my surprise he had been working with a pediatric pulmonologist specializing in cystic fibrosis. I was given a referral to them (and discovered they were the same office that had seen me during the sweat testing in middle school). I did not know at the time I arrived for the appointment that they were for CF I just knew they were another doctor and I really had very little hope that anything would be different this time. MUCH TO MY SURPRISE I WAS MET BY A TEAM OF SPECIALISTS AND DIAGNOSED WITH CYSTIC FIBRORIS WITHIN 10 MINUTES!! I STARTED CYRING AND WHEN THEY TRIED TO CONSOLE THEM I TOLD THEM THEY WERE TEARTS OF JOY!!! Finally I was believed and understood.

Sensitivities...or lack thereof

Culture shows moderate mucoid PA (normal) and Achromobacter which wasnt there last time but seems to be there more (my theory anyway) when I'm sick.

PA is susc to colistin, zosyn, and piperacillin
AB is susc to ceftazimide, meropenem, and piperacillin

Germ Factories started early & Clinic Tracking

This year in MI the germ factories seem to have started early and whatever has been going around has left a number of people with pneumonia. We were not overlooked. After all three of us had a cold I was just starting to feel better but had a cough hanging on and then WHAMMO I started feeling worse. I was wondering if my lungs were going down hill when Lillian came down with a fever and I knew we had.....round two. Lillian had a fever for 6 days and ended up needing antibiotics. The bugs in my lungs went wild and I was very productive and increased cough.

After checking my last culture showed up sensitive to cipro which I havent used in a few years and for the record I detest and nromally doesnt work. We decided based on my numbers below that something had to be done so we decided to give cipro a go and change our minds if needed based on the culture and how I did.

7Oct2010 FVC94 (down 33) FEV1 88 (down 26) FEV25-75 82 (down20)
Notes: I'd been sick for 3 weeks. I've fallen off the anti-inflammatory eating but am still taking 5LAC, Lauricidin, and doing green smoothies. New clinic new machine reference numbers so need to start tracking volumes. FVC3.81 FEV1 3.00 FEV25-75 2.94

23Apr2010 FVC 127 FEV1 114 (up 14% WOW) FEV25-75 102 (up 12% WOW)

Notes: this is especially fantastic given my allergies are running wild and I have seen a drop in my peak flow the past few days from it. I normally write down my PEF (peak flow) but he pointed out that mine was off the chart this time, my Peak flow was 11.82 which equates to 150 L/min higher than two months ago i.e. the little plastic things we use measures in L/min.

Clinic Notes: Discussed recent treatment for candida. Fatigue, chronic pain, pleural pain, all gone. Lung functions are the best on record and it is after no drugs or steroids where as the 108% last year was after serious steroids. Please see here for all details:

18Feb2010 FVC 110 FEV1 100 (down 4% more-total8%) FEV25-75 90 (up 2%)
Clinic Notes: This was post IV's (stopped Christmas Eve) and 2 rounds prednisone totaling 5 weeks (1st round stopped New Years day and 2nd round was 3 weeks in January). Infection is gone but still having chronic pain on left side when breathing, especially deep breathing, still intermitten pleurisy, still fatigued and not feeling right, feel like I do right before I get a bleed. Discussed potentially entering chronic pain phase of CF (I do not accept this). Also started drinking mucomyst N-acetylcysteine since last visit so reported good results in gastro area from this, no large effect noted on the lungs. Discussed going to CA to consult with Dr.Moss on inflammation and also discussed pursuing testing for candida with family doctor.

**oops missed a couple, need to dig around and find those**

3May2009 FVC 118 FEV1 104 (down 4%) FEV25-75% 88 (up 1%)

Clinic Notes: re-check post steroids and pre-pregnancy (attempt). Everything looks great, feeling good, allergies are problematic and doc did say that my theory on my allergic reactions having residual inflammatory effect on my lungs (which I did another week steroids for) was very possible. His pregnancy recommendations are to be vigilent with physiotherapy especially hit it hard in 2nd tri' to get ready for 3rd when lungs are most compromised and there is the biggest risk.

March2009: FVC FEV1 108 FEV25-75% 87
Clinic Notes: Recheck after end of steroids, feeling good. Best FEV1 ever!

29Feb2009 FVC 111 FEV1 100 (down 3%) FEV25-75% 88 (down 14%)
Clinic Notes: feel inflammatory in nature start 2 weeks steroids 40mg taper. Still got streaking in day 2 steroids.


15Dec2008 FEV1 103 FEV25-75 102%
Clinic Notes: summer steroids early winter cold w 3 weeks cipro)

21Feb2008: FVC 105.3 FEV1 99.3 FEV25-75% 89.1 BP 114/68 HR 59 Wt152
Clinic Notes: was getting huge variability and felt something 'stuck'

25Jun2007: FVC 105 FEV1 97 FEV25-75% 82

4Dec2007: FVC 99 FEV1 91 FEV25-75% 77