CF Info

Information on Selected Aspects of Cystic Fibrosis

Email: LarryV@pobox.com.

This page contains information on the following aspects of cystic fibrosis (CF): 

• Reversing diabetes.
• Controlling hemoptysis.
• Controlling nasal polyps.
• Reducing lung congestion.
• Benefiting from tea tree oil and magnesium.

The information on tea tree oil and magnesium was provided by Kim Payne at paynekimj@YAHOO.COM.  She is interested in collecting feedback from people who try magnesium or essential oils. 

All the other information presented on this web page is drawn from the experience and careful observations of an adult male (born in 1956 and still breathing with original lungs) who has two copies of the delta F-508 gene, the most prevalent mutation causing CF.  Nothing presented on this page can be considered scientifically valid until it has been tested in randomized, controlled clinical trials.  Nonetheless, this information may be of use to individuals with CF.

*** Please consult with a medical professional before changing your regimen or acting on any information you see here. ***

Reversing CF-Related Diabetes
(Updated Dec. 29, 2005)

This write-up discusses the case of a male with cystic fibrosis (CF) who is close to reversing CF-related diabetes (CFRD) through modest daily alcohol consumption.  He has so far failed to reverse diabetes because he is one of the rare individuals with CF who easily absorbs copper and iron and he discovered that stored iron and an elevated serum level of copper are toxic to beta (insulin-producing) cells.  The vast marjority of individuals with CF have a below-normal level of copper and stored iron and should be able to reverse their CF diabetes using the information provided here.  Stored iron is measured by transferrin or total iron binding capacity (TIBC).  This discussion draws on medical studies and theory to explain the progress of this particular case.  A subsequent section discusses the practical steps needed to effect the reversal of CFRD.

Background

There is little evidence that the beta cell destruction which occurs in CFRD is caused by an autoimmune process (the process that causes type 1 diabetes).  Pancreatic tissue from patients with CFRD frequently contains amyloid deposits similar to those seen in patients without CF who have type 2 diabetes.  These amyloid deposits are derived from an islet amyloid polypeptide (IAPP) produced within the beta cells and normally secreted together with insulin.[1]  Autopsy findings have shown that "amyloid depositation is found in islets from patients with CFRD but not in islets from patients with cystic fibrosis without diabetes."[2]

Since association does not prove causation, it remains to be established whether the the amyloid deposits are the cause of type 2 diabetes or only a marker for the disease.  

Amyloidosis is associated with type 2 diabetes and is a disorder of protein folding.  Beta cells excrete IAPP as part of normal functioning. The body has a mechanism to remove IAPP.  However, in individuals with type 2 diabetes, IAPP, which is normally soluble, turns (folds) into an insoluble mass which collects outside beta cells, blocking normal insulin secretion and destroying beta cells which are at the stage of cell division.  Pepys and colleagues propose that the glycoprotein serum amyloid P component (SAP) binds to the amyloid fibrils and protects them from degradation and removal.  They discuss the identification of chemical compounds which dissociate SAP from amyloid deposits, allowing the deposits to be cleared through normal biological mechanisms.[3]

There are numerous studies which indicate that moderate consumption of alcohol reduces the risk of developing type 2 diabetes.[4]  This raises the possibility that alcohol is one such compound which dissociates SAP from amyloid deposits, allowing them to cleared and allowing beta cells to be re-generated and protected.  Individuals with CF are advised to minimize alcohol consumption because CF puts them at increased risk of liver disease, which alcohol may exacerbate.  Therefore one would expect to find a high percentage of abstainers among the CF population.

Case Study

The patient under discussion is homozygous for delta F-508, the most prevalent mutation causing cystic fibrosis.  He was diagnosed with diabetes mellitus in May 2002 at age 46, presenting with an HbA1c of 9.3% and a postprandial blood glucose of 434 mg./dL.  He has engaged in regular vigorous exercise all his adult life.  He weighs about 165 lbs. (within normal range for his height of 5 ft. 11 in.).  He was diagnosed with diabetes later than most patients with CF who get the disease.  In one study, the cumulative incidence of CFRD was found to be 76% in patients who are 30 years of age.[5]

Prior to developing diabetes, the patient largely abstained from alcohol consumption.  At the end of June 2002, he began consuming a glass of dry red wine with his evening meal.  After noticing a favorable effect on his blood glucose, he continued this practice each evening.  The patient kept a detailed record of the number of carbohydrates consumed with each meal, the amount of insulin injected and pre-meal blood glucose readings.  The patient's HbA1c was measured in Oct. 2002 at 6.6%, in Feb. 2003 at 5.8% and in Aug. 2003 at 5.7%, indicating good blood glucose control.  (Note:  In 2005, the patient discovered that having a drink before bed instead of with the evening meal more than triples the number of beta cells which are generated and protected each night.)

The author proposes that the human pancreas undergoes a seasonal variation in the production of beta cells.  This variation may have evolved to match the seasonal supply of carbohydrates available to pre-historic humans.  If present, such a variation would be apparent only in individuals who have a fraction of the normal supply of functioning beta cells.

The graph below shows the number of units of insulin injected daily by the patient from September, 2002 to May 2004, adjusted to reflect his average daily carbohydrate intake of 392 grams.  The author proposes the following explanation of the data:  During the first six weeks of 2003, a sharp increase in injected insulin was needed to replace the beta cells lost to apoptosis.  These cells had not been previously replaced due to years of accumulation of IAPP which finally resulted in the onset of diabetes.  

The decrease in injected insulin which occurred from spring through mid-summer of 2003 occurred as the pancreas was preparing for nature's seasonal abundance of carbohydrates.  The regular consumption of wine was allowing the body to clear IAPP, which allowed newly generated beta cells to begin accumulating.  

During the early autumn of 2003, most of the last of the older generation of beta cells expired, requiring a mild rise in injected insulin.  During the first six weeks of 2004 there was only a very slight rise in injected insulin, unlike the case a year earlier, because there were only a few aged beta cells which were expiring.  However, the sharp decline in injected insulin from mid-February to March 1st 2004, mirrored the decline during the same period in 2003.  

During 2002 and 2003, the patient's level of exercise and level of iron intake was largely unchanged.  In early March 2004, the patient substantially increased his intake of iron (due to increased exercise) which remained at an elevated level until the end of March, at which time he resumed his former level of iron intake.  The author proposes that this abnormally high level of iron consumption led to increased stored iron which led to destruction of beta cells which, in turn, led to an increase in injected insulin.  A recent study, published in JAMA, shows a correlation between elevated iron stores and risk of diabetes.[6]

Once iron consumption was reduced, beta cell production resumed as shown in the chart for the month of April.  At the end of April, disaster struck.  I increased my copper intake by eating more copper-containing foods.  I did this because copper pulls in more iron and I was hoping to strike the right copper/iron balance to allow me to exercise more while still maintaining a low level of stored iron.  However I overshot the mark and noticed that I was losing beta cells again.  Once I realized that I would not be able to tightly control my copper/iron intake, depression set in because my goal of getting rid of diabetes was in doubt.  Depression caused insomnia, high levels of stress and lack of deep sleep.  I then discovered, much to my horror, that severe stress also kills beta cells.  My supply of beta cells, which had been carefully nurtured over two years, was destroyed in the course of two weeks and I fell into deeper depression which lasted for months.  As of December 2005, my insulin requirements continue to rise and fall as I struggle to get my copper under control.  Once I accomplish this my diabetes will be history.  Stay tuned.

Reversing CF-Related Diabetes:  Practical Details
(Updated Jan. 4th, 2006)

Who can benefit?  One drink of alcohol taken just before bedtime each night should allow anyone with regular CF diabetes to reverse it (i.e., get rid of it) over a period of months, even if diabetes has been present for many years, providing that one's pancreas is still able to manufacture beta cells and providing you have a low level of stored iron, as measured by a blood test for transferrin or total iron binding capacity (TIBC).  If your insulin requirement (for a given amount of carbohydrates) changes from week to week or month to month it is very likely that your pancreas still makes beta cells.

Can someone who does not have CF, but does have type II diabetes use this method to get rid of it?  Yes.  However, the first step should be to get your salt level down to normal (see "first steps" below).  Once that is done and the diabetes persists, try one drink a day before bedtime for a few months.

Do I have to worry about copper?  Probably not.  If your copper level is high, it will most likely be reflected in an elevated level of stored iron (transferrin or TIBC).

What if my stored iron level is high?  Very few individuals with CF have this problem.  However, if a blood test shows your iron stores are too high, you can try cutting back on foods high in copper (see section on hemoptysis for a list of such foods) and foods high in iron, such as red meat.  I have been fighting this problem for years.

Contraindications:  Diabetes that is caused by steroids (such as those used after transplantation) will not be helped by alcohol consumption because steroids are directly toxic to beta cells.  Also, alcohol interferes with anti-rejection meds and should not be consumed by anyone who has had a transplant.  Furthermore, anyone with severe lung disease should probably not consume alcohol because it can lower O2 saturation.

What are the first steps?  Have your liver function tested (blood test) by your physician to rule out any existing liver problems.  Discuss the risks of alcohol consumption with your doctor.  Some people are allergic to alcohol.  Have your sodium chloride (salt) level checked; if it is above normal, reduce your intake of salt.  Insulin resistance rises rapidly as your sodium level rises above normal, which means you must use more insulin for the same amount of carbohydrates.

What should I drink, how much and when?  I chose dry red wine because it is low in carbs and high in antioxidants.  If you prefer a bottle of beer, it should work just as well.  I consume a glass of wine just before bedtime.  Drinking at other times of the day will help little or not at all (depending on the length of time between the drink and your nightly sleep).  The best time to drink the alcohol is just before bedtime because it then provides maximum protection for the beta cells which are only generated during deep sleep.  Too much alcohol will have the opposite of the intended effect.  In high doses, alcohol is directly toxic to beta cells.  So, binge drinking is about the worst thing you can do (from the perspective of getting rid of diabetes).

If drinking just before bedtime interferes with sleep you can move the drink back to an earlier time.  The only drawback will be less beta cell generation each night.  So, it will take longer to get rid of the diabetes.  For a long time, I was taking a drink with my evening meal.  This was still was getting the job done (until my copper crisis occurred), but very slowly.

What is the best time of year to start the experiment?   Anytime.  I previously thought that beta cells were only generated during spring and summer.  However, I was wrong.  It appears that during spring and summer beta cells can be generated every night if conditions are right.  However, during fall and winter, there are days at a time when no beta cells are generated even if all conditions are perfect.  However, during most days of fall and winter, new beta cells can be generated (if conditions are right).

How soon will I see results?  Not right away.  It will take at least 4 to 6 weeks of consuming one drink a day to clear out all the plaque in your pancreas that is preventing beta cell generation.  Anytime after that you can expect your insulin production to take off like a rocket and keep going (except for breaks taken during fall and winter -- see previous paragraph), providing you continue to consume one drink each day as close to bedtime as possible.

Do I still have to hassle with measuring the carbs I eat?  Yes.  If you start to take a drink a day and are still injecting insulin it would be wise to measure carbs for at least one meal per day so you can track your progress.  Once your pancreas starts to manufacture and retain new beta cells, you will need less insulin.  There can be a significant jump in the body's production of insulin from one day to the next.  If you are not carefully measuring your carbohydrate intake, you risk severe hypoglycemia (low blood sugar).  The reason every bottle of insulin has a warning against consuming alcohol with the insulin is because of the risk of low blood sugar.  (One would think some smart researcher would have put two and two together and studied the ability of alcohol to reverse diabetes.  But, Nooooooooo. :-)

What if I have elevated blood glucose but don't yet take insulin?  Get clearance from your medical team for alcohol consumption (see Who can benefit?, above) and start with a drink a day before bedtime.  If the theory is correct, you should never get diabetes as long as you are able to continue drinking and don't have to take steroids.  See next question.

What other things are essential to increase my supply of beta cells or improve insulin utilization?  1) Make sure a blood test shows your level of stored iron, as measured by transferrin or total iron binding capacity (TIBC), is at or just below the lower end of normal.  Many individuals with CF have low iron stores.  2) Make sure you are not consuming too much salt because high levels of salt cause insulin resistance.  Have your sodium level measured the next time your doctor does blood work.  Try to keep your salt level within the normal or even low-normal range.  3) Make sure you are getting an adequate amount of Vitamin D.  It is needed to manufacture beta cells.  

What other things might help, but are not essential for getting rid of diabetes?  1) Talk to your nutritionist about taking 200 mcg. per day of chromium picolinate.  It improves insulin utilization.  2) Start a program of regular exercise, even if this is just walking.  It will help your lungs and improve insulin utilization.  Try to exercise for the same length of time each time you do it so you can more easily calculate the effect of exercise on your insulin and carbohydrate intake.  You have to experiment to find how exercise affects you.

Note:  If you are able to get rid of your diabetes using this method, please let others with diabetes know about it.

Atypical Hemoptysis
(Updated August 27th, 2006)

Atypical hemoptysis is characterized by moderate to severe bleeding (more than 200 mL of bright-red blood coughed up in a 24-hour period) which often begins an hour or two after a large meal.  It occurs predominately in CF males and non-menstruating females.  Unlike regular hemoptysis, it is not positively correlated with acute lung infection (i.e., an intravenous clean-out may have just been done, or lungs may have recently been pronounced clear of acute infection).  Atypical hemoptysis is more likely to occur in CF individuals who are generally considered to have better than average pulmonary status.  Once it occurs, it is likely to recur repeatedly in the following days, often triggered by routine physical activity.  However, when it finally vanishes, it may not recur for months.

Atypical hemoptysis occurs when copper rises to 1.5 to 2 times its normal level in the bloodstream because of the failure of the bile duct to excrete it into the duodenum.  Copper, by itself, is a powerful oxidizing agent.  CF arteries have little or no plaque lining the artery walls and may be particularly susceptible to oxidation.  The combination of an elevated level of this oxidizing agent (copper), a weaker than normal artery wall and the high pressure present in a pulmonary artery causes the rupture and bleeding.

Impaired copper excretion in the bile duct occurs when the pH level becomes too acidic.  This acidic pH is caused by lack of bicarbonate excretion in the bile duct, which, in turn, is caused by lack of bicarbonate/chloride exchange.  Bicarbonate/chloride exchange is impeded by the lack of available chloride.  Finally, the lack of available chloride occurs when a mild to moderate deficiency in dietary potassium iodide shuts down an alternate chloride channel.  The primary (CFTR) chloride channel is defective in all individuals with CF.  Note:  This hypothesis has yet to be studied scientifically or confirmed by medical studies.

Atypical hemoptysis can be easily diagnosed by measuring serum copper during or shortly after an episode of hemoptysis.  Individuals with cystic fibrosis typically have a low copper level, so an elevated level will stand out prominently.  

One way you can uncover suspected atypical hemoptysis without medical testing is to keep a record of foods you eat.  When hemoptysis occurs, look up the copper content of the foods recently eaten (see list below).  Another way to test for atypical hemoptysis is to deliberately eat foods containing a moderately high level of copper over a period of several days to see if hemoptysis occurs.  Warning:  Be very careful with this second approach; in susceptible individuals, copper accumulates like water behind a dam and can cause sudden and substantial hemoptysis.

Controlling Atypical Hemoptysis

My previous hypothesis put the blame on a malfunctioning gallbladder (common in CF) which (I thought) pushes accumulated sludge into the common bile duct, thereby inhibiting normal bile flow from the liver to the intestine.  I was completely wrong about this.  My gallbladder was surgically removed, under general anesthesia, on April 6, 2006.  For about three days after surgery, I thought my hypothesis had been right because I was able to eat foods moderately high in copper without killing beta cells (the first sign of elevated copper serum) and without hemoptysis.  However, shortly thereafter, my beta cells began to die off in great numbers and it became clear that my original hypothesis, however plausible, had been wrong.  I suspect the 3-day relief I experienced after surgery was due to the removal of a source of acidity (namely, my atrophied gallbladder).  After 3 days, the previous acid/base balance had re-established itself and I was back to square one.  So, there seems to be no reason to rush into gallbladder surgery (unless other symptoms warrant it).

Another idea I came across in my search for a solution is drug-induced cholestasis.  Some of the antibiotics used to treat CF can cause bile duct inflammation or injury, theorectically resulting in impaired copper excretion, a build-up of copper in the blood stream and hemoptysis.  For example, amoxicillin, ampicillin, dicloxacillin, and tetracycline may cause a form of cholestasis.  For a longer list of such drugs, refer to the Cleveland Clinic's summary page on drug-induced cholestasis.  For additional information, refer to the Clinic's detailed discussion of Cholestatic Liver Disease.   In my case, intermittent hemoptysis and an elevated copper serum level were immediately (though only temporarily) reversed by discontinuing dicloxacillin on Jan. 6, 2006.  On April 15th, 2006, I discontinued my only other antibiotic, Bactrim D.S., to see if that would help my problem.  Again, the improved copper excretion was very brief.  So, this idea came to naught.

In the early summer of 2006, my symptoms got much worse and things looked very bleak.  However, by chance, I discovered that the underlying problem appears to be a deficiency of potassium iodide (the nutrient that is added to iodized salt).  For years, I avoided potassium iodide because too much made my acne worse.  Over time, I developed a substantial deficiency, which, it appears, led to my decreasing ability to excrete copper.  It appears to be the case that the iodide opens an alternate chloride channel (not the CFTR chloride channel which is defective in all people with CF).  This alternate chloride channel is needed in the pancreas and bile duct, where it allows the proper exchange of chloride for bicarbonate.  This exchange is needed to maintain a proper pH balance.  I am currently supplementing with pills containing potassium iodide.  Once my level of iodide is back to normal, I will be able to see if that is the solution to the copper problem.

Because iodide is preferentially sequestered by the thyroid gland, (assuming my latest hypothesis is correct), even a mild deficiency of potassium iodide would cause an elevated copper serum level.  Only a full tank of iodide, which is topped off every day with a supplement containing the recommended daily allowance or with iodized salt will prevent the copper problem.  Time will tell if I am right.

Warning:  Although copper can cause hemoptysis, it is nonetheless a valuable ally in the fight against CF.  Copper increases iron absorption, may help with bone formation, forms part of the antioxidant superoxide dismutase, and independently fights both bacterial and viral infections.  I have fewer colds and no lung exacerbations when my copper serum level is elevated.  Driving your copper level too low will result in a substantial increase in lung infection.  Finding the right level is a process of trial and error.

On the negative side, even a mildly elevated copper serum level kills beta (insulin producing) cells, which provides a fast-track to insulin-dependent type II diabetes.

For years, I controlled my atypical hemoptysis is by limiting foods high in copper, by taking a low dose of chelated zinc (such as zinc gluconate) with one or two meals a day, and by exercising regularly.  Exercise appears to increase copper excretion by raising the body's pH level (making it more alkaline).  The exercise need not be vigorous.  Rapid walking for a half hour each day would help a lot.  Zinc suppresses the absorption of copper in the gut.  Discuss zinc dose levels with a nutritionist or a physician.  

The prescription drug Actigall (Ursodeoxycholic acid - UDCA) is supposed to improve bile flow.  However, I found that discontinuing this drug improved my stools and allowed me to get my copper below the level that was causing hemoptysis.  So, you may want to experiment with stopping this drug if you are already taking it.

Also, consumption of the micronutrient molybdenum may increase copper excretion.

If you think you have atypical hemoptysis, have your copper level measured as soon as possible after hemoptysis occurs and again several months after your most recent episode of hemoptysis to establish a baseline level.

You can measure your iodide level, indirectly, via a urine test which indicates how much you are excreting.  The less your body excretes, the lower your body's store of iodide is.  Taking too much potassium iodide causes other problems, so measurement is important.

***** The following lists are not exhaustive. *****

Foods Very High in Copper (more than 500 mcg. per serving)

Multi-vitamins which list copper as an ingredient, oysters, lobster, squid, octopus, blue crabs, crab cakes, buckwheat flour, sesame seeds, sunflower seeds, liver, heart, other animal organs, raw coconut milk, tahini sauce, navy pea beans, potatoes with skins, almonds, brazil nuts, cashews, filberts/hazelnuts, mixed nuts, peanuts and peanut butter, pecans, pistachios, black walnuts, most other nuts.

Foods Moderately High in Copper (200 - 500 mcg. per serving)

Chocolate, bran cereal, clams, sardines, shrimp, raw blackberries, pineapple, prunes, whole wheat flour, avocado, kidney beans, lima beans, great Northern beans, black-eyed cowpeas, lentils, green peas, peas in pods, tofu, roasted soybeans, goose, potatoes without skins, potato skins only, vegetable juice, black strap molasses, and some types of mushrooms (shiitake, for example).

I have found that the copper from some foods, such as nuts and chocolate, is more readily absorbed than the copper from other foods.  Only a process of trial and error will let you discover the foods and amounts which must be avoided.

An inexpensive paperback which shows the copper content of many foods, along with the counts for other vitamins and minerals, is:  The Corinne T. Netzer Vitamin and Mineral Counter, by Corinne T. Netzer.

An expensive but very thorough reference which contains the copper content of a large number of foods, along with the counts for carbohydrate and a variety of nutrients is:  Bowes & Church's Food Values of Portions Commonly Used, by Jean A. T. Pennington.

The following USDA web site lets you search for the copper content of particular foods:

http://www.nal.usda.gov/fnic/foodcomp/search/

For a PDF file of foods, sorted by copper content, visit the following USDA web page.  I disagree with many of the rankings (based on personal experience).  You will have to decide for yourself.

http://www.nal.usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17w312.pdf

Fighting Nasal Polyps
(Updated Dec. 29, 2005)

I discovered, quite by accident, that eating a small (6 oz.) white or sweet potato (without skin) once a day reduces the swelling of my nasal polyps and, I'm hoping, reduces their growth rate and the frequency of sinus surgery.

I have only my personal experience to back up this claim.  I had nasal polyps removed in 1968, 1981, 1989, Sept. 1996 and Sept. 1999, and Nov. 2004.  I have also been a regular potato eater most of my life.  However, in January 1996, I stopped eating potatoes completely in an attempt to reduce my copper intake (see previous item on hemoptysis).  My nasal polyps grew rapidly in 1996 and had to be removed in September.  Three years later they had filled my sinuses again, the quickest relapse I've ever experienced.

By August 1999, with polyps filling just about every square inch of my sinuses, I was experiencing a regular pattern:  My polyps would swell slowly during the day and by evening it felt as though an inflated, pressurized water balloon filled my sinuses, which caused substantial discomfort.  Overnight, the swelling would ease and the pattern would begin again the next day.  This pattern repeated day after day, without exception.  

One day, being quite sick of my bland diet, I decided to throw caution to the wind and eat an exquisite sweet potato as part of supper.  That evening I experienced no sinus swelling.  I assumed it was just a fluke, so I waited a few days until the normal swelling pattern resumed and tried another sweet potato.  I got the same results.  After surgery, the first thing I did (after trying to flirt with the nurses on my floor) was to wolf down some potatoes.  I have been eating them regularly since then.

I have found one food and one supplement which appear to dramatically increase polyp growth.  Red seedless grapes appear to promote vigorous polyp growth and artichoke leaf extract (which I was taking to improve bile flow) appears to do the same.  I have discontinued consumption of both.  I assume green grapes would have the same effect as red grapes, but I am not sure and do not plan to test them.  Red wine does not appear to promote polyp growth.  I don't know about raisins.

Reducing Lung Congestion

In addition to following accepted medical protocol for treating CF, I have found the following to be very beneficial in reducing lung congestion:

• Adding the spice turmeric to my diet.
• Adding the herb cayenne to my diet.
• Eating enough copper-rich and iron-rich foods to maintain proper blood levels of those minerals.
• Exercising regularly.

Turmeric

I have found that eating a 1/2 teaspoon per day of the spice turmeric per day has noticeably improved my lung function numbers.  I usually sprinkle it on my lunch-time sandwich.

Turmeric is a powerful anti-inflammatory which seems to help break the cycle of inflammation and infection.  Turmeric is also an anti-oxidant, which is all to the good.  Some people may have GI sensitivity to it. 

I get the Whole Foods brand of turmeric for $2 per 1.92 oz. bottle.  I have heard a similar-size bottle can be purchased at WalMart for $3.

Here are some online references:

• Turmeric has anti-inflammatory effects.

• Curcumin/Turmeric.

• Turmeric Is A Known Anti-Oxidant, Anti-Inflammatory, Anti-Carcinogenic Agent.

• Holistic Online:  Turmeric.

Cayenne

I've found that the substance capsaicin, which is contained in hot chili peppers and in the herb cayenne, has the ability to dramatically reduce mucus production in the lungs.  It also improves digestion by stimulating gastric secretions and peristaltic activity.[1]  I sprinkle a half capsule of cayenne on my evening meal.  A full capsule contains 450 mg. of cayenne of strength 40,000 H.U. (heat units).  As a result of taking this herb, my lung function has improved substantially (due to reduced inflammation caused by less mucus.) 

Warnings:  If you are taking the asthma drug theophylline, cayenne may increase the amount of theophylline which is absorbed, possibly to dangerous levels (see The Natural Pharmacist link below).  Cayenne may act as a mild anticoagulant.  Also, according to Rodale's Illustrated Encyclopedia of Herbs: "Consumption of cayenne can be dangerous for people with intestinal disorders such as duodenal ulcers or chronic bowel diseases.  Even in individuals with health digestive systems, cayenne in excessive amounts can cause severe stomach upset and even kidney damage."[2]

The following are some links to information on capsaicin and cayenne. 

• Weekly Wire.  Information on the benefits of capsaicin including benefit to the lungs.
• Whole Health MD.  More information on cayenne.
• Supplement Watch.  Technical and medical information on capsaicin.
• Not Just Vitamins.  Herbs are in alphabetical order.  Scroll to "cayenne."
• Purple Sage.  More information on cayenne.
• MD Consult.  If desired, sign up for a free trial.  Then, search on "cayenne" under the section "Patient Handouts."  Then select the 4th handout: "Cystic Fibrosis, Alternative Therapies."

Iron and Copper

I have found both iron and copper to be very valuable in reducing the congestion in my lungs.  According to one nutrition book, white blood cells, which "serve as the body's primary defense mechanism against bacterial infections, depend on iron-containing enzymes to do their job. . ."  They note further that the "production of antibodies also requires iron-dependent enzymes. . . "[3]  Moreover, increasing one's intake of iron improves the blood stream's ability to carry oxygen which is used to oxidize (destroy) bacteria.  

When I consume a substantial dose of iron (for example, by eating a large steak), production of green mucus initially increases as bacteria, which need iron to thrive, have a field day.  However, their victory is short-lived because the increased iron boosts the body's ability to destroy bacteria.  Overall, maintaining an adequate level of iron in my blood stream decreases mucus production and reduces its consistency.  Consuming iron also helps me get over colds quickly.

It is important to understand the interaction of iron with other vitamins and minerals.  Taking iron (in high-iron foods such as red meat or in supplement form) at the same time as Vitamin C helps increase iron absorption in the gut.  Taking iron with calcium supplements or with calcium-containing dairy products dramatically reduces iron absorption because calcium binds with the iron, making it unavailable.  I consume needed calcium (in food and in pill form) during breakfast and lunch and avoid dairy products and calcium supplements at dinnertime, to maximize my iron intake during that meal.  Having an elevated level of copper in the blood stream also increases iron absorption.[4]  Unlike Vitamin C, the copper does not have to be taken at the same time as the iron.  Copper also plays an independent role in fighting bacterial infection.[5]

If you are taking an iron supplement and still have a low level of iron in your blood stream, ask your nutritionist about taking a multi-vitamin which contains B vitamins and 1-2 mg. of copper.  As an alternative, there are some foods, such as nuts, seeds, and seafood, which are naturally high in copper.  Be sure to read the previous item about the connection between copper and hemoptysis.

Exercise

In 1981, when I first started playing tennis seriously, my stamina could be measured in minutes.  I had barely started running around on the court when I would become winded, feeling as though someone had pored glue in my lungs.  Taking a brief rest allowed me to resume play.  As I continued to play I found I was gradually able to increase my endurance on the court.  Today, I play tennis 3 times per week at the local tennis club throughout the year.  I can play just over an hour of singles tennis at a normal pace against an opponent with no lung impairment.  And, I win my games as often as I lose!

There are several secrets to exercising with CF.  Find an athletic activity you genuinely enjoy.  If you regard exercise as a chore, you are less likely to stick with it.  Try several different sports before making a choice.  For example, if you live in a warm climate, you might go crazy about inline skating.  Build up gradually, set modest but frequently-changing goals for yourself and be persistent.  I find the benefits of regular exercise are well worth the time spent:  Any junk in my lungs is easily coughed up.  My lungs feel larger after playing, as though their capacity had increased.  And, I have an increased feeling of well-being, which is reported by many people who exercise regularly.

It's my understanding that some lung transplant centers put their candidates on a systematic and rigorous program of exercise.  This tells me that physicians consider exercise to be beneficial, regardless of the state of one's lungs.  If you regret not having started exercising earlier in life, forget about it; that's old news.  Today is a good day to start and tomorrow is a good day to stick with it.

Tea Tree Oil and Magnesium

by Kim Payne
at paynekimj@YAHOO.COM.

Tea Tree Oil:  Many of us swear by melaleuka alternifolia (tea tree oil).  When my 24-year old son with CF begins to feel inflammation and congestion building, he'll add a couple drops of tea tree oil to a bowl of freshly boiled water and inhale the vapors to help keep respiratory issues at bay.

When we're in a hurry, I just open the bottle and wave it under my nose for a few whiffs; my son does this too whenever he flies to help guard against in-flight germs.

On occasion when I have stuffy sinuses, sinus and ear pain, I put a small drop of tea tree oil (TTO) on a cotton ball and stuff the cotton into my ears overnight.  Next day, no more pain or puffy face.  Since most sinus infections are fungal not bacterial, this is a good alternative to oral antibiotics, which may do nothing for the infection anyway.

TTO has excellent antibacterial, anti-fungal, anti-parasitic and anti-yeast properties. Look for TTO in dark brown or dark blue glass bottles -- not clear bottles and definitely not plastic bottles.  Make sure the label says 100% pure essential oil.  Avoid any essential oils that say "distillate," "floral water," or "absolute." Those three are not pure, but rather the by-product of processing; they are best used in candle or perfume making, not for medicinal purposes.

TTO on a Q-tip is great for zapping a zit, and for women who get frequent yeast infections (or infants with diaper rash/yeast), bathing in a tub with TTO added helps clear up issues.  Just be sure not to splash the water in your eyes.

Magnesium (Mg): In mid-January 2002, we got the results of a sputum culturing showing my son was growing S. maltophilia and aspergillus.  Previously he'd only cultured pseudomonas and in 1998, he also began culturing mucoid pseudomonas aeruginosa (PA).  The doctor didn't want to treat these two new organisms, but we didn't want them to take up residence in his lungs.  So I started searching for something to help him.

Knowing that CF lungs are more acidic than non-CF lungs, and that bugs love an acidic environment, I started looking for a way to raise lung pH.  (Editor's note:  Water has a neutral pH.  Anything with a pH lower than that of water is acidic.  Anything with a pH higher than that of water is alkaline)  By the way, cancer cells also love an acidic host, and our typical diet in the US reinforces this acidic environment.

That's where Mg came in; Mg is an alkaline mineral -- the second most abundant intracellular mineral and necessary for over 300 enzymatic actions in the body.

For example, Mg is responsible for holding calcium in the bones and teeth. Without Mg, it wouldn't matter how much calcium (Ca) you consume, your body just won't hold on to Ca unless you balance it with Mg.

So, the last week of January 2002, my son started taking Mg supplements every day and inhaling TTO nightly (he'd inhale the vapors for about five minutes or until the water cooled).  He did skip a nightly inhalation now and then.

By April 10, 2002, we happened to be in the ER for an ankle injury so I asked the doctor to also do a sputum culture. They were flabbergasted to learn he had CF because he looked so great.  You would not have believed the turn-around in his health and appearance -- the difference between January and April was amazing.

The culture came back the following week, and the aspergillus and S. maltophilia didn't show up on the culture.  We were also surprised to see that his mucoid PA was now sensitive to all antibiotics.  He first cultured mucoid PA sometime in 1998 and from the very beginning it had *always* been resistant to aminoglycosides (tobramycin, gentamicin, amikacin) -- though his non-mucoid PA was sensitive to aminoglycosides.

The nurse in the CF clinic (Northwestern in Chicago, where Brian is not a patient but we happened to be in their ER so we had culture results sent up to the clinic) told me they have over 40 adult patients and none of them are sensitive to all antibiotics; she was amazed. So were we.

Eight months later in December 2002, Brian was home over Christmas and saw his own CF doctor for his annual exam.  The results from that sputum culture came back still showing no aspergillus, no S. maltophilia, and this time, not even mucoid PA.  The only thing that showed up was nonmucoid PA.

In the meantime, I had continued digging around and found some research papers pointing to PA resistance to aminoglycosides during magnesium deficiency (MgD).  The studies also showed this was reversible when MgD was corrected.

Also, studies showed that PA becomes mucoid during MgD, but again the study showed this was reversible when MgD was corrected.  My son could have been a poster child for the study because this was exactly what happened in his case.  But because everyone is different, not everyone may experience the same happy results.

Other crucial points to keep in mind:

1) Nearly every med used in CF depletes Mg.  These include antibiotics (nearly every type known), steroids, bronchodilators such as Xopenex, albuterol and theophylline.  Caffeine and alcohol deplete Mg; stress is a big depleter of Mg, as is surgery, malabsorption, vomiting, diarrhea, and sweating (all together now, can we say, "CF?"). Heart meds and antidepressants also deplete Mg.

2) With so many people with CF (PWCF) taking Zithromax, it's crucial to watch your Mg., because it depletes Mg.  And if you are Mg deficient, you greatly increase your risk of torsades des pointes, a serious heart condition.  In just the past year, cardiologists have increasingly become aware of this and now macrolide antibiotics carry the warning on the patient insert.  But is *your* doctor aware of this importance?  Probably not.

3) Timing of Mg (really, any mineral) is important because minerals often compete with antibiotics on the cell receptor site, and the antibiotic loses the contest.  For example, if you take Cipro (which greatly depletes your Mg stores) too close to Mg, then you reduce the efficacy of Cipro by 50%.

There's a 2-hour rule of thumb for taking Mg when you're taking antibiotics.  You can take Mg two hours *after* antibiotics (do not take sooner than two hours after antibiotics).  If you take Mg first, then you must wait at least 4 hours before you can take an antibiotic. However, in the case of Cipro, you must wait a full 7 hours after taking Cipro before you can take Mg.

The only antibiotic my son takes is Zithromax, 500 mg. M-W-F.  To comply with the 2-hour rule, he takes all his vitamins and minerals before noon, and takes Zithromax before bed.

We don't worry about the 2-hour rule on the occasions he inhales TOBI, but we would be conscious of it if he had to take other oral or IV antibiotics throughout the day.  One benefit he found to correcting MgD was that he no longer has to do the 28 day on/off TOBI cycle.  He now only inhales TOBI if he feels he's getting something that he can't kick.

4) A few studies indicate increased risk of ototoxcity (hearing damage) if you are Mg deficient while taking aminoglycosides.  Another study shows that if you take Mg before and during IV aminoglycoside therapy, you reduce this risk; yet another study showed slight improvement of symptoms if MgD was corrected within a short time after first experiencing ototoxic symptoms (eight days, I think).

5) Another study showed that taking iron or iron-containing supplements while using aminoglycosides increases the risk of ototoxcity.

6) Nearly without fail, certain groups always have lower Mg: people with asthma, diabetes, depression, migraines, attention disorders, seizure disorders, pancreatitis, kidney stones and gall bladder issues, heart disease, and osteoporosis.  Sadly, many meds prescribed to offset the symptoms of these illnesses further cause MgD, causing a vicious cycle that does little to help the root problem, but only ease symptoms.

7) Doctors do not routinely test for Mg.  Look at your last lab.  CF clinics may test Ca or potassium, but not Mg.  And even if they do test Mg, a blood test is not the way to go.  Only a fraction of 1% of Mg is in the blood; roughly 60% is in bone; 40% is intracellular.

If you have blood drawn to test Mg, and the results come back "in range," you can be "low out of range."  And if the blood test comes back "low out of range," then studies have indicated you are likely dangerously low out of range.  I had a blood Mg test done after supplementing 200-300 mg. a day for a couple months.  My blood test came back on the low end of in range.  Imagine if I'd not been supplementing.

And imagine my son's Mg levels after years of taking theophylline, Zithromax, other oral antibiotics, surgery resulting in a 3-week course of Cipro and 2-month back-to-back course of TOBI, malabsorption issues, college-kid diet, and inhaling albuterol twice daily for years.  In fact, albuterol depletes calcium, phosphorus, potassium and Mg, and within one hour, Mg levels fail to return to pre-treatment levels. That's a scary fact when doctors tell parents to give their kids albuterol treatments every 2 hours without recognizing rebound and how MgD contributes to bronchoconstriction.

Therefore, the only accurate way to test Mg levels is to test intracellular Mg by taking a small cell scraping from under the tongue for analysis. This site explains it in more detail: http://ww.exatest.com.

8) Not all magnesiums are created equal.  Magnesium oxide (MgOx) is the cheapest, most available form; you'll find it listed in nearly every multivitamin/mineral on the market.  However, it's the least bioavailable form, and at high doses it can cause loose stools or diarrhea, which only makes MgD worse.  Other common forms are magnesium chloride (MgCl) and magnesium citrate, which aren't the greatest choices either for the same gastric reasons as MgOx.

A lot of us (including my son and me) use a magnesium chelated to the amino acid, glycine (Mg gly).  This was developed by a very reputable company, Albion Labs (http://www.albionlabs.com).  Albion sells their minerals to other companies for marketing under their own labels.  We buy Solgar, which labels it as "magnesium amino acid chelate."

Grandmom Bev at the Florida CF Pharmacy (1-800-741-4427) worked with us to get Solgar magnesium glycinate at the absolute best price: $12.95 for a 250-ct. bottle (each tablet contains 100 mg.).  If you order over $25, they pick up the shipping costs, and you can't beat that!

I found that I absolutely must have a minimum 4 tablets (400 mg.) daily (in addition to whatever Mg is contained in my multivitamin).  Otherwise migraines, insomnia, back muscle spasms and IBS flare up within three days.  Solgar's Mg glycinate has been a blessing; I tried other forms of Mg but it didn't work for me at all.  And as for Brian, like me, he continues to take a good-quality complete multivitamin/mineral in addition to 400 mg. Solgar Mg each day.

Since finding tea tree oil and correcting his Mg balance, he has been able to discontinue Prilosec, TOBI and Pulmozyme.  He uses TOBI and Pulmozyme only when needed.  And shortly after starting Mg, his PFTs stopped dipping; previously they were declining at each visit.

I know most of you are thinking, "If it's so important, why hasn't my doctor mentioned it?"  Because your doctor doesn't know.  So there. I said it but it's true.  Ask your doctor why he or she doesn't know how important this is.  Ask why they haven't read the ebook on Mg printed by the USDA and backed by the NIH.  That document states that Americans are not getting enough Mg, even with proper diet and even when taking a multivitamin/mineral (and very few Americans actually take a multivitamin).  For those inquisitive enough, here's the link to the USDA site that contains the ebooks: http://www.nal.usda.gov/fnic/etext/000105.html.  Scroll down to find the one on Mg.

For more Mg info, here's the PubMed site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi.  Type "magnesium" or "magnesium deficiency" into the search box.  For hours of fun, type in "magnesium and cystic fibrosis", "magnesium and pseudomonas", "magnesium deficiency and diabetes", "magnesium and CFTR", "magnesium and ATP", or "magnesium and aminoglycoside".  The list goes on.

For more than a year, beginning in January 2002, I spent 16 hours a day (yes, I did) reading about implications of MgD and contacting researchers in the field.  And I'm still learning and still amazed that doctors know so little and are so unwilling to humbly accept the research of their colleagues when a parent brings it to them.

Other sites worth reading are:

http://www.mgwater.com. 
http://www.krispin.com. 
http://magnesiumresearchlab.salu.net. 
http://www.life-enthusiast.com/twilight/shealy/magnesium.htm. 

And if you consume anything with aspartame, you absolutely must read the following and stop consuming all aspartame products.  Aspartame is highly toxic stuff:  http://www.alkalizeforhealth.net/Lsweetdebate24.htm. 

Kim

Update on Brian received on May 27, 2005:

In December 2004, Brian had another check up.  He had gone two years without seeing his CF doctor and having tests done.  He is still free of mucoid PA, though he still cultures PA.  And, he is still sensitive to all antibiotics.  All other lab work is normal.

Kim Payne

Footnotes

1. Mark K. Robbins and David A. Ontjes, "Endocrine and Renal Disorders in Cystic Fibrosis," in Cystic Fibrosis in Adults, ed. by James R. Yankaskas and Michael R. Knowles (Philadelphia: Lippincott-Raven, 1999), p. 392-393.

2. Dana S. Hardin and Antoinette Moran, "Diabetes Mellitus in Cystic Fibrosis," Endocrinology and metabolism clinics of North America, 1999 Dec; 28(4): 790.

3. M.B. Pepys et al., "Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis," Nature, 2002 May 16; 417: 254-259; Robert A. Ritzel, Peter C. Butler, "Replication increases [beta]-cell vulnerability to human islet amyloid polypeptide--induced apoptosis (Islet Studies)," Diabetes, 2003 July.  Online at http://www.findarticles.com/cf_dls/m0922/7_52/105161579/p4/article.jhtml?term=.

4. See, for example:  Wannamethee SG, et al., "Alcohol drinking patterns and risk of type 2 diabetes mellitus among younger women," Archives of Internal Medicine, 2003 Jun 9; 163(11): 1329-36; Carlsson S, et al., "Alcohol consumption, Type 2 diabetes mellitus and impaired glucose tolerance in middle-aged Swedish men," Diabetic Medicine, 2000 Nov; 17(11): 776-81; Carlsson S, et al., "Alcohol consumption and the incidence of type 2 diabetes: a 20-year follow-up of the Finnish twin cohort study," Diabetes Care, 2003 Oct; 26(10): 2785-90; Nakanishi N, Suzuki K, Tatara K, "Alcohol consumption and risk for development of impaired fasting glucose or type 2 diabetes in middle-aged Japanese men," Diabetes Care, 2003 Jan; 26(1): 48-54.

5. Peter R. Durie and Gordon G. Forstner, "The Endocrine Pancreas," in Cystic Fibrosis in Adults, ed. by James R. Yankaskas and Michael R. Knowles (Philadelphia: Lippincott-Raven, 1999), p. 392-393.

1. Elson M. Haas, Staying Healthy with Nutrition:  The Complete Guide to Diet and Nutritional Medicine (Berkeley, California: Celestial Arts Publishing, 1992), p. 276.

2. Claire Kowalchik and William H. Hylton, Editors, Rodale's Illustrated Encyclopedia of Herbs (Emmaus, Pennsylvania: Rodale Press, 1998), p. 77.

3. (Editors of Prevention Magazine), The Complete Book of Vitamins and Minerals for Health (Emmaus, Pennsylvania: Rodale Press, 1988), p. 177.

4. Elizabeth Somer, The Essential Guide to Vitamins and Minerals (New York: HarperCollins Publishers, Inc., 1995), p. 99.

5. Ibid., p. 101.

6. Jiang R, et al., "Body iron stores in relation to risk of type 2 diabetes in apparently healthy women," JAMA, 2004 Feb 11; 291(6): 711-7.  Abstract can be found online at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14871914