My MS/LDN story/1988 - 2015

[Art]

I was diagnosed with multiple sclerosis April 1988.

I was very ill for two years after the initial attack. I could barely walk straight, the left side of my face was numb, my eyesight was extremely blurry for a few weeks, and had terrible fatigue. I never thought I would recover and become independent again. I was very depressed, and briefly considered suicide. I was hospitalized for over one month and out of work for over four months. It took me many, many months to get back into action.

I gradually pulled out of the attack with the help of much IV Solumedrol and oral Prednisone, which is all the doctors had to offer back then. CRAB/Novantrone/Tysabri meds were unheard of.

I eventually made a full recovery and was symptom-free until around 1994. It was as if I never had MS. I wasn't under the care of a neurologist, which, in hindsight, was a mistake. 1994 is when I started seeing him again on a regular basis.

I was originally diagnosed with Relapsing/Remitting type MS, but after a few years the neurologist upgraded it to the next level, called Secondary Progressive Multiple Sclerosis.

1996 was a very rough winter here in New York. There was a major blizzard, followed by heavy snowfall after heavy snowfall. I work as a maintenance supervisor for a real estate company and part of my job is to see that the snow is removed from their properties. It was a very stressful winter for me both mentally and physically. My MS returned with a vengeance, and my neurologist put me on Avonex, which I took for over three years. Self injected, too. Not fun.

I eventually developed neutralizing antibodies against interferon meds so my neurologist put me on Copaxone which I took for over three years. He also had me on eight treatments of Novantrone. I had many, many IV Solumedrol / Prednisone taper-offs in between all of this. Nothing was holding the MS off. Nothing. He then wanted to put me on Beta Seron and I asked him why, as I thought I was immune towards interferons. He said, "Well, we have to try something". He also thought about putting me on Tysabri, right before it started harming people and was pulled from the market. It was then I realized he was only experimenting on me and really didn't have definite answers.

I am 6'7" and weigh 220 lbs, but my eyes filled with tears in his office.

Fortunately, his nurse saw me and suggested I look into LDN, even though the neurologist was against it. She also suggested Prokarin, which I took for a few months.

I have been on LDN since March 2005 and shudder to think where I'd be without it. Among other things, it has helped my blurry vision and balance, improved my bladder control, lessened my fatigue and given me a general sense of well-being. If that weren't enough, it has slowed the progression of my disease. My only regret is that I didn't start LDN sooner than I did. I am certain I wouldn't be dealing with the physical problems I now have.


Besides taking 3mgs LDN every other night at 9pm, I also use:

Tysabri
Neurontin (Gabapentin) 800mgs
Ampyra
Ativan (Lorazepam) 1mg
Provigil (Modafinil)
Vitamin D3
Citrucel fiber tablets
Multi-vitamin
Magnesium Glycinate


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I actually used Copaxone for at least 6 or 7 total years.

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I also have spinal stenosis and 3 herniated discs in my lower back. July 2011 I had back surgery which didn't help very much.

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No alcohol, was never a drinker, no cigarettes, quit June 1993, after being up to three packs a day.

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The summer of 2013 I was diagnosed as having Babesiosis. Get it from a tick bite and it's in the malaria family. After being in the hospital for a while and out of work for a few weeks the infectious disease doctors said I was cured.

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If you have MS you better get off your ass and start researching EVERYTHING out there. Don't rely on your mainstream doctors ONLY for help! If you do, you will be sorry. Trust me.

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Helpful sites:

LDN Now
www.ldnnow.co.uk/

LDN brochure
www.ldn-help.com

LDN Aware
www.ldnaware.org/

How LDN works
tinyurl.com/how-LDN-OGF-worksskydrive.live.com

Dr. Gluck's LDN website
www.lowdosenaltrexone.org/

LDN Yahoo discussion group
health.groups.yahoo.com/group/lowdosenaltrexone/

Skip's Pharmacy
skipspharmacy.com/ldn.php

The Compounder
www.thecompounder.com/

Crystal's website
www.freewebs.com/crystalangel6267/index.htm


www.ldners.org/

LDN stories
www.health.gov.au/internet/nhhrc/publishing.nsf/Content/056-ch/$FILE/56%20-%20Attachment%20-%20CASE%20Health%20Booklet.pdf

Larry's LDN story
www.larrygc.com/mystory

LDN discussion site
disc.yourwebapps.com/Indices/148285.html#64425

forum.ldnresearchtrust.org/

forum.lef.org/default.aspx?f=37&m=16685

The Accelerated Cure Project for Multiple Sclerosis (ACP) is a patient-founded national non-profit organization dedicated to accelerating advances toward a cure for MS.
www.acceleratedcure.org/

Jack LaLane Power Juicer
www.powerjuicer.com/

Dr. McCandless LDN Africa
www.ldnafricaaids.org/

Tart cherry juice
www.brownwoodacres.com/cherry_juice_concentrate.php

DMSO info
www.dmso.org/

Vitamin info
www.wholehealthmd.com/ME2/default.asp

Prokarin
www.edmsllc.com/

Lyme disease test
www.igenex.com/Website/

LDN Science
www.ldnscience.org/low-dose-naltrexone-ldn/questions-and-answers

Dr. Ian S. Zagon
Introduction to Low Dose Naltrexone (LDN)
www.ldnresearchtrustfiles.co.uk/docs/Dr%20Zagon.pdf

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It is not what you have lost but what you have left that counts. -- Harold Russell, the only actor to win 2 Oscars for the same role, The Best Years Of Our Lives (1946)

If I knew I was going to live this long, I'd have taken better care of myself. -- Mickey Mantle (1931-1995)

[Art]

From Dr. Lawrence
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Gamma Amino Butyric Acid in Multiple Sclerosis

Gamma amino butyric acid (GABA) is an amino acid, a natural substance that has been found to stimulate the production of growth hormone by the posterior pituitary gland at the base of the brain.

The effects of growth hormone are most well known in teenagers when, during the rapid growing phase of adolescence, it is produced in massive quantity. It is this growth hormone that stimulates the normal growth and maturation changes that occur at this time.

Less well known is the fact that growth hormone continues to be produced, to a lesser degree, throughout life. At this time, its purpose is to stimulate the various processes of regeneration and repair that maintain the body in a state of fitness and functional efficiency.

In normal health and within the limits of moderate age this process is maintained in reasonable order, but in illness and with increasing age, the production of growth hormone begins to diminish. It is considered that this reduction in growth hormone production is contributory to the degeneration of the body seen in old age.

In MS, where brain function is inhibited by the inflammatory auto-immune process, the production of growth hormone is believed to be further retarded.

Thus, there is a clear logic in using a substance, such as GABA, in an attempt to restore the more normal production of the hormone that would be expected to enhance the repair of the damage caused.

Effects of GABA

1) Gaba promotes increased muscle growth and strength.

2) By promoting growth hormone production it would be expected to enhance the process of remyelination (repair of the myelin sheath in the brain and spinal cord).

3) By improving circulation to the brain it increases vigour and vitality.

4) It often has a dramatic effect in relaxing muscle tone, thus reducing muscle spasm and pain, and aiding relaxation during sleep.

The crystalline powder is extremely hygroscopic (absorbs water from the air) and should therefore be kept well-sealed, in a cool, dry place.

The GABA should be taken in modest quantity, using just one level teaspoonful each day, dissolved in a little water, usually taken before bedtime. If muscle spasm is more apparent in the daytime, the GABA may be taken at whichever time provides the most convenient response.

The treatment should be taken on an empty stomach but should not be taken just before food. Because GABA acts as a vasodilator (increases blood supply to the muscles and other body tissues) it may prompt a slight fall in blood pressure. Eating soon after taking GABA could therefore result in discomfort due to gastric colic, and faintness due to a further fall in blood pressure.

This therapy, within five to ten minutes, may result in some transient side-effects, including: flushing and/ or tingling of the skin and, occasionally, slight shortness of breath. These slightly disturbing effects are usually mild and brief, lasting no more than a minute-or-so.

[Art]

From Dr. Lawrence
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The use of Diet and Nutritional Therapy in Multiple Sclerosis

Fundamental to the effective treatment of MS is the need to follow a restricted diet and take a range of nutrient supplements intended to compensate the well-known and common deficiencies existing in MS.

The restricted diet requires the exclusion of all red meat, all dairy (cow’s milk) products, all wheat products, caffeine, chocolate, citrus fruit, and strong, spicy food.

Red meat includes beef, pork, mutton and lamb. Possibly, lean pork may be eaten occasionally, perhaps once per month. Poultry or fish may be eaten freely.

Cow’s milk, even skimmed milk, must be avoided completely. Sweetened soya milk may be used as an alternative in milk puddings or cereals. Unsweetened soya milk, to most people, is unpleasant and unpalatable. A non-dairy coffee whitener may be used in decaffeinated tea or coffee.

Wheat appears to be a specific sensitivity in MS as the incidence of similar sensitivity to other gluten cereals (inc oats, barley, and rye) is very low, at about 10%, or less.

Caffeine, although used in small doses in the histamine therapy, is detrimental in larger doses. Caffeine drinks, such as tea, coffee, or cola should be decaffeinated. Avoid caffeine in such as analgesic tablets or artificial stimulants.

Chocolate, in significant quantities, is detrimental. When the diet and suitable therapy is found to be effective, small amounts may be eaten with relative impunity.

There is an acute sensitivity to citric acid, contained in citrus fruit. These include oranges, lemons, grapefruit, and limes. Citrus fruit must be avoided completely.

Spicy food contains high levels of natural salicylates. Similar to aspirin, these compounds block the conversion of essential fatty acids (EFAs) into prostaglandins (PGs). PGs are vital cell mediators that provide a variety of important functions throughout the body, including the function of the immune system.

Some spices, such as turmeric, and possibly cumin, are found to be beneficial in MS or other conditions. These are available as nutritional supplements from various healthfood companies.

Occasionally, there may exist a sensitivity to the deadly nightshade family of plants. This group includes tomatoes, potatoes, capsicums,(red or green peppers), courgettes, and cucumbers. In this circumstance, exposure to these foods will tend to increase certain symptoms of the MS, such as fatigue or numbness of the hands or feet. If such symptoms occur, the foods involved should be avoided.

Nutrients should include, most essentially, essential fatty acids (EFAs), zinc, copper, and the basic range of antioxidants. Flavonoid antioxidants (anthocyanidins) are also considered greatly beneficial in MS.

EFAs should include significant quantities of all three groups of essential fats: omega 3 (N3); omega 6 (N6), and omega 9 (N9). It has been known for over 60 years that people with MS lack many of the essential fats within this group.

The N3 fats include the fish oils, or such as flaxseed oil, which contains a predominance of the N3 fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).. These are essential in providing the basis for anti-inflammatory leucotrienes (cell activators) that naturally reduce the level of inflammation in the body.

N3 fats also contribute to the structure and regeneration of the brain. All the cells of the brain consist predominantly of N3 fatty acids.

The N6 fats include such as evening primrose oil, borage seed oil (Starflower oil) or, to a lesser extent, sunflower oil.

N6 fats contribute to the structure of all living cells, forming the cell wall and certain internal structures of the cell. N6 fats provide the building blocks forming, and permitting the regeneration of the myelin in the brain.

They also may be converted to a range of vital prostaglandins (PGs). PGs are active in maintaining a vast range of essential physiological functions in the body, including the efficient activity of the immune system.

N9 fats are the monosaturated fats, most abundantly available as olive oil. The N9 fats are heat-stable up to 400 deg C and are therefore preferable for cooking. They are not denatured by the heating process when, under similar circumstances, N6 fats are readily converted to saturated fats. N9 fats are also useful in salad dressings.

N9 fats are effective in reducing cholesterol in the blood, thus benefiting the heart and circulatory system. They also contribute to the structure and integrity of the skin. In MS a deficiency of N9 fats will often result in intense urticaria (itching) thus leading to further skin damage through scratching. A regular daily supplement of N9 fats will prevent this.

Zinc is a vital element in the treatment of MS. It too is contributory to a wide range of functions in the body including the activity of the immune system and the conversion of N6 EFAs into prostaglandins.

Most importantly perhaps, is the action of zinc on the adrenal gland. The adrenal gland is vital in maintaining both vigour and vitality; providing protection against infection, and in defending the body from the effects of stress.

Because MS is invariably accompanied by major zinc deficiency the adrenal gland is equally underactive. This is why emotional or physical stress has such a marked adverse effect on the disease process, often triggering a relapse of the MS.

The provision of a suitable supplement of zinc each day, usually at least 50 to 100 mg, is effective in boosting adrenal function to diminish any such adverse responses.

The precise estimation of zinc needs may be assessed by means of the zinc taste test, an inexpensive, simple, and non-toxic test that may be repeated frequently to assess the ongoing response to zinc therapy.

In addition, with high doses of zinc, a single low dose of copper (2 to 4 mg) should also be taken.

The basic range of antioxidants includes selenium (200 mcg); vitamin E (400 units); vitamin C (1000 mg) and beta carotene (15 mg).

These antioxidant nutrients are active in support of the antioxidant enzymes, including superoxide dismutase; glutathione peroxidase; and catalase, which together protect the body from the damaging effects of free radicals.

It is the reactive increase in these antioxidant enzymes that provide the benefits after hyperbaric oxygen treatment (HBO).

Free radicals are produced as a result of normal metabolism, from traffic pollution, and from such abnormal abuses such as smoking tobacco. Smoking cannabis, sometimes used in the treatment of MS, will increase the damage due to smoking by about twenty times. Also considering the wide-ranging side-effects of cannabis itself, this is why cannabis cannot be recommended in the treatment of this disease.

The flavonoid antioxidants (anthocyanidins) are particularly effective in reducing the symptoms of MS. These include such as grapeseed extract, extracts of various dark berries, such as bilberry or bluberry, or pinebark extract (pycnogenol - a patented product).

Flavonoids enhance the activity of the basic antioxidants, such as vitamin C or E, by promoting their reactivation within the body. The recommended dose is from 250 to 1000 mg/ day.

Vitamin D may also be found to be deficient in MS. If so, a maximum supplement of 2000 international units (50 mcg) per day is recommended. Doses higher than this have been recommended by some practitioners but, because vitamin D preparations also contain high doses of vitamin A, these high dose of vitamin A may be considered detrimental.

High doses of both vitamin D and vitamin A may be teratogenic in pregnancy. This means that such high doses could cause developmental abnormalities in the developing infant.

Thus, the maximum dose recommended in pregnancy is 1000 international units (25 mcg) of Vit D, and 1000 international units of vitamin A.

Vitamin B12 is of particular importance as MS is occasionally associated with auto-immune pernicious anaemia. In this condition the absorption of B12 is prevented due to the deficiency or absence of gastric intrinsic factor (a glyco-protein produced in the stomach).

Vitamin B12 (referred to as the extrinsic factor), is normally absorbed by combining with the intrinsic factor in the stomach. It is then absorbed in this combined form in the small bowel.

If the intrinsic factor is deficient or absent the absorption of B12 is diminished and pernicious anaemia occurs. Because B12 is also essential for the process of remyelination, repair of the myelin is impossible without adequate vitamin B12.

It is thus essential to be given a regular, at least monthly, injection of B!2, as hydroxycobalamin 1000 mcg, in order to prevent these problems.

To be most effective, vitamin B12 must be accompanied by a high-strength vitamin B complex, either B50 or B100, containing an average dose of either 50 or 100 mg of each individual vitamin.

Muscle spasm in MS is a common symptom. This is initially minimised by taking an adequate dose of both calcium (1200 mg) and magnesium (500 mg).

Calcium is effective in maintaining a relaxed and appropriate muscle tone; magnesium is essential in maintaining appropriate and efficient muscle strength.

Vanadium is a rare mineral that is known to be often deficient in MS. Vanadium deficiency (together with zinc deficiency) is specifically associated with depression, a common MS symptom. The recommended dose is 10 mg/ day, as vanadyl sulphate.

[Art]

From Dr. Lawrence
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Anthocyanidins in the Treatment of Multiple Sclerosis

Oligomeric proanthocyanidins (OPCs), or anthocyanidins, are natural compounds within a group of plant-derived substances called flavonoids. They have very powerful antioxidant properties.

Anthocyanidins are derived from sources such as pine-bark extract, grape-seed extract or from berries, including cranberry and bilberry. These have a primary disadvantage in that they are relatively expensive but other more economic, but perhaps less effective, sources such as citrin or rutin have been used for their potential benefit.

There is presently an increasing interest in this group of compounds in the treatment of multiple sclerosis and other conditions.

The beneficial effects of this range of compounds may be summarised as follows:-

1) Antioxidant/ free radical scavenger: OPCs scavenge certain common free radicals 50 times more effectively than vitamin E and twenty times more effectively than vitamin C. As bioflavonoids they potentiate the absorption of vitamin C and protect vitamin C and carotenoids in the body. These, in turn, permit the recycling (and therefore conservation) of vitamin E. Thus, they increase the beneficial effect of other antioxidant vitamins.

2) Collagen binding and stabilising: OPCs bind to collagen, a protein in connective tissue, to maintain and restore its flexibility and integrity. Collagen is a primary component of the skin, blood vessels, joint tissues respiratory tract, intestinal tract, etc.

3) OPCs are anti-inflammatory; anti-allergic; they enhance the effect of vitamin C and protect capillaries.

A number of sources, including several references on the internet, have revealed some additional important facts.

With specific regard to MS, OPCs are effective in:-

!) Maintaining the blood/ brain barrier, which prevents cells of the immune system reaching the brain and spinal cord. Here, they are able to attack the myelin cells surrounding nerve fibres, thus promoting the range of disabilities characteristic of MS.

2) Crossing the blood/ brain barrier where they are able to further inhibit those T-lymphocytes which are already present in the tissues.

Pine-bark extract is probably the best-known source of OPCs. It has been patented under the trade-name of Pycnogenol and, as such, tends to be expensive. Pycnogenol products vary widely in price. The more expensive brands do not provide any additional benefits.

Alternative sources of OPCs tend to be more economically priced. Lamberts Coladeen (Anthocyanidin Complex), for example, costs £12-95 for 60 x 80 mg tablets.

Taken at a dose of one capsule twice daily 60 capsules would last for one month.

For such as MS, higher dose have been recommended by some internet sources. Doses as high as 500 – 1000 mg/ day have been used. The compound has been said to be free of side effects but in local tests, temporary symptoms, such as dizziness, tinnitus, nausea, dyspepsia, headache or disturbed sleep have been reported.

An American product, Revenol, contains 60 mg of OPCs together with low doses of vitamin C, vitamin E, and beta carotene. Revenol costs about £20 for 60 tablets.

Another product, Procydin, also contains a mixture of various berry extracts.

Local tests, using Colladeen, for periods up to six months, have shown significant beneficial responses. Improvements in muscle spasm, muscle function, balance and mobility, reduced pain, improved sleep and improved sense of well-being, have all been reported.

The flavonoids may be destroyed by the bacteria normally found in the bowel and, if taken in company with food, their movement through the bowel will be retarded. This will give more time for the bacteria to destroy the active ingredients so reducing their effectiveness.

Thus, despite the frequent recommendation that they should be taken with a meal, it would be preferred that they be taken on an empty stomach, at least one hour after the last meal. Their transition through the bowel will then be rapid providing optimum opportunity for absorption unchanged.

Due to some initial introductory side effects, it is recommended that the starting dose should be no more than two 80 mg tablets.

If no side effects occur, this dose may be increased slowly by adding two tablets to the daily dose each week.

Thus, during the first week – take two tablets each day (160 mg);
Second week – take four tablets each day (320 mg);
Third week – take six tablets each day (480 mg). This dose seems a practical and economic limit but higher doses may be safely considered if desired.

Tablets should be taken as a single dose each morning or as divided doses in the morning and at mid-day.

Taking the tablets late at night tends to increase the increase the likelihood of disturbed sleep or dreams.

[Art]

From Dr. Lawrence
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The Treatment of Neuro-muscular Spasm in Multiple Sclerosis

One of the most common symptoms occurring in MS is neuro-muscular spasm.

This troublesome symptom may be of two types, either tonic or clonic spasm.

Tonic spasm is when the resting muscle tone is abnormally increased. This is often simply apparent as stiffness, when the limb appears rigid and difficult to move despite the absence of absolute paralysis.

Clonic spasm: this is perhaps the most distressing of the two forms as the affected limb or muscle may jerk violently without warning, causing the individual to lose balance and perhaps fall.

The conventional means of treating these symptoms is with drugs including such as Baclofen or Zanaflex. The main penalty of the use of these drugs is the side-effect of sometimes extreme muscle weakness. Zanaflex is also quite toxic and can cause liver damage with the sustained use of high doses.

Other methods, utilising nutritional supplements are also available.

Although these are often less reliable and unpredictable and, it must be admitted, sometimes totally ineffective, they are harmless, and may be taken, at the advised doses, without risk or penalty.

Calcium and Magnesium: These minerals are both essential to the normal function of muscles, not only in providing the function of muscle contraction but also in maintaining an appropriate level of muscle tone during periods of relaxation. The occurrence of muscle cramp, due to spasm, is well known to be associated with calcium deficiency.

The normal therapeutic daily dose is, at least, calcium 1000mg and magnesium 500 mg. These are best taken at night because calcium levels tend to fall most significantly during sleep when muscle cramp is most likely to occur.

Gamma amino butyric acid (GABA): is a natural amino acid, which, at therapeutic doses, is able to stimulate the production of growth hormone. Growth hormone is normally produced throughout life and is necessary for any process of regeneration and repair.

When first tested it was anticipated that this would stimulate the regeneration of myelin. This may well be so but so far, the process remains unproved.

Its use however was found, in some, to dramatically reduce the incidence of pain and spasm, thus improving mobility and increasing comfort at rest.

Threonine: an amino acid, which, it is suggested, may reduce spasm in some individuals. The necessary dose is one gramme taken twice daily. Amino acids must be taken on an empty stomach for maximal benefit.

Niacin (Vitamin B3); This vitamin is also found to be effective in some individuals. The necessary dose is 500 mg taken three times daily with food. It must be taken with a daily dose of vitamin B complex to be fully effective.

Vitamin B complex is considered to be an essential routine vitamin for use in the treatment of MS.

Niacin may cause uncomfortable skin flushing in some individuals. A non-flush preparation is however available but is more expensive than the basic vitamin.

Methyl-sulphonyl-methane (MSM): a natural sulphur-containing compound, commonly used in the treatment of arthritis, when it is effective in facilitating the regeneration of joint cartilage and other connective tissues of the body.

In MS, it is suggested to be effective in restoring the integrity of the blood-brain barrier, thus reducing the invasion of CD4 T-cells into the brain and diminishing the process of auto-immune attack.

The substance also appears to be effective in reducing the incidence of muscle spasm. The appropriate dose is one or two grammes each day.

Anthocyanidins: taken in sufficient dosage (approximately 250 mg/ day, or more) these too appear to be helpful in reducing muscle spasm and so restoring mobility.

[Art]

History of Naltrexone


Naltrexone, short for Naltrexone Hydrochloride (C20H23NO4-HCl), is an
opiate antagonist. At a therapeutic dose of 50mg per day, Naltrexone
blocks the parts of the brain that "feel" pleasure when a person uses
alcohol or narcotics. When these areas of the brain are blocked, a
person feels less need for "one more drink" or "one more hit."

FDA-approved for the treatment of alcohol and opiate abuse,
Naltrexone has recently shown great promise in the treatment of other
medical conditions.


The Beginnings

Naltrexone was originally synthesized in 1963 and patented in 1967
as "Endo 1639A" (US patent no. 3332950) by Endo Laboratories, a small
pharmaceutical company in Long Island, NY, a company with extensive
experience in narcotics.

In 1969, DuPont purchased Endo Labs. DuPont had been struggling to
develop its drug business since the late 1950s, and the acquisition
of Endo provided DuPont with valuable expertise in drug manufacturing
and marketing.

In the purchase, DuPont acquired the rights to several successful
Endo drugs, including: Coumadin (warfarin), an anticoagulant;
Percodan, a prescription narcotic; and Naloxone, a drug used for
narcotic overdose.

Naltrexone, still in its early development phase, came to DuPont as
part of the overall purchase of Endo.

At the time it seemed unlikely that DuPont would develop naltrexone,
because at the time, naltrexone seemed to have relatively low market
potential, and its patent would probably expire before the completion
of any clinical trials.


The Federal Government Steps In

In June 1971, President Nixon created the Special Action Office for
Drug Abuse Prevention (SAODAP). The first director of SAODAP, Dr.
Jerome Taffe, was determined to improve access to drug abuse
treatment by shifting services from prisons and hospitals to
community-based services. "I regarded the development of naltrexone
as one of my high priorities," said Dr. Taffe.

SAODAP recognized that the development of naltrexone was of no
burning interest to the private pharmaceutical industry, and that
governmental funding would be necessary to bring it to market.

In March 1972, Congress passed the Drug Abuse Office and Treatment
Act, calling for development of "long-lasting, non-addictive,
blocking and antagonist drugs or other pharmacological substances for
the treatment of heroin addiction." This Act provided substantial
financial support for research.

By mid-1974, as SAODAP began to phase out of existence, the narcotic
antagonist development project fell to the newly formed National
Institute on Drug Abuse (NIDA).That same year, NIDA approached DuPont
with the idea of developing naltrexone as a drug addiction therapy,
and asked for DuPont's assistance in facilitating naltrexone's
transit through the FDA approval process. DuPont agreed to assist
NIDA with the development of naltrexone. In return, NIDA agreed to
pay for the bulk of clinical development costs.

When asked later, DuPont representatives said that the primary reason
for helping the government was Dupont's "public spirit", and that
naltrexone would probably not have been developed without the
government's clinical and financial support.

The clinical trials for naltrexone as a treatment for heroin
addiction began in 1973 (Schecter 1974, O'Brien 1978).


Difficulties in Clinical Trials

Early trials of naltrexone in rats, rabbits, dogs and monkeys had
determined that the drug was nontoxic at therapeutic levels, with
very few side effects. The subsequent human trials confirmed that
the drug was safe for humans, but the efficacy trials ran into some
unexpected problems.

Dr. Arnold Schecter, who conducted many of the early studies,
reported that many opiate-addicted patients feared a new drug, lacked
a desire to become drug free, were unwilling to possibly receive a
placebo, and disliked the rigid protocols associated with the
clinical trials (Schecter 1980).

Patients had to remain opiate-free for a minimum of 5 to 10 days
prior to treatment because naltrexone causes severe withdrawal
symptoms in patients with opioids in their system (Schecter 1974).
Many addicts were unable to comply, due to the physiological effects
of withdrawal.

Taking naltrexone does not provide any drug reinforcement ("high"),
and produces no negative consequences (withdrawal) when discontinued.
Unlike methadone, which helps suppress cravings, naltrexone has no
effect until the addict attempts to use heroin. Some patients feared
naltrexone would make them more vulnerable to these cravings, and
felt that methadone was more effective in controlling them.

Because of these recruiting difficulties, researchers made no effort
to screen out patients who might be difficult to manage in clinical
trials -- e.g., patients who were poorly compliant -- and this may
have compromised the results of the trials (Schecter 1980).

Since naltrexone is non-addictive and lacks the reinforcing effect of
methadone, it requires more extensive psychosocial support services
than methadone. Support services are expensive. Schecter estimated
that total clinical treatment with naltrexone was almost twice as
expensive as methadone -- not because of the medication itself, but
because of the more intensive support services.

Early trial results showed that, compared with the methadone
patients, the patients who were attracted to naltrexone therapy were
relatively "more motivated and emotionally stable." Other studies
showed that although naltrexone was an effective opiate block,
clinical success (a reduction in heroin use), was limited to fully
compliant patients. As a result of these findings, the product
labeling for naltrexone reads, "[Naltrexone]… does not reinforce
medication compliance and is expected to have a therapeutic effect
only when given under external conditions that support continued use
of the medication".

The final results of the clinical trials showed that naltrexone was
modestly successful in the reduction of heroin use.

In 1984, the FDA approved naltrexone in a 50mg dose as a treatment
for heroin addiction. Dupont brand-named the drug Trexan.

The same year, DuPont's naltrexone patent expired.

On March 11, 1985, the FDA designated naltrexone as an orphan drug,**
which provided seven additional years of market exclusivity for
naltrexone for DuPont.


Marketing Strategy for Trexan

The DuPont sales force had trouble explaining the mechanism of
naltrexone and its benefits to a lay audience. The consumer
marketplace had many misunderstandings and negative perceptions about
naltrexone. One former member of the DuPont sales force said these
misunderstandings were a great barrier to the use of Trexan.

DuPont also had an extremely difficult time trying to convince
methadone clinic personnel to use Trexan. Most facilities could not
afford to implement naltrexone therapy due to the combined price of
the drug, the drug treatment program, and the additional time and
staff necessary for psychosocial counseling.

Methadone clinics were also reluctant to refer patients for Trexan
because of their need to keep their own censuses high enough to
receive funding (Schecter 1980).

Pro-methadone treatment providers argued that because methadone was
dependence-producing, it was easier to maintain a patient on
methadone, and thus more likely that treatment would be successful.

As a result of these problems, Trexan failed to penetrate the highly
regulated federal treatment market for opioid addiction.

By 1995, Trexan sales were approximately $5-8 million annually, which
represented approximately 15-25,000 patients per year, or less than
5% of the estimated number of heroin addicts (Scrip 1993).


Naltexone as a Treatment for Alcoholism

Dr. Joseph Volpicelli first recognized naltrexone's potential to
treat alcoholism while experimenting with rats as a graduate student
in University of Pennsylvania. In 1981, he began to publish his
findings.

In 1985, Volpicelli and Dr. Charles O'Brien, a professor at Penn and
chief of psychiatry at Philadelphia's Veterans Administration Center,
began a naltrexone study using volunteers at the Veterans
Administration Hospital.

"We did it without any outside funding," says O'Brien. "We got it
started against pretty great odds." According to O'Brien, the
researchers had difficulty recruiting subjects because the idea of
treating alcoholism with medication was not commonly accepted in
the 1980's.

They tracked 70 men for 12 weeks in an outpatient detox program. Half
received naltrexone, half a placebo. While 54% of the volunteers who
received a placebo reverted to drinking, only 23% of those who took
naltrexone experienced a relapse.

In 1991, researchers at Yale University School of Medicine tested the
effects of naltrexone in conjunction with psychological therapy in
104 alcohol-dependent men and women. Patients who took naltrexone
were nearly twice as successful in their clinical outcomes as those
who took a placebo.

After the Penn and Yale studies were published in the Archives of
General Psychiatry in November 1992, DuPont showed interest in
marketing naltrexone specifically as an alcoholism treatment.

Governmental funding for the development of naltrexone as a therapy
for alcoholism was provided by the National Institute on Alcohol
Abuse and Alcoholism. The FDA modified existing regulatory
requirements to encourage DuPont to develop naltrexone as an
alcoholism therapy. They offered DuPont three additional years of
post-approval market exclusivity for naltrexone as an alcohol therapy.

Marketing exclusivity allows a pharmaceutical company to sell its
drug for a certain length of time free of competition from generic
versions of the drug. This type of marketing exclusivity is often
granted to encourage pharmaceutical companies to develop a use for a
drug whose patent has expired or to encourage a company to develop an
already approved drug for a new use. With market exclusivity, the
expected returns are higher, thus improving the profitability of the
drug.

The FDA also linked phase IV clinical trial requirements to annual
sales. No phase IV trials would be required if naltrexone as an
alcoholism therapy did not meet certain sales thresholds. If the drug
did well in the alcohol-abuse market, DuPont would have to conduct
phase IV trials based on the level of sales.

By allowing for flexible phase IV studies, the federal government
lowered post-marketing costs, improved profitability projections, and
made investment in naltrexone as an alcoholism therapy more
attractive to DuPont.


Clinical Trials

Clinical trials for naltrexone as an alcoholism therapy encountered
familiar problems -- difficulties with patient recruitment and
compliance, high cost of clinical support services, and low funding
of treatment centers.

Because researchers had difficulty recruiting patients, they accepted
all patients who agreed to participate, and didn't reject any
unsuitable patients. This may have negatively affected the results of
the clinical trials by including a high proportion of high-risk
patients, who may have been motivated more by payment for
participating in the trial than a desire for treatment, which led to
poorer compliance and higher drop-out rates (Schecter 1980).

The study found that naltrexone as an alcoholism therapy did not
perform significantly better than a placebo unless it was
administered as part of a comprehensive, multidisciplinary treatment
program (O'Malley 1995).

Although the government funded and supported the clinical trials, the
funding fell short of the amount necessary to provide the necessary
intensive psychosocial support. As a result, the labeling for ReVia
(the brand-name eventually chosen by DuPont) includes the following
stipulation, "ReVia should be considered as only one of many
factors determining the success of treatment of alcoholism."
Understandably, this labeling had a profoundly negative effect on
marketing strategy and sales.

In 1995, the FDA approved naltrexone in a 50mg dose as a treatment
for alcohol abuse.

The FDA surprised the researchers by authorizing naltrexone's use in
alcoholism treatment in just six months. According to Volpicelli, the
FDA was "pretty confident" that the drug was safe: It had been
researched for 20 years and was on the market for 10 as a treatment
for heroin addiction.

At this point, Dupont changed the brand name from Trexan to ReVia
(pronounced "REV-ya"..


Marketing Strategy for ReVia

Because the alcohol treatment system is less regulated than the
heroin treatment system, DuPont had more flexibility in marketing
ReVia directly to clinics and treatment providers. Despite ReVia's
clinical effectiveness and less restrictive distribution
channels, however, DuPont's sales force encountered marketing
problems.

Like Trexan, ReVia is most successful in highly motivated patients
who have a strong psychosocial support and access to counseling
services.

DuPont was not successful in selling ReVia, except in comprehensive
alcohol treatment programs such as VA hospitals and "white collar"
treatment centers. These patients tended to be more highly motivated
and have a stronger support network. ReVia became the treatment of
choice for more upscale patients, such as physicians, nurses,
pharmacists and attorneys (O'Brien).

Another roadblock to naltrexone's wider acceptance was insurance
regulations. "Insurance companies often don't allow naltrexone to be
prescribed by a primary care physician," said Tania Graves,
spokeswoman for the Arizona Medical Association. "Their point of view
is that drug or addiction problems should be sent to a specialist."

Some insurance companies do not accept naltrexone at all. For
example, a chain of California treatment centers using naltrexone as
the primary treatment had to suspend operations after only six
months, citing managed care companies' unwillingness to cover the
treatment (Behavioral Health Treatment 1996).

Some physicians were reluctant to prescribe naltrexone due to
the "black box" warning of liver toxicity in the package insert. The
warning was included based on liver enzyme elevations reported with
the100-300mg/day dose (the recommended dose is 50mg) that was given
during a study of naltrexone treatment for obesity. A review of
literature and adverse effect reports from Dupont demonstrates that a
50 mg/day dose poses no risk for liver damage, but the warning
remains (Galloway).

From the American Council on Alcoholism website, 2005:


Many physicians and non-physicians in treatment programs are unaware
of the usefulness of naltrexone or how to use it. In other areas of
medicine, it is highly probable that the development of such an
efficacious medication would prompt physicians to use it readily.
The biggest obstacle to using naltrexone for the treatment of
alcoholism is the 'pharmacophobia' of many alcoholism-treatment
professionals. This near-hysterical resistance to medication for
treating alcoholism (or other substance-abuse disorders) has deep and
tangled roots. Many recovering professionals learned in their
recoveries that MDs and their prescription pads were evil purveyors
of pharmacological lies and temptations. This attitude is often
accompanied by a deeply rooted and strongly held belief that recovery
has only one successful formula (usually the 12-step program) and
that any modification to that approach is unethical. Scientific
evidence is irrelevant to these individuals. They believe they have
the 'truth' about recovery and don't want to be bothered with other
points of view. [http://www.aca-usa.org/pharm2.htm]




Poor Sales

DuPont never expected either Trexan or ReVia to become major revenue
generators, but sales fell far short of even DuPont's modest
expectations. In 1994, just prior to the launch of ReVia, Trexan
sales were approximately $5-8 million annually, which represented
approximately 15-25,000 patients per year, or less than 5% of the
estimated number of heroin addicts in the US (Scrip 1993).

When ReVia was launched in January 1995, DuPont expected US sales of
ReVia to rise to $15-25 million annually. As of October 1996,
however, ReVia had not even reached the FDA's threshold of the
200,000 prescriptions required to trigger phase IV clinical trials
(Pink Sheet 1996).

In 1997, ReVia's market exclusivity agreement lapsed. Other companies
were now free to manufacture and market generic naltrexone. In May
1998, the first generic version of ReVia was produced by Barr
Laboratories in Pomona NY. At this time, ReVia had annual sales of
approximately $20 million.

In 2001, Bristol Myers Squibb acquired DuPont Pharmaceuticals. In
April 2002, Bristol Myers Squibb sold the ReVia brand-name rights in
the U.S. and Canada to Barr Laboratories.

As of February 2005, Barr manufactures ReVia in 50mg pills in the U.S
and Canada. Bristol Myers Squibb continues to market ReVia in
countries outside of the U.S. and Canada.

Other versions of naltrexone are currently manufactured in the U.S.
by Eon Labs and Amide Pharmaceutical; Mallinckrodt Pharmaceuticals
manufactures 50mg and 100mg naltrexone pills in the U.S. under the
trade name Depade.

Other 50mg versions of naltrexone are named Nalorex (manufactured by
Bristol-Myers Squibb in the UK); Nodict (manufactured by Sun Pharma
in India); Naltima (manufactured by INTAS in India), Narpan (by
Duopharma in Malaysia), Antaxone (by Pharmazam in Spain), Celupan (by
Lacer in Spain), Narcoral (by Siton in Italy), Nemexin (Bristol Myers
Squibb in Germany), as well as Revez,
Naltrexona, and Naltrexonum.



The Future of Naltrexone

Researchers continue to explore the potential of naltrexone as a drug
and alcohol therapy. Attempts to address compliance issues have
resulted in the introduction of a ReVia implant (2003). In addition,
Alkermes, Inc. recently developed Vivitrex, a naltrexone injection
which lasts a month. (Phase III clinical studies are set to begin in
2005.)

Over the years, researchers have tested naltrexone for a wide variety
of medical conditions, including obesity, schizophrenia, and chronic
obstructive pulmonary disease. In March 2005, Yale researchers began
investigating the use of the naltrexone to help men and women quit
smoking without gaining weight.

The FDA has awarded orphan drug** status to naltrexone to treat
symptoms of childhood autism. Another orphan grant has been issued
to naltrexone as a therapy for self-injurious behaviors. (Naltrexone
therapy for self-injurious behavior is already used extensively in
veterinary medicine.)

In addition, researchers have used derivatives of naltrexone to treat
other conditions. For example, the FDA granted orphan drug status to
methyl-naltrexone as a drug that blocks the side effects of morphine
without interfering with pain relief in cancer treatment. (Oncology
1996)



Low Dose Naltrexone

Naltrexone in substantially lower doses (Low Dose Naltrexone) is
showing great promise as a treatment for multiple sclerosis, Crohn's
disease, AIDS, rheumatoid arthritis, celiac disease, CFIDS, lupus,
and certain forms of cancer.

Unfortunately, obtaining FDA approval for LDN will not be a
straightforward process. Since naltrexone is now a generic drug, no
pharmaceutical company currently holds exclusive manufacturing
rights. No company is eager to fund an expensive clinical trial for a
drug that will make them so little profit.

However, even without governmental approval or corporate support, LDN
is gaining significant grass-roots attention among patients and
doctors. The exchange of research information over the internet has
greatly accelerated the recognition of the off-label use of LDN.

In the past, the federal government and the pharmaceutical
corporations cooperated to create an environment where naltrexone was
tested, approved and made available to patients who needed it.
Perhaps someday soon they will find a way to do the same for Low Dose
Naltrexone .

[Art]

Frequently-Asked Questions About
Low Dose Naltrexone (LDN) as a
Therapy for Multiple Sclerosis


What is Low Dose Naltrexone?

Naltrexone is short for Naltrexone Hydrochloride (C20H23NO4-HCl), an
opiate antagonist. Naltrexone was approved by the FDA (at a 50mg
dosage) in 1984 for opiate addiction, and again in 1995 for alcohol
abuse. At a much lower dose (1.75-4.5mg), it has been gaining
popularity as a treatment for symptoms of auto-immune disorders such
as Multiple Sclerosis. Low Dose Naltrexone is administered orally,
usually in capsule form.


What MS symptoms does LDN help?

Primarily neuromuscular spasm, fatigue, and urinary problems,
although patients have also reported improvements of other symptoms.
In addition, patients who start LDN while in the middle of an acute
relapse often show rapid resolution of the attack.


Does LDN halt progression of MS?

Evidence suggests that LDN can significantly reduce the chances of
either a relapse or progression for many MS patients.


How does LDN work?

It is believed that LDN briefly obstructs the effects of brain
endorphins (the brain's natural painkillers). Sensing an endorphin
deficit, the pituitary signals for increased production of
endorphins, which re-balances the immune system, thus reducing the
activity of the MS. The effect lasts around 18 hours.


But how can this work? Isn't MS is caused by an overactive immune
system?

Although there is a long-held theory that MS might be caused by an
overactive immune system, this theory has never been proven. Recent
clinical studies indicate that this theory might not be true at
all. The October 2004 issue of The Archives of Neurology reports a
clinical study which found that intravenous immunoglobulin therapy
applied after the first signs of MS significantly reduced the
probability of developing clinically definite multiple sclerosis.
Patients receiving this immune-system boosting therapy also suffered
fewer brain lesions. [Intravenous Immunoglobulin Treatment
Following the First Demyelinating Event Suggestive of Multiple
Sclerosis; a Randomized Double Blind, Placebo-Controlled Trial; Arch.
Neurol. Oct. 2004; 61:1515-1520.]


How fast does LDN work?

Although some patients have no symptom changes, around two-thirds of
MS patients report some symptom improvement within the first few
days. Other patients report improvement over the course of several
weeks or even months.


What dosage and frequency are usually prescribed?

The usual adult dosage of LDN for the treatment of MS is 1.75-4.5mg
taken orally once daily at bedtime.Because of the natural rhythms of
the body's hormone production, LDN is best taken between 9pm and
2am. It is generally recommended that the patient begin on 3.0mg per
day, and adjust the dosage if necessary. Prescribing 1.5mg capsules
allows easy adjustment of dosage. (For example, the patient can take
either 2 capsules for 3mg, or 3 capsules for a 4.5mg dose.)


How is LDN prepared?

LDN is usually prepared by a compounding pharmacist, who makes
capsules by either grinding up 50mg Naltrexone tablets, or using
Naltrexone powder purchased from a primary manufacturer.(The most
popular Naltrexone tablet is the 50mg "ReVia" Naltrexone tablet,
usually prescribed for treatment of drug and alcohol addictions.)

LDN may also be prepared in a solution of distilled water, with 1mg
per ml dispensed with a 5ml medicine dropper. If LDN is used in a
liquid form, it is recommended that it be refrigerated.


Are there any side effects?

All sources indicate that LDN has virtually no side effects. Some
patients report vivid dreams, and occasionally, during the first week
of use, patients may complain of difficulty sleeping. (Reports
indicate that sleep disturbance is rare, occurring in less than 2% of
users.) If this persists after thefirst week, dosage can be reduced
from 4.5mg to 3mg.

Full-dose Naltrexone (50mg 3x day) carries a cautionary warning for
patients with liver disease. (This warning was placed because adverse
liver effects were noted in early experiments involving 300mg daily,
given for alcohol abuse.) The 50mg dose does not apparently produce
impairment of liver function nor, of course, does the much smaller
3mg - 4.5mg dose.

LDN is virtually non-toxic, simple to administer, and, compared with
other MS drug therapy, very inexpensive – usually costing less than
$40 per month.


What about cautionary warnings?

Because LDN blocks opioid receptors throughout the body for three or
four hours, people using narcotic medication such as Ultram,
morphine, Percocet, Tramadol, Duragesic patch or codeine
should not take LDN until such medicine is completely out of the
system. Steroids would counteract the effects of LDN, and so should
not be combined. LDN should probably not be taken during
pregnancy. (This thought is open to discussion)

LDN should not be used by people already receiving interferon (Beta
Seron, Avonex, or Rebif). Because LDN stimulates the immune system
and interferon suppresses it, the two therapies are incompatible.
The combination of these therapies does not cause any adverse
reactions, but it is believed that they cancel out each other's
effectiveness.


What does it feel like to be on LDN?

At both high and low dosages, patients taking Naltrexone usually say
they are largely unaware of being on medication. Naltrexone usually
has no psychological effects and patients (at both high and
low dosages) don't feel either "high" or "down" while they are on
naltrexone. It is not addicting.


Why isn't LDN routinely prescribed for MS?

Many physicians simply have not yet learned about the positive
effects of LDN on MS symptoms. Because Naltrexone is a generic
medication, there are no commercial marketing campaigns to
increase awareness of LDN in the medical community. Other doctors may
be hesitant to prescribe LDN because it hasn't yet been approved as
an MS treatment by the FDA.


Why hasn't LDN been approved by the FDA for MS?

Naltrexone (in the higher 50mg dosage) was approved by the FDA in
1984 for opiate abuse therapy, and again in 1995 for alcohol
addiction. Its safety and efficacy have been proven in clinical
trials. In the much lower dosage of 3 or 4.5mg, Naltrexone has not
yet been submitted for FDA approval. Federal regulations prevent the
FDA from approving LDN as an MS therapy until it undergoes specific
clinical trials for MS.


Why hasn't LDN gone through a clinical trial as an MS therapy?

Clinical trials are usually initiated and funded by pharmaceutical
companies, and these companies are not interested in promoting or
marketing LDN.


Why aren't pharmaceutical companies interested in exploring the
possibility of LDN as an MS therapy?

Naltrexone was developed so long ago, it is now a generic drug,
manufactured by many different companies. Since no single company
owns exclusive manufacturing rights, Naltrexone can be
manufactured and sold very inexpensively by any pharmaceutical
company.

This means that LDN can't make anyone any money. Pharmaceutical
companies are not eager to fund clinical trials for a drug that will
make them no profit. Also, if LDN were FDA-approved and became a
preferred treatment for MS, the pharmaceutical companies who make the
expensive ABCR drugs could lose millions of dollars.


Are there any plans for a clinical trial for LDN as an MS therapy?

In May 2007, the MindBrain Consortium, the Department of Psychiatry
of Summa Hospital System of Akron, Ohio, and the Oak Clinic for the
treatment of Multiple Sclerosis, announced a study of the effects of
treating MS with LDN.

In March 2007, the University of California, San Francisco Medical
Center, implemented a double-blind, randomized, placebo-controlled,
crossover-design study of the effects of LDN on 80 MS patents.

In December 2006, a study of LDN in MS was begun in Milan by
neurological researcher, Dr. Maira Gironi.

In August 2004, the LDN Research Trust (www.ldnresearchtrust.org) was
created in England. Organized by a group of patients who have been
helped by LDN, the Trust's mission is to raise funds for the
initiation of clinical trials for LDN. In conjunction with the Trust,
Dr Alasdair Coles, a neurologist and MS specialist from Cambridge
University, and Dr Robert Lawrence of Wales, himself an MS patient,
are currently working on a proposal for a clinical trial of LDN for
the treatment of MS.

Since LDN has also shown promise as a therapy for other autoimmune
disorders, there has research activity in that area. In September
2007, the Institutional Review Board in Bamako, Mali, approved
plans for a clinical trial of LDN in HIV-infected citizens of Mali.
In July 2007, Stanford Systems Neuroscience and Pain Lab began
organizing a study of LDN for the treatment of fibromyalgia.


Has LDN as an MS therapy been reported in any of the major medical
journals?

Most medical journals are not interested in reviewing a drug therapy
that has not yet had a clinical trial.However, the peer-reviewed
medical journal Medical Hypothesis recently published an article
about the LDN's success as an MS therapy.

(For full text, see:ldners. org/Articles/LDN_Medical_Hypotheses.pdf )


Can a doctor legally prescribe LDN?

Yes. While it is illegal for a pharmaceutical company to market or
promote a drug for a use other than that approved by the FDA, it is
NOT illegal for a physician to prescribe an FDA-approved drug
for a non-FDA-approved use. This is called an "off-label"
prescription, and physicians do it all the time. (Neurontin, for
example, was approved by the FDA in 1993 for the treatment of
epilepsy; yet it is routinely prescribed off-label for the treatment
of MS.) All physicians understand that the responsible off-label use
of an FDA-approved medication such as Naltrexone is perfectly ethical
and
legal.


Who first thought of using Low Dose Naltrexone for MS?

Initial research on LDN was conducted by Ian S. Zagon, Ph.D.,
Professor of Neural and Behavioral Sciences at Pennsylvania State
University. The use of LDN for MS is credited to Dr. Bernard Bihari,
a practicing neurologist in New York. Dr. Bihari, who received his MD
from Harvard and is board-certified in psychiatry and neurology,
began prescribing LDN for his MS patients in 1985.


Does anyone profit from the promotion and sale of LDN?

No. Some people are initially suspicious of LDN, thinking that it
might be an internet "snake-oil" scheme, but no one markets or sells
LDN for profit. Naltrexone is an inexpensive, generic medication,
manufactured by a number of large pharmaceutical corporations. Low-
Dose Naltrexone is compounded at individual compounding pharmacies,
and is not marketed by anyone.


How many MS patients are taking LDN for Multiple Sclerosis?

No one is sure of the exact number, but it is known that thousands of
MS patients worldwide are now using LDN, and the number is
increasing. Without the financial support of the pharmaceutical
industry, the growing reputation of LDN has been driven solely by
positive reports from MS patients.


Are MS patients getting positive results from LDN?

A review of the anecdotal evidence shows that most MS patients taking
LDN have experienced considerable improvement, often within days or
weeks of beginning the treatment.

The first annual LDN Conference was held on June 11, 2005, at the New
York Academy of Sciences, New York City. It was attended by more than
80 members of the medical community –doctors, patients and
researchers from all over the world.

The Second Annual LDN Conference was held on Friday, April 7, 2006 in
the Lister Hill Center Auditorium of the National Library of Medicine
(NLM) in Bethesda, Maryland.

The Third Annual LDN Conference will be held October 20, 2007 at
Vanderbilt University in Nashville.

For more information about the conference, visit:
www.lowdosenaltrexone.org/events.htm.

[Art]

Dr. Kamau B. Kokayi Interviews Dr. Bihari
September 23, 2003
WBAI in New York City

"Global Medicine Review"


Dr. Kokayi: …the story about Low Dose Naltrexone is really
fascinating. How did you get the idea?

Dr. Bihari: Well, we were treating heroin addicts, and in 1984 a new
drug for the treatment of addiction came out. It was called
Naltrexone, and it was designed to block the heroin "high"and it was
a flop. I used it for a lot of patients, as did most addiction
doctors across the country. At 50 milligrams a day, it made people
feel terrible. Not that it blocked the heroin so much as it blocked
their own endorphins, which is a source of our sense of well-being,
so that people couldn't sleep.

Dr. Kokayi: Your own opium, basically.

Dr. Bihari: Right. Your own equivalent. That's what heroin is.
And I knew from work that had been done by the National Institute on
Drug Abuse in developing the drug that it had the ability to trigger
the body into making more endorphins, but at the high 50 milligram
dosage, the dose was too high. It blocks those endorphins.

About six months later our addicts began dying in large numbers of
AIDS. I ran HIV tests on about a hundred addicts, and fifty percent
were already HIV positive. This was in 1985; currently it's eighty
eighty-five percent around the country. And we began looking for
some way to approach this new disease, with a view to the idea that
this disease was likely to turn into a worldwide epidemic.

Dr. Kokayi: That was about the time where people were just being
blasted with AZT with horrific results.

Dr. Bihari: Right. There was nothing else available. When I
discovered that people with HIV had less than twenty percent of the
normal levels of endorphins, that meant that the virus not only kills
the immune system cells, it also weakens the whole immune system, so
that it's not as able to fight the virus.

We began looking for ways to use this drug to raise endorphins
without blocking them. We hired a laboratory scientist to measure
endorphin levels. We'd measure in the afternoon, then we'd give the
first dose at bedtime that night. Then we'd measure again at the
same time the next day; then again at one week, and again at one
month.

We found that doses in the range of 1.75 to 4.5 milligrams (which is
just a fraction of the recommended dosage to addicts) would trigger
or jumpstart endorphin production during the night.

Except with exercise, endorphins are made only between two and four
in the morning. The brain sends a message out to the adrenal and
pituitary glands and tells them to make endorphins. Giving a dose
three, four, five hours before that, at bedtime, is enough to make
that message from the brain much stronger.

Dr. Kokayi: Were you able to document that the levels of endorphins
were then actually raised?

Dr. Bihari: The level of endorphins went up by two hundred to three
hundred percent. We then started a little foundation and did a
placebo-controlled trial in which half the patients got the drug and
half got sugar pills. A year later when we broke the code, we
discovered that people with HIV who took the drug had only an eight
percent death rate in the year, while people who were on the placebo
had a thirty-three percent death rate. And of course they had many
more infections and their immune system declined. That was a
startling discovery.

Dr. Kokayi: Now let me jump ahead, because I'm always curious about
why this therapy hasn't gotten the kind of publicity specifically for
this disease.

Dr. Bihari: Well, at that time there was very little treatment.
AZT came out about '87, and as you mentioned, it was not only a flop
but made some people sicker. At the time we did the study, there was
nothing available.

So I met with doctors in New York and in San Francisco (where the
largest number of HIV doctors were at that time) and described this
drug and how it worked, and about forty to fifty doctors on the east
and west coast began using it. Unfortunately, they measured
effectiveness by whether or not the numbers of the immune system
cells that are crucial in AIDS -- the CD4 cells -- were rising. On
this drug, CD4 cells don't rise in people with AIDS. As I knew from
the study, and have known since, they simply stop dropping. That
means you can freeze the disease wherever it is. And if somebody is
only mildly immune-suppressed, they stay that way.

Dr. Kokayi: That's so important…

Dr. Bihari: It stops progression. It stops the count from growing.
I have patients going back as much as seventeen years who haven't
lost an immune system cell in that time. They're very healthy.

Dr. Kokayi: Wow, that needs to be on the evening news.

Dr. Bihari: The trouble was, we wrote a paper, but couldn't get it
published. Nobody understood the concept.

Dr. Kokayi: You're using the dose homeopathically. You're using it
not for the effect that the medicine has on the person, but for the
body's reaction to the medicine.

Dr. Bihari: It strengthens the body's own defenses. Rather than
directly attacking, the way antibiotics attack bacteria, or the way
chemotherapy tries to attack cancer cells, or the way anti-viral
drugs attack viruses, the purpose of this is to take a weak defense
(which people with AIDS or cancer have), and strengthen it so that
the body can fight the disease more effectively.

Dr. Kokayi: I've often made the point that therapies like
acupuncture, therapies that are foreign to the cultural mindset of
doctors and the American public, these therapies can be effective,
but they won't be included or in mainstreammedicine because the
concept is so foreign.

Dr. Bihari: It's a different model of understanding the body -- how
it works and how disease works. I think eventually there will be
changes in the paradigm of the way we think about diseases, and it's
going to be a struggle. But I think oncologists in particular are
getting more and more frustrated with the failure of chemotherapy.

Dr. Kokayi: Well, about time.

Dr. Bihari: The people I talk to at the National Cancer Institute,
and the Food and Drug Administration, are very negative. All they
get from drug companies are proposals to test new, more toxic
chemotherapies, and they're really looking very hard for non-toxic
ways of modifying the behavior of the cancer cells so that they stop
the cancer from growing.

Dr. Kokayi: Over the years have you had to modify what you were
actually doing with Naltrexone? Or is the initial model impetus
pretty much on point?

Dr. Bihari: The initial model was pretty much on point. A small
dose at bedtime increases endorphin production during the night. In
somebody who has a disease which is related to low endorphins, the
endorphins go back up to normal by the next day.

… [station break] ….

Dr. Kokayi: … can you tell us about some of the work with Naltrexone
and cancer?

Dr. Bihari: During that year, when we were doing our first AIDS
trial, an old friend of mine called. Five years earlier, she'd had
Non-Hodgkin's Lymphoma. It had initially responded to chemotherapy,
but it had grown back after her husband died. Her oncologist refused
to treat her, saying it would be resistant to chemo the second
time.

She knew what I'd been doing, and she called me and said, "Bernie, do
you think your AIDS drug would help my cancer?"

So I dug around and I found a large body of literature showing that
when you give endorphins, metenkephalins, beta endorphins and even
low dose Naltrexone to mice that had human cancer transplanted, that
there is about an 80 percent recovery rate. I gave her the drug in
the same dose we were using in the AIDS trial. She had large masses
in her groin, her neck, her chest, and her abdomen, and they all
slowly shrank and disappeared over a (inaudible) period.
(Inaudible) taking the drug every night.

Dr. Kokayi: Wow! You know, even if that's just an anecdote….

Dr. Bihari: Yes.

Dr. Kokay: I mean, everyone who has that disease deserves a chance
to see if they're going to be an anecdote as well.

Dr. Bihari: It was actually her idea. She stayed on the drug, and
died about eight years later, in her late seventies, of her third
heart attack, which was unrelated.

Then I was in Paris the following summer, presenting a paper at an
AIDS conference, and I met a woman who had a cancer called malignant
melanoma. It starts in the skin, and in her case it had spread to
the brain. She had four large brain tumors. The oncologist told her
family that she had perhaps three months to live. When I got back
to New York, I shipped her the drug from a pharmacy that was making
it for our study. She started on it, and her neurological symptoms
from the tumors in her brain slowly disappeared. Seven or eight
months later she went back to the oncologist, had a cat scan of the
brain done, and the tumors were gone.

Dr. Kokayi: Fantastic.

Dr. Bihari: That was eighteen years ago, and she stayed on it.

Dr. Kokayi: This is such a non-toxic, simple [inaudible].

Dr. Bihari: There are absolutely no side effects. I continued
doing a lot of the AIDS work, but the last four or five years I've
gotten much more interested in other uses. We stumbled on the fact,
also by chance, that the drug works very well for almost all,
if not all, of the autoimmune diseases like multiple sclerosis,
rheumatoid arthritis, lupus, sarcoidosis, and --

Dr. Kokayi: When you say "it works", what actually happens? What's
been your experience?

Dr. Bihari: Well, what happens is that the disease activity stops,
as long as people stay on it. If they have damage to the brain and
spinal cord with multiple sclerosis, that doesn't disappear, because
that's due to scarring, but they stop getting new attacks.

I've had people on Low Dose Naltrexone for years. The longest is a
friend of my daughter, who's been on it for eighteen years and has
not had an attack as long as she stayed on it.

Dr. Kokayi: So it's almost as if it's up-regulating the endorphin
production but somehow the endorphins actually block or inhibit the
effect of the antibodies from attacking the tissue.

Dr. Bihari: Not directly. It's more that the autoimmune diseases
are beginning to look more and more like they're diseases of
endorphin deficiency. [Inaudible] models of all the diseases I
mention that can be bred in mice, the endorphin levels are always
fifteen to twenty percent of normal compared with normal mice.

[Female Voice] How can you naturally increase endorphin levels?

Dr. Bihari: There's only three or four ways that I know. First,
Naltrexone increases them substantially, two to three hundred percent
in people with low levels. Second, aerobic exercise increases them,
but not as much. If you do an hour of exercise four or five times a
week it will last three, four hours, and that's one of the reasons
that exercise helps prevent cancer. A third way, oddly, is
acupuncture. Acupuncture, especially when used in treating addicts,
increases endorphin levels in the blood and the spinal fluid. And
chocolate increases it.

Dr. Kokayi: [Inaudible] will be glad to hear that.

Female Voice: [inaudible] It actually works out, because you're
going to eat your chocolate and then run to the gym.

Dr. Bihari: Chocolate has a substance in it called Phenylalanine,
which slows endorphins from being broken down in the body.

Dr. Kokayi: And that's basically an amino acid that we find….

Dr. Bihari: Yes, that's the food that has it in the largest
amount. And only people with a rare disease called [inaudible]
can't eat chocolate.

Dr. Kokayi: So some people will run to the health food store and
get Phenylalanine.

Dr. Bihari: Well, Phenylalanine is helpful if you're raising your
endorphins by other means. Then it keeps them from decaying. They
last much longer. But the crucial thing still seems to me to be the
Naltrexone. Over the last five or six years, I've treated about 420
patients who have various kinds of cancer with low dose Naltrexone.
Occasionally, for people who come to me with very advanced cancer, I
add intravenous metenkephalin, which is an endorphin...
intravenously, three times a week. It improved immune function
substantially, and had no side effects, but that's generally not
needed.

Among the people I've treated with Naltrexone for various kinds of
cancer, on the average the cancer stops growing in about two-thirds.
For half of that group, it eventually -- after six, seven, eight
months -- goes on to slowly shrink and disappear.

Dr. Kokayi: And that's about forty percent.

Dr. Bihari: Higher.

Dr. Kokayi: Well, it's about forty percent of the total number.

Dr. Bihari: Sixty-five percent actually benefit and don't go on to
develop [inaudible]. Thirty percent go into remission.

Dr. Kokayi: That's phenomenal. I don't think there's any chemo or
radiating oncologist with numbers like that.

Dr. Bihari: There's no downside. One of the reasons that the war
on cancer failed is that the oncologists doing the research failed to
take into account that chemotherapy really wipes out the immune
system, which the body needs to fight cancer cells. So they are
giving drugs that kill cancer cells, but at the same time weakening
the body's defense against cancer. Naltrexone strengthens the body's
defense, and the increased endorphins kill cancer cells directly.
Also, the immune system when it's strengthened kills cancer cells
through its natural killer cells.

Dr. Kokayi: What you're saying is, that a boost in endorphin
levels also activates other components of the immune system.

Dr. Bihari: The endorphins are the hormones centrally involved in
regulating the immune system. About 95% of the regulation or
orchestration comes from endorphins. People with cancer --
especially adults – have very low natural killer cells. They have a
weakened immune system. I've discovered, after seeing such a large
number of people, that the vast majority of them have experienced
major life stresses lasting weeks, months to years – anywhere from
two to six years before they get the cancer.

Dr. Kokayi: That was one of my other questions. What really can
keep those endorphin levels down in the body?

Dr. Bihari: If a child gets sick -- children are supposed to
outlive us -- so if a child gets sick and dies, or if you have a very
bad marital break-up, or if you discover a business partner is
embezzling money and it takes a couple of years to straighten out…
If you wake up every morning under stress -- really serious stress,
not everyday stress -- really serious stress, this can lower your
endorphin production, and it never returns to normal. So the person
then walks around with low endorphins. The body makes cancer cells
all the time, but usually the immune system kills them as
they are forming. But if your endorphin levels are low, then your
immune system is weak, the cancers grow and you become much more
vulnerable. The same thing with exposure to really toxic
substances.

Dr. Kokayi: Right. I'm wondering, I'm sure the listening audience
would like to get an idea. If you could just run down a list of some
of the cancers that you have successfully treated, types of cancers
that have seemed to respond where the opiate levels play a prominent
role.

Dr. Bihari: Well, first one of the things we discovered was that
almost all cancers have a lot of receptors for endorphins on the cell
surface, and that seems to be necessary for it to work. Some of the
cancers that respond most dramatically are Multiple Myeloma,
Lymphoma, Hodgkin's disease, breast cancer, all the cancers of the
gastrointestinal tract, like pancreatic cancer, non small-cell cancer
of the lung, the kind associated with smoking. I've got several
patients with tumors that have stopped growing; they have no
symptoms, and then after a year, year and a half, in about half
of that group, the tumors start shrinking and disappear.

Dr. Kokayi: This is lung cancer?

Dr. Bihari: These are lung cancers due to smoking.

Dr. Kokayi: Because there's really --

Dr. Bihari: Very common.

Dr. Kokayi: It's very common, but therapeutic effectiveness --

Dr. Bihari: There's nothing --

Dr. Kokayi: There's nothing, right --

Dr. Bihari: My own attitude about chemotherapy in patients I see
with cancer, is if they have one of those rare cancers that's very
sensitive to chemotherapy, like cancer of the testicle, I encourage
them to do that, to take it, and take Naltrexone afterwards to
prevent recurrence. These drugs are licensed to treat cancer.
Naltrexone is not yet licensed to treat cancer, although it's a
licensed drug. It's been on the market for nineteen years. It's use
in these low doses is called an "off-label" use. Any doctor
can prescribe it. And growing numbers of oncologists and
neurologists in the country are prescribing it.

Dr. Kokayi: I think it would be interesting you know just to talk a
little bit about the process … a lot of physicians don't really know
about it and it's not talked about. This is a big deal.

Dr. Bihari: Well, I think it could turn out to be a big deal when
it's picked up, if it's picked up. We set up a web site,
www.ldninfo.org, which brings up about thirty pages of written
material describing all the diseases, and how they respond, and how
many cases we have of them. There's some small trials going on,
there's two trials in people with Crohn's Disease, which is an
autoimmune disease of the small intestine, one in Jerusalem, and one
in New York. There's a trial in Israel for multiple sclerosis. The
national cancer institute has copies of twenty charts of my patients
who have agreed to share their charts. These are people who have
done well on Naltrexone when nothing else could explain how well
they've done. They intend to present them to a committee for
recommendations as to whether to invest and test it in the network of
cancer research.

Dr. Kokayi: You know, when I think about Africa and AIDS, this is
exactly the kind of medicine there needs to be there….

Dr. Bihari: This is perfect. In fact, we've been working with the
largest pharmaceutical company in the developing world called
(inaudible) in India to get a trial going, probably in Africa, in the
Republic of South Africa, in which half the HIV patients get the
drug, half get a placebo, and they should be able to show in about
nine months, using two to three hundred patients, that this drug
stops progression.

Once it does, it will be manufacturable at less than ten dollars per
year per person. That's been the big problem -- the anti-HIV drugs
are so expensive. The average income in Africa is about eighty
dollars per year.

Dr. Kokayi: I can only imagine just the financial stress that
you've had to go through just to keep this whole project alive. It's
one thing to prescribe things as an individual doctor, but to get
recognition within the scientific community is a bit difficult.

Dr. Bihari: It really bothers me when doctors say, "Oh, I can't
prescribe that, because he hasn't done a placebo-controlled trial."
That's a full-time job, for two, three years involving eight or nine
centers around the country. I'm working with a number of diseases in
my office, and a lot of money goes out paying for the website, for
patents to cover low dose naltexone, and (inaudible) things like
that. It's very very expensive. But I can't stop doing it. My wife
and I would love to do some traveling -- I think we've earned it --
but I really can't stop until the drug is out there. It's as much of
a burden as it does a pleasure.

Dr. Kokayi: I really hope that at least your sharing with our
listening audience today helps to make people more aware. People
should be clamoring for it. We're running out of time, but I wanted
to go back to the treatment of autoimmune diseases. I always
pictured them as the body is attacking its own tissues. I pictured
these antibodies actually honing in there. But you're saying that,
in large measure it's an actual endorphin deficiency.

Dr. Bihari: It's an endorphin deficiency which weakens the immune
system, so that certain cells in the body forget to distinguish
between the body tissues and bacteria or viruses, so when these cells
are activated by an infection they attack the bacteria and they
attack you. Restoring the immune function to normal stops that. So
far, the drug works dramatically in all the diseases that are labeled
autoimmune diseases.

Dr. Kokayi: And you've treated lupus with this.

Dr. Bihari: I've treated -- I have two dozen cases of lupus. I
have about the same number of people with rheumatoid arthritis. I
have about twenty people with Crohn's Disease. A number of
rheumatologists who specialize in these diseases in New York
re now beginning to use it, because we have cases in common, and
they see.

Dr. Kokayi: Right

Dr. Bihari: Because they're using cancer drugs

Female Voice: Dr. Bihari, is this being used with children with ADD?

Dr. Bihari: I doubt that it would work, knowing the nature of
ADD. I doubt that it would work. It doesn't do everything for
everybody. I don't think it would.

Dr. Kokayi: Again, going back to the idea of giving a medicine that
at ahigher dose actually blocks the chemical system, but a lower
dose actually augments it.

Dr. Bihari: And enhances the body's defenses -- that's essential.

Dr. Koyayi: This idea gives the pharmaceutical industry something
to do, rather than giving people high doses of medication.

Dr. Bihari: It certainly would. It will take this drug to be
licensed, picked up by a pharmaceutical company and tested, licensed,
and once it's widely used, then this approach to medicine -- every
medical researcher will start thinking about it. It's an entirely
different approach to the body and illness.

Dr. Kokayi: What is the next step? Is there anything that the
listening audience can do that might be helpful for to make this
more -- not even make it more available, because it's just a
prescription any doctor can write. I guess it's the information --

Dr. Bihari: The information, getting it from the website, getting
doctors to prescribe it. I'm always happy to take calls from doctors
and spend as much time as I need, because the more doctors prescribe
it, the more widely used it will be. Currently, as far as we can
calculate it, over eighty thousand people in the U.S. and western
Europe are on the drug, and the numbers are increasing rapidly.

Dr. Kokayi: I'd like you to give your website one more time and the
number where people can reach you …

…

Well with that, thank you again and I'm sure we will be talking to
you again soon.

[Art]

LDN FILLERS

If your Low Dose Naltrexone comes from a compounding
pharmacy and arrives as a liquid, then you're getting pure
naltexone powder dissolved in distilled water. This is probably
the "purest" way to ingest naltrexone. You don't need to worry
about fillers.

BUT -- If you get your LDN in any other form, you're
swallowing filler.

A "filler" is an inert, inactive ingredient that accompanies every
dose of naltrexone you take.

If you make your own LDN --

If you make LDN by crushing ReVia (pronounced REV-yah)
or another commercially manufactured 50mg naltrexone tablet,
you're still injesting filler, because each tablet is comprised of
about 16% Naltrexone and 84% filler.

What kind of filler is in your tablet? This depends on the
manufacturer. Here are the main manufacturers:

Barr Labs – Barr manufactures naltrexone under the brand
name ReVia for the US and Canadian markets. This tablet
contains 50mg naltrexone and these inactive ingredients:
lactose monohydrate, colloidal silicone dioxide, magnesium
stearate, crospovidone, microcrystalline cellulose, purified
water, Opadry beige (coloring). [Information from Barr Labs
phone representative.]

Bristol Myers Squibb – BMS manufactures naltrexone under
the brand name ReVia in markets other than the US and
Canada. As of 2002, their 50 mg tablets contain 50 mg of
naltrexone hydrochloride, plus these inactive ingredients (filler):
lactose, microcrystalline cellulose, crospovidone, silicon
dioxide, magnesium stearate, and pale yellow Opadry
(colouring). [Information from a 2002 leaflet by Australian
Prescription Products Guide.]

Mallinckrodt – makes a 50mg naltrexone pill called Depade.
This tablet contains 50mg naltrexone, plus these inactive
ingredients (filler): crospovidone, hydropropyl methylcellulose,
lactose monohydrate, magnesium stearate, microcrystalline
cellulose, polyethelene glycol, polysorbate 80, silicone dioxide,
titanium dioxide, yellow iron oxide, and red iron oxide.
[Information from Mallinckrodt website.]

[Historical Note: The original ReVia was made by Dupont.
The inactive ingredients were: lactose, microcrystalline
cellulose, crospovidone, silicon dioxide, magnesium stearate,
and pale yellow Opadry (colouring). In 2001, Bristol Myers
Squibb acquired DuPont Pharmaceuticals. In April 2002,
BMS sold the ReVia brand-name rights in the US and Canada
to Barr Laboratories. BMS continues to market ReVia outside
of the US and Canada.]

If your LDN is made by a compounding pharmacy –

Ask your pharmacist how it is made.

1. Some compounders make LDN by crushing commercially
manufactured 50mg tablets and putting the powder into
capsules. Because the amount of powder that goes into each
capsule is not enough to fill the capsule, most pharmacies add
additional filler. If this is how you get your LDN, you can find
out which commercially manufactured tablet is being used and
what kind of additional filler is being added.

2. Other compounders don't crush 50mg tablets; instead, they
use pure naltrexone powder (purchased in bulk from
pharmaceutical companies), which they mix with filler. From
these pharmacists, you can learn what kind of filler you are
taking.

Here are some of the most common fillers used by
compounding pharmacists:

LACTOSE: Lactose is a naturally-occurring simple
carbohydrate, or sugar, found only in the milk of mammals. For
this reason, it is also commonly referred to as "milk sugar."

Lactose has long been used as a soluble filler in the manufacture
of orally administered pharmaceuticals. It is safe, stable,
inexpensive, and has a fast dissolution rate. Pharmaceutical-
grade lactose powder is highly pure, and specifically produced
to meet government standards of safety and purity.

Lactose is easily tolerated by most patients. However, if you
are lactose-intolerant (that is, if milk products give you nausea,
diarrhea, abdominal cramping, bloating, or flatulence), you
might want to try another filler.

Note: Dr Bihari asks his patients to use lactose, unless they
have an adverse reaction… not because he believes lactose is
better than other fillers, but because he began his study of LDN
with lactose, and he wants his records to be consistent.

ACIDOPHILOUS – (pronounced Ah-SID-uh-FILL-us) – is
lactic bacteria, or one-celled micro-organisms, used by the
body to promote immunity and proper nutrition. Sold over the
counter as a nutritional supplement and digestive aid,
Acidophilus is sometimes used as a treatment for diarrhea and
constipation. It is commercially available as powder, tablets,
capsules or liquid.

Lactose-intolerant patients sometimes switch to Acidophilus
filler in their LDN capsules.

AVICEL – a brand name for microcrystalline cellulose. Avicel
has been used safely and effectively for 35 years in the food
and pharmaceutical industries. Virtually inert, it is not absorbed
into the system, and will not interfere or interact with other
nutrients, vitamins or minerals. Avicel is made of wood which
has been purified and powdered into extremely tiny particles --
between 0.000039 and 0.0001560 of an inch of pure fiber,
with the consistency of a very fine face powder.

Avicel is the filler used by Skip's Pharmacy in Boca Raton.
For a fun history of Avicel, "Let Us Have Nothing To Eat,"
CLICK HERE.

CALCIUM CARBONATE – a mineral that occurs naturally
in limestone, marble and coral. Crushed to a fine, flavorless,
odourless powder, it is a natural food additive, and the most
common ingredient in calcium supplements and antacids.

Calcium is absorbed by the small intestine and is used by the
body to build bone tissue. Calcium supplements are generally
well tolerated, but in some patients may cause constipation,
bloating, gas and flatulence.

People with kidney stones, hypercalcemia, sarcoidosis,
hyperparathyroidism, hypervitaminosis D or cancer should not
take calcium carbonate.

People taking calcium supplements are usually advised to take
them with food.

There has been some concern among LDN users that calcium
carbonate is occasionally packed too tight in the capsule, which
can cause a slow-release reaction, rather than the desired fast-
release.

IMPORTANT: Make sure to specify that you do NOT want LDN in a slow-
release form.

Reports have been received from patients that their pharmacies have
been supplying a slow-release form of naltrexone. Pharmacies should
be instructed NOT to provide LDN in an "SR" or slow-release or timed-
release form. Unless the low dose of naltrexone is in an unaltered
form, which permits it to reach a prompt "spike" in the blood stream,
its therapeutic effects may be inhibited.

Fillers. Capsules of LDN necessarily contain a substantial percentage
of neutral inactive filler. Experiments by the compounding
pharmacist, Dr. Skip Lenz, have demonstrated that the use of calcium
carbonate as a filler will interfere with absorption of the LDN
capsule. Therefore, it is suggested that calcium carbonate filler not
be employed in compounding LDN capsules. He recommends either Avicel,
lactose (if lactose intolerance is not a problem), or sucrose fillers
as useful fast-release fillers.




Any questions about filler should be referred to your
doctor or your pharmacist.

--

[Art]

From Dr. Lawrence.
--

Zinc and the Zinc Taste Test


Zinc is an essential trace element. It is one of the most important of the trace elements needed by the body. Of the many hundreds of protein enzymes present in the body, which allow its chemistry to work, zinc is required by over two hundred of them. It can thus be seen how a deficiency of zinc can affect so many different functions (see below).

Zinc is also important in the production of prostaglandins (PGs). PGs are vital to numerous body functions including, for example: the function of the immune system; the expression and control of inflammation; skin and wound healing; function of the heart and cardiovascular system; absorption of various minerals; body temperature control and the important functions of fertility, conception, and delivery of the infant.

The way in which zinc influences PG production is by potentiating (or supporting the function of) the enzymes which permit the conversion of the polyunsaturated fatty acids into PGs. Zinc thus has a very direct action in stimulating the normal production of PGs thereby maintaining or restoring normal health and fitness.

Zinc is of vital importance in MS and other auto-immune diseases, partly because of its effect in promoting the production of PGs but, more importantly perhaps, because, by acting in its capacity as an antioxidant co-factor in the enzyme, superoxide dismutase, it helps maintain the integrity of the essential fatty acids that contribute to the regeneration of the myelin.

Zinc deficiency can result in many symptoms, including: loss of appetite, growth retardation, diarrhoea, tremor, hair loss, dandruff, a dry skin rash, white lines on fingernails, increased allergic sensitivity, disturbance of menstrual periods, pre-menstrual syndrome, delay of wound healing, loss of taste or smell sensation, dyslexia, poor night vision, photophobia (sensitivity to light), depression, sleep disturbance, hyperactivity, reduced fertility, loss of sex drive, pre-eclampsia (toxaemia) of pregnancy and post-natal depression.

It has been observed that those suffering with any of the auto-immune diseases (such as multiple sclerosis, rheumatoid arthritis, psoriasis, etc); atopic problems (allergy, eczema, asthma or migraine); or many of the inflammatory diseases (such as osteo-arthritis, ME or irritable bowel syndrome), have a consistent, and often severe, zinc deficiency, which is greatly benefited by a programme of zinc replacement therapy.

Zinc supplements in MS will increase both energy and vitality, increase muscle strength, improve sleep and prevent fatigue. Perhaps in company with vanadium, another common mineral deficiency in MS, which contributes to the occurrence of depression, it will also prevent this distressing symptom.

The zinc taste test is used to evaluate this common state of deficiency. This simple and non-toxic test was devised and developed by Professor Derek Bryce-Smith, Professor of Biochemistry at Reading University. Professor Bryce Smith is an established authority on zinc and numerous other biochemical topics.

The test solution is zinc sulphate in purified water, at a concentration of 1 gramme/ litre.

Once prepared the solution should be stored in a refrigerator and discarded after six months. The solution should be removed from storage and left at room temperature for about two hours before carrying out the test.

The test is based on the knowledge that the functions of taste and smell are dependent upon there being sufficient zinc available in the body. Thus, if zinc is deficient then taste function will be diminished. This principle is utilised in the taste test by offering a standard test solution of zinc sulphate for tasting. The response is then compared with a series of defined standards and the zinc status thus determined.

The test involves taking a sip of the solution (approximately 5-10 mls - using the beaker supplied) and holding it in the mouth for ten seconds, timed with a watch. Due to the possible influence of recently consumed food or drink on the taste experienced it is essential that neither be taken for approximately one hour before the test.

The defined standards are:

Grade one response: no specific taste sensation: tastes like plain water. This indicates a major deficiency of zinc requiring a supplement of at least 150 milligrammes (mg) of zinc per day.

Grade two response: no immediate taste is noticed but, within the ten seconds of the test, a `dry' or `metallic' taste is experienced. This indicates a moderate deficiency requiring a supplement of 100 mg of zinc per day.

Grade three response: an immediate slight taste is noted, which increases with time over the ten second period. This indicates a deficiency of minor degree requiring a supplement of 50 mg per day.

Grade four response: an immediate, strong and unpleasant taste is experienced. This indicates that no zinc deficiency exists. If this is the response to the first test done then obviously the diet already contains sufficient zinc and no supplement need be taken.

If this is the response, however, after a period of zinc supplementation then the diet, prior to the supplement being given, must be assumed to have been deficient. Thus, if a relapse to this deficient state is to be further prevented a regular maintenance dose of zinc is required. One 15-20 mg dose per day is usually sufficient for this purpose.

During any period of supplementation the taste test should be repeated at appropriate intervals and the subsequent dose of zinc adjusted according to the above instructions. In addition, it should be noted that when starting any programme of zinc supplementation, the starting dose should always be a minimum dose of 15-25 mg. This is then increased slowly in the following manner stopping at the required level as demanded by the results of the taste test.

Thus in the first week: take one 15 mg (or 25 mg) dose per day.

Second week: two 15 mg (or 25 mg) capsules or tablets per day.

Third week: one 50 mg dose per day.

Fourth week: two 50 mg doses per day.

Fifth and subsequent weeks: three 50 mg doses per day.

The reason for this protracted introduction is that zinc treatment, in the presence of zinc deficiency, may initially induce a feeling of fatigue or depression: a slow introduction reduces this possibility.

Zinc should be taken each day after food. If unusual tiredness occurs during the initial stages of treatment it should be taken at night before retiring to bed. In this way it will benefit any difficulty in sleeping and promote increased vitality the following day.

Various zinc preparations may be used, including possibly chelated zinc, zinc citrate, zinc picolinate, or zinc gluconate. Zinc sulphate is the most common (and cheapest) presentation but should be avoided due to the frequent occurrence of gastric irritation and dyspepsia. To avoid such a possibility, as a precaution, any zinc preparation should be taken after food. The most efficiently absorbed is the chelated form. This is where the zinc is combined with an amino acid, which assists in its absorption.

High doses of zinc (50 mg/day or more) should also be accompanied by a small dose of copper. This is because a large amount of zinc in the diet will compete with, and reduce the absorption of, copper. It therefore becomes necessary to take a regular supplement of copper to prevent a state of copper deficiency developing. The appropriate dose of copper is 2 - 4 mg per day. This single dose is usually all that is required whatever the dose of zinc used.

High doses of zinc will also tend to reduce the absorption of iron. This is not usually a problem but, in strict vegetarians, when the intake of iron is low, there may be a need to take a small, regular dose of iron to prevent the occurrence of iron-deficiency anaemia.

[Art]

Note: This poll was not conducted by me, although I did participate in it. The person who did conduct the poll had it posted on her website which has since been shut down for reasons unknown to me. I post it here as an FYI. -- Art
--

The Low Dose Naltrexone
Height/Weight/Gender/Dosage Poll

In Spring 2006, the Yahoo LDN board had an ongoing discussion about dosage.

Does body size and gender affect the dosage of LDN? Should men take more
than women, or less? Should large people take more than small people?

In the notorious absence of actual clinical data for LDN, I opened a poll.

I asked the members of the Yahoo board to submit their height, weight, gender,
and the dosage they were most comfortable with. I asked people who had not yet
settled on a dosage to refrain from participating in the poll.

Forty-seven people responded to the poll.

Keeping in mind that I am not a statistician, here are the results:

1 person (2% of all respondents) takes 2.5mg
1 person (2% of all respondents) takes 4.0mg
3 people (13% of all respondents) take 6.0mg
17 people (36% of all respondents) take 3.0mg
25 people (53% of all respondents) take 4.5mg

Gender Differences --

Total Men Responding: 18

8 men (39% of the men) take 3.0mg
10 men (61% of the men) take 4.5mg
-- Conclusion – more men take 4.5 than take 3.0.

Total Women Responding – 29

1 woman (3% of the women) takes 2.5mg
8 women (30% of the women) take 3.0mg
1 woman (3% of the women) takes 4.0mg
15 women (56% of the women) take 4.5mg
3 women (7% of the women) take 6.0mg
-- Conclusion: more women take 4.5 than 3.0.
-- We can also conclude that women are more likely to take “odd” dosages
of LDN (like 2.5 or 4.0) than men are.



Height/Weight/Dosage Correlation....?

Each respondent provided their height and weight. For each person, I converted
this information to a Body Mass Index number. The thinner you are in proportion
to your height, the lower your BMI. To figure out your BMI, you can go here:

www.consumer.gov/weightloss/bmi.htm

(There is a BMI calculator at the bottom of the page.)

Our 47 respondents had a BMI range between 16.5 and 47.5.

Below is the list of all 47 BMIs. Each individual’s BMI is followed by their dosage.
I listed the BMI numbers in ascending order – going from small and thin to tall and
large -- to see if I could discern any pattern.


16.5 – 4.5
17.6 – 3.0
18.0 – 3.0
18.5 – 6.0
18.9 – 4.5
19.4 – 4.5
19.5 – 4.5
20.1 – 3.0
20.1 – 4.5
20.6 – 3.0
20.8 – 4.5
21.0 – 4.5
21.3 – 3.0
21.3 – 4.5
22.1 - 3.0
22.2 – 4.5
22.4 – 4.5
22.5 – 3.0
23.4 – 4.5
23.4 – 4.5
23.4 – 3.0
23.9 – 6.0
24.1 -- 6.0
24.4 – 4.5
24.4 – 4.5
24.8 – 4.5
24.8 – 4.5
24.8 – 4.5
24.9 - 4.5
25.1 – 3.0
25.1 – 4.0
25.6 – 4.5
25.7 – 3.0
26.1 – 3.0
27.0 – 3.0
27.1 – 3.0
27.1 – 4.5
27.3 – 4.5
27.9 – 3.0
28.2 – 4.5
28.6 – 4.5
28.6 – 4.5
31.1 – 3.0
33.0 – 3.0
36.6 – 4.5
47.5 – 3.0

Conclusion: If there's a pattern here, I don’t see it.

Some patients believe that if you're short and thin, you should take less LDN, and
if you are tall and large, you should take more.

This list seems to contradict that idea.

Note: I’m sure there’s a way to convert this list to a chart, or a graph, but I’m not a
statistician, so I don’t know how to do that. If anyone else wants to take a crack at
it, feel free.

[Brenda]

I remember that poll being taken. A few comments I might add is Dr. Bihari always put his patients under 100 pounds on no more than 3.0mg. Rarely, and only for a temporary period of time did Bihari put anyone on 6.0mg. He would consider putting someone weighing 400 to 500 pounds and above on doses of 5.0mg and 6.0mg and if a person were to lose weight he would lower that dosage. Dr. Bihari also felt for LDN to halt the progression of the more advanced forms of multiple sclerosis one needed to be on no less than 3.0mg. Bihari would put all his cancer patients on 4.5mg unless they were grossly underweight.

I had a long interview with Dr. Bihari years ago and learned alot from him. I am so glad I got the privilege.

Good post Art.

[Art]

Below by Dr. Lawrence

The use of Glyconutrient Therapy in Multiple Sclerosis

I am currently greatly interested in the increasing use of glyconutrients.
This is a group of what is now recognised as essential sugars, in the same
manner as essential fatty acids. By attaching to cell surface binding sites
these apparently enhance the process of inter-cell communication, thus
optimising normal physiological function, including that of the immune system.

These seem to be effective in a vast range of diseases, like LDN, in
auto-immune diseases, chronic viral and bacterial infections, and numerous cancers.

Case studies have shown that a regime of glyconutrient therapy has been
effective in reducing disabilities, and the size and number of brain lesions
shown on MRI scan.

This, according to clinical studies, has the effect of increasing the
release of intrinsic stem-cells from the bone marrow by up to 400 times, in turn stimulating all the various processes of repair and regeneration. As
Gaba has the same basic purpose and effect, this would be further increased by also taking Gaba.

This should provide a response better than stem-cell therapy as the benefits will be self-sustaining, constant and ongoing. The response to stem-cell therapy is relatively transient, short-lived, and very expensive.

Mannatech has been providing a form of glyconutrient therapy, as Ambrotose, containing just three of the necessary glyconutrients, but this is at a very low dose and is very expensive and ineffective at such low doses, at least £25 per month for one teaspoonful each day. The recommended dose for MS is perhaps 6 spoonfuls each day, obviously costing £150 per month.

Further research has revealed that the eight essential glyconutrients can be provided by just three common food supplements, kelp, aloe vera and whey (milk) or egg protein.

The frequent and common sensitivity to either cow's milk or eggs makes it diffiicult to take the last of these but the remaining seven can be readily
provided by just kelp and aloe vera.

I suggest that a higher than normal dose be employed as the dose needs to be maximal for optimal effect.

The suggested dose is kelp, four tablets each day, and Aloe vera, 15 mls
twice daily.


If you decide to try this new and exciting method I would be greatly
interested in your response.

Dr. Bob Lawrence, contact information is below.


Registered Office
Dietary Research Limited, 10 Heol Gerrig, Treboeth, Swansea, SA5 9BP
Telephone: 01792 - 417514; Company Registered Number 2615367

--

For those of you who have received the welcome package from Aletha--
which include Dr. Lawrence's recommendations re: supplements, LDN,
diet--there's a document called Glyconutrients. In it, Dr. Lawrence
discusses Ambrotose, the Mannatech product. He recommends it, but
also suggests a much less expensive alternative. I have been
following his recommendations since January and have a little more
energy. Here's what I take:

1. 15 ml of aloe vera liquid 2x/day
2. kelp: 660 mg (Dr. Lawrence recommends 400 mg, but it's difficult
to find that in the U.S.)
3. shark cartilage OR glucosamine/chondroiton (they supply the
same sugars):
- four capsules of the combined tablet containing glucosmaine
(500 mg)& chondroiton(400 mg): two in the morning, two at
night (not beef-derived) OR
- shark cartilage: 500-1000 mg 2x/daily (often found in 750 mg
tablets)

All the glyconutrients can be started at the same time.

[Art]

Website of Dr. Lawrence:

www.msrc.co.uk/index.cfm?CFID=8153172&CFTOKEN=19107767

[Art]

NO REGRETS

--------------------------------------------------------------------------------


I have no regrets for the pain of life,

For it has given me strength.
Nor for the sorrow,
For it has made me real and
helped me to understand myself.
Nor for the despair,
For I have cast off illusion.
--------------------------------------------------------------------------------

I have no regrets for the loneliness,
For I have made friends with the night.
Nor for the rage of anger,
For through it I have found inner peace.
Nor for having made enemies,
Who taught me what not to be.
--------------------------------------------------------------------------------

I have no regrets for the death of loved ones,
For the they showed me how to live.
Nor for rejected love,
For I have learned to love myself.
Nor for the passage of time,
That which has given me my memories.
--------------------------------------------------------------------------------

I have no regrets for the shackles of deception,
For I have broken through the walls of
the prisons of my mind.
Nor for the wandering,
Which has led me home.
Nor for the road taken,
Which has opened my eyes to destiny.
--------------------------------------------------------------------------------

I have no regrets,
For life is born of struggle
And the will to survive.

[Art]

The Unseen Tormentor


For most of us who suffer with chronic illness, coping with the pain is one
of the greatest challenges. Nature has so created us that we cannot remember pain past. We remember what we did and said in response to it but cannot actually recall the pain itself. Certainly this may be a great blessing. Who would ever have a second child if she could actually recall the pangs of labor? But, our lack of memory also makes suffering a lonely experience. Even those who have been where we are and, are now freer-perhaps in remission-often look at us blankly when we speak of our pain. Others choose not to hear for fear that our words will call forth their own buried experiences. We ourselves often choose to not talk about or think about pain, hoping, perhaps, it will go away. Sometimes we are right. Business and distractions provide temporary relief. But then, often in the dark hours between midnight and dawn, our body reminds us of the battle experience that is ours alone. A battle that never ends and is never won.


If you are coping with chronic pain, I offer you a few insights but not a
solution. Your pain is its own solution. Following are seven insights:


(1) All pain is invisible,don't expect others to understand how you feel.
Often when we desperately need soothing we resent having to ask and direct others as to how to help, as though this negated the care. We want them to read our minds.


(2) All pain is relative to the sufferer. His or her pain is always most
significant. To justify our pain by comparing it to another's is absurd,and
degrades both experiences. Your pain is valid and worthy of comment simply because it is yours.


(3) Pain is more difficult to bear when we see no end to it.
Opportunities for relief can become scheduled "vacations" whether via
therapy or medication.


(4) Pain drains us. It takes a great deal of energy to cope with pain on
a day in, day out basis. It is therefore important to schedule activities and
responsibilities to accommodate our pain, not just our disability.


(5) Pain distorts our self-image. We begin to see our bodies
differently, not as our greatest tool of self-expression but as a hindrance,
a jailer, a tormentor. Often our ability to see ourselves accurately in the
mirror is hampered. Instead of long slender fingers we see pain; instead of
sky blue eyes we see hurt. Instead of self, we see suffering.


(6) Pain affects our perception of reality. We become more sensitive. We often feel fragile and vulnerable. We can become more negative in our
thinking and in our expectations. We can feel unloved and unlovable. We can become crabby and even lash out undeservedly and unexpectedly.


(7) Pain that is ignored or fought rarely goes away. However,it is
possible to negotiate a friendly peace with our pain but the key is honesty
and intentionality. Learn to take time daily to focus on your pain, to
really feel it and absorb it. You may find it to be a safe place where you
can go and hide or a wall that protects you from outside dangers.


Pain has a way of clearing the head so that we might choose anew who we are and what we are going to be about. It is in this authentic relationship between the sufferer and the pain that an inner growth can be found.

[Art]

The Fraud of Medical Marijuana

Pot smokers usually agree that smoking pot is more fun than
drinking alcohol. Pot smokers seem like a harmless lot. There are
no pot smokers whom you can see laying in the gutter covered with
their own excrement, urine and puke. They generally do not dig
through garbage cans for something to eat or beg for money to
feed their pot habit. Neither are these people found in the
emergency wards after passing out and falling under a tram or an
automobile or having their heads wrapped in bandages after
blacking out and falling flat onto their faces. You do not
usually find these pot smokers belligerently picking fights and
suffering the cuts and contusions that result thereby. Neither do
they suffer from liver and kidney malfunction, high cancer rates,
arthritis and heart disease. They do not have a high incidence of
auto accidents where they drive over innocent pedestrians. Also,
arson, destruction of property, vandalism, assault and battery,
murder, theft, etc., are not noticeably high among this group.
However, you DO find such things and many other evils besides
among those people who drink alcohol to excess.

So, why is it that alcohol is condoned and encouraged while
marijuana smoking is prohibited? Who writes the laws that allows
this discrepancy to occur? As is usual in the West, the laws are
written by those who benefit from them and not by those who must
suffer under them.

And so, once again, we must ask ourselves the question: Who
Benefits? Obviously the first beneficiary is the booze industry.
Who else benefits from the drunkenness of the People?
When drunks fall down, they need doctors and hospitals.
Drunks get into legal trouble and need lawyers. Gambling and
prostitution are vices which benefit from the drunkenness of their
clients.

In short, all of the services that benefit from drunks becoming
inebriated and drunks destroying themselves and others, are
services that are highly profitable. So, of course, they write laws
that benefit themselves. They promote alcohol consumption and
discourage the smoking of marijuana. And when marijuana is illegal,
then its price is very high so this is beneficial to the criminals of
Mexico and other pot growing locations who get high profits from
their crops and for transportation and distribution. If marijuana
growing was legal, then the price would be nearly zero because it can
be grown anywhere. Pot smokers would grow their own intoxicants and
drink less alcohol.

Now, I am not condoning the smoking of pot but merely pointing
out something odd about the medical marijuana debate. In this
debate, society is being manipulated by the Media to be
either for or against medical marijuana for sick people. Those
with cancer and other debilitating diseases have all agreed that
by smoking pot they are able to withstand the effects of
chemotherapy and to eat their food without up-chucking.

But the actual debate is being waged for the hearts and minds of
the ordinary citizens who neither smoke pot nor have a disease.
The debate is being waged for the votes of the average citizen.
The citizens are being asked to decide medical drug laws for
which they are neither qualified nor interested in deciding. Why
is this?

You see, the issue is really not at all about whether marijuana
should be given to sick people. From a medical standpoint, if the
drug relieves suffering without dangerous side-effects, then it
is a good therapy. So, the ordinary citizen should not be
required to decide whether it should be allowed or not since it
is a medical decision alone. The ten thousand other drugs that
physicians use are not placed before a committee of laymen to
decide whether they should be used or not, so what is so special
about marijuana? Why is such an issue put on the ballot for the
uninformed and uneducated people to vote on? Quite simply -- the
people are being brainwashed.

When the Media rages through both sides of the debate --
some saying "Yes" and some saying "No" -- without
really attempting to clarify the situation, then you know that
neither a "yes" nor a "no" is their goal. The main goal in fomenting
this debate is to brainwash the People with the idea that marijuana
is a pharmacological drug that is prescribed by doctors to people who
are sick and NOT a recreational substance on the same level as
alcohol. They want the People to begin thinking of marijuana as
something that a pharmacy dispenses for a fee and not as an
agricultural product that anyone can grow. They want to keep
marijuana banned as an illegal drug even though the marijuana plant
produces more paper pulp per acre than do pulp forests. The marijuana
plant has 10,000 useful products that can be made from it including a
very nice. soft cloth, strong rope, eatable seeds, as well as oils,
paints and plastics. It is an extremely valuable agricultural product
that can benefit any country that grows it commercially. But because
it causes those in liquor, medicine and law to not make money,
they want it banned. Or if not banned outright, they want it
classified as a controlled substance in such a way that they can
reap a profit by selling it through their already established
commercial channels.

The Medical Marijuana Debate is just another swindle. Its
goal is not to determine the advisability of letting cancer
patients take an illegal drug or not. After all, most of the
drugs that cancer patients take are not only highly illegal
without a prescription but extremely toxic as well. But there is
no debate on whether to allow cancer patients to take morphine
patches or swallow a hundred other drugs prescribed by their
doctors. Why is this?

The goal of the Medical Marijuana Debate is to convince people
that marijuana should be a controlled substance that only the
doctors and pharmacists should be allowed to dispense. Those
in the medical profession, in the legal profession and in
the liquor industry are bribing the politicians. You see, once
they can make money, then ANYTHING is okay to do. An example
is the Las Vegas gambling arena controlled by organized crime
syndicates where EVERY vice is condoned.
But if they lose money, then it is made to be illegal no
matter how beneficial it is to all of the rest of Mankind.

[Art]

'A place to share ideas and experiences'

Welcome All who are dealing with Multiple Sclerosis, Lyme Disease, or any other related illnesses, and/or their loved ones. This site has been set up by individuals who are personally dealing and care about people who are dealing with these “SUPPOSEDLY” incurable diseases. We have all come here collectively, to share our thoughts, experiences, and personal treatments, as well as develop friendships, share laughter and have fun. This site will be used as a forum to exchange ideas that may help other Multiple Sclerosis, Lyme, and other related illness sufferers. This site, by no means, proposes or is intended to “DIAGNOSE” or “CURE” any diseases. OUR GOAL HOWEVER, IS TO BEGIN THE JOURNEY TO DO JUST THAT. . . We are all here looking for symptom relief, quality of life, and extinction of these challenges. Blessings, and much Health & Happiness, to all that come to our forum.

disc.yourwebapps.com/Indices/226358.html#20911

[Art]

Coping With an Unprofitable Cure


PUBLISHED MAY 1, 2004


I am a Columbia undergrad with Multiple Sclerosis. You wouldn't recognize me
as someone with MS, because I look just like you. I don't have a wheelchair
or a cane, and I keep my diagnosis a secret (and am writing this article
anonymously) in order to improve my chances of being employed after I finish
school. In fact, you and I were probably similar in a lot of ways up until
nine months ago, when I was diagnosed and put on a $10,000 per year designer
drug that I inject every other day with the hope of slowing the progress of
my condition.


I know it's not pleasant to think about what your life would be like if what
happened to me had happened to you. Probably, like me, you would be very
angry. Some of this anger is irrational and useless, focused on people who
are just plain luckier than me. But some of it is very justified, and it has
to do with research and support institutions that are not doing everything
they can to find a cure.


MS is a chronic illness--that means you have it all your life--which affects
the nervous system. The illness is poorly understood, but we do know that
scars develop on the brain and/or spine of MS sufferers, and that the
insulating material that surrounds their neurons deteriorates, making it
much harder for the nervous system to move information around. Symptoms
range from numbness, dizziness, and trouble concentrating to memory loss,
blindness, and paralysis. About 400,000 Americans have MS; about 100,000 of
them are in wheelchairs.


Being an enterprising Ivy Leaguer, I've spent a lot of time since my
diagnosis familiarizing myself with the disease and the efforts to cure it.
Just like you would, I want to both find the best immediate treatment for
myself and make sure that real efforts are being made to cure the disease in
the long-term future. However, in the course of my research, I came across a
lot of defeatism among people with MS. In fact, I found a large Web
community of people who had given up on the designer drugs altogether.
Whether because they couldn't afford them, because they couldn't tolerate
the devastating side effects, or because their symptoms just weren't
affected by the drugs, these people have turned to less conventional
therapies. The most common and fastest growing of these is Low Dose
Naltrexone, a drug with a ton of anecdotal evidence but no scientific
studies proving that it helps MS sufferers. At least 1,000 people in the
U.S. alone probably use LDN, which works by stimulating the body to create
more endorphins, modifying both pain reception and immune response.


This piqued my curiosity. If so many people are using LDN and claiming that
it works, then why isn't it being tested for FDA approval in treating MS?
The answer should have been obvious: LDN can't make anyone any money. The
active ingredient, Naltrexone, was developed so long ago that no one holds a
patent. Generic versions of the drug can be created and sold for a few bucks
a dose, like ibuprofen. If LDN were certified for MS by the FDA,
pharmaceutical companies would lose millions.


This means that no pharmaceutical company would ever pay to test LDN. Fine,
then, what about research institutions? Well ... no institutions are
stepping forward either. Large research interests like Columbia's Medical
Center also put a premium on intellectual property, and doctors there are
pressured to find drugs from which they and their employers can profit. It
is possible that a good-hearted doctor will eventually apply for a grant to
do a study on the relationship between LDN and MS, which would probably cost
between $600,000 and $3,000,000. Maybe Dr. Ian Zagon, a researcher at Penn
State who has already done important work demonstrating the effectiveness of
LDN in cancer treatments, will study MS next. Dr. Bernard Bihari, a New York
neurologist who has prescribed LDN for both MS and AIDS, is another
candidate. As of yet, no one has stepped up.


Attempts to cure MS are financially dominated by pharmaceutical companies
that have no interest in unprofitable solutions. The National MS Society
only funds projects that are initiated by outside researchers, and they
spend just 20 percent of their funds on research. There is no large-scale
institution dedicated to advocating and developing new trends of research in
MS, especially when those trends don't promise to be lucrative. Luckily, the
internet now provides a forum for this problem to be recognized and
remedied. Through message boards and Web sites built by non-profits like the
Boston Cure Project, people with MS are starting to recognize and address
the shortcomings of MS research.


It's easy to make people with MS care about new approaches to finding a cure
regardless of the profit model. It's much harder to convince the people who
have the resources to make the cure possible, who usually do not have MS. If
you've read this far, maybe by now you have some interest in finding a cure.
Maybe you agree that it's not right to allow commercial economics to
determine how a disease is researched and treated. Maybe you can help find a
way to fix this. After all, I used to be a lot like you.


www.columbiaspectator.com/?q=node/15130

[Art]

Provigil Warning!!!
For all of you that have been prescribed Provigil (modafinil) for MS-related
fatigue: the FDA has issued a warning that Provigil has been linked to
serious skin rashes and psychiatric symptoms.
Instead of me trying to restate these warnings, I give you this, straight
from the FDA letter:

a.. Skin rashes: "Rare cases of serious or life-threatening rash,
including SJS (Stevens-Johnson Syndrome), Toxic Epidermal Necrolysis (TEN),
and Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) have been
reported in adults and children in worldwide post-marketing experience. The
reporting rate of TEN and SJS associated with modafinil use, which is
generally accepted to be an underestimate due to underreporting, exceeds the
background incidence rate. Estimates of the background incidence rate for
these serious skin reactions in the general population range between 1 to 2
cases per million-person years."
b.. "Psychiatric adverse experiences (including anxiety, mania,
hallucinations, and suicidalideation) have been reported in patients treated
with modafinil. Caution should be exercised when PROVIGIL is given to
patients with a history of psychosis, depression, or mania. If psychiatric
symptoms develop in association with PROVIGIL administration, consider
discontinuing PROVIGIL."
Bottom line: Contact your doctor if you are on Provigil and concerned (and
IMMEDIATELY contact your doctor if you experience ANY sort of unusual rash
or mood changes while taking Provigil).
Wednesday October 31, 2007

[Art]

DL-PHENYLALANINE

DL-Phenylalanine (DLPA) is an essential amino acid, meaning the body
produces this from the diet. DLPA is a mirror image of the amino
acid phenylalanine, it shares a lot of the same benefits as
phenylalanine, but in the DL form, its properties for controlling
pain naturally are truly amazing.

It has been shown by several researchers to be far more effective in
the control of pain than almost any other analgesic on the market.
The only problem from the analgesic stand-point is that it requires
anywhere from seven to fourteen days to be effective for relieving
most pain. It is not a fast acting pain killer and should not be
expected to produce results for some short duration pains that may
last only a few hours, headache or slight sprain, for example.

However once pain relief effects are established, they can last for
extremely long periods after discontinuing, since they stayed stored
within the body and are called upon when needed. Another short term
analgesic (such as White Willow), with anti-inflammatory properties
must be taken in conjunction with DLPA in order to alleviate the
short term pain, giving DLPA time to activate the natural pain-
killing systems within the body. The two such elements, a short-
term analgesic and DLPA, taken in combination biologically compliment
each other and become one of the most effective OTC weapons available
to fight rheumatoid and osteo-arthritis, migraine, menstrual cramps,
lower back and joint pain, postoperative pain, and neuralgia.

It has been discovered that the human brain responds to pain by
producing and activating morphine-like hormones, called endorphins.
These hormones constitute the active portion of a naturally built-in
pain relief system. DLPA operates to protect this pain relief
system from certain destructive enzymes (carboxypeptidase A and
enkephalinase enzymes). DLPA consequently allows the pain relief
system to exert its powerful pain-relieving influence for an extended
period of time.

DLPA has other features such as, anti-depressant, weight control,
stress, appetite suppressant, and mood elevator.

In conclusion DLPA is a very effective painkiller, it is safe for
long term use with no know toxicity levels, so therefore toxic
overdose is impossible. It is important to know that DLPA does not
cure the disease, which causes the pain, you must continue your other
therapies.

The dosage recommended: two capsules of 500 mg, three times per day,
thirty to forty minutes before meals for a period of seven days.
Thereafter, a maintenance dosage of two capsules a day should be
taken. DLPA is not recommended for use by pregnant or lactating
women or phenylkertonerics (PKU). Those suffering from high blood
pressure should take their tablets immediately after meals.

www.internalhealth.com/dl_phenylalanine.htm

--

Free-form DLPA means the amino acids is in its purest form they do not need any digestion and are absorbed directly into bloodstream.

--

I take 500 mgs around 10:00AM and again around 3:00PM. Must be taken on an empty stomach.

--

I thought this was a simple, easy way of explaining how DLPA works:

"DLPA destroys the enzyme that causes endorphins to self-destruct,
and so extends their life."

--

[Art]

This half hour video describes how LDN halted the progression of Progressive Relapsing Multiple Sclerosis. It also explains how LDN works and the reasons why after 20 years of saving lives it is still unknown.

video.google.com/videoplay?docid=4440379733824898139

[Art]

Not an LDN-related website.

www.multiplesclerosissucks.com/

I don't agree with everything he says, but the site is interesting, entertaining and worth a look.

[Art]

4-AP: All You Need to Know, Part One

By Wise Young, M.D., Ph.D.

4-aminopyridine, or 4-AP, is a drug that improves the function of surviving nerve fibers in your spinal cord. Most people with spinal cord injury still have some connections, but many have lost their myelin (an insulating material) and cannot conduct signals well. 4-AP allows these demyelinated axons to send signals.
The drug, not approved by the Food and Drug Administration, is available in compounding pharmacies with a doctor's prescription. A compounding pharmacy makes drugs from ingredients that doctors prescribe. The FDA allows such drugs to be made even though they have not been formally approved. A list of compounding pharmacies can be obtained from the Internet by doing a search for "compounding pharmacies."

4-AP works only while it is taken, and the effect goes away within hours after you stop. It is not an innocuous or miraculous drug. Indeed, it is a powerful substance with beneficial effects on spinal cord injury but with complex effects on the body; it also has interactions with many drugs.
An estimated 10,000 people in the United States with multiple sclerosis or spinal cord injury are taking 4-AP, yet more studies are needed to establish its safety and efficacy.

What are the effects of 4-AP?

4-AP's effects can range from reduced spasticity and pain, increases in strength and in some, walking. The worst effect is seizures, but the risk is low when dosage is kept lower than 40 milligrams per day.
Several clinical trials have reported beneficial effects of the drug in multiple sclerosis and spinal cord injury. Over 100 people with spinal cord injury have received various formulations of 4-AP in clinical trials.
It appears that about a third of people with spinal cord injury have clinically detectable improvement in spasticity or sensory, bladder, bowel or motor function. Most of these people are more than a year after injury.

Many studies have documented the effects of 4-AP on motor function in animals and humans after spinal cord injury. In 1993, Hansebout and colleagues reported that 4-AP significantly improved motor and sensory function in eight patients with chronic spinal cord injury. The drug was given intravenously over two hours. Three patients showed no effect, but the remainder had increased motor control and sensibility below the injury site, with reduction of chronic pain and spasticity. The sensory effects outlasted the motor effects by as long as 48 hours after drug infusion.

When can I expect to start feeling the effects of 4-AP?

The beneficial effects of 4-AP depend on the symptoms and the injury. Sensory improvement should be fairly rapid (within hours), while motor function may take days or weeks to appear. Spasticity changes should be fast, but bowel and bladder improvements frequently occur within days. For some people, 40 milligrams per day may not be sufficient, but if you are not seeing any beneficial effects within four weeks at 40 milligrams per day, I suggest discontinuing the drug until the sustained-release formulation is available.

Does 4-AP have side effects?

At doses of up to 40 milligrams per day, oral immediate-release formulations of 4-AP appear to have few side effects. Sustained-release formulations may allow higher doses with fewer side effects.
At high doses, 4-AP may cause hyperexcitability, dystonic movements, seizures, cardiac arrythmias, blood pressure changes and other problems that can be treated with anti-convulsants, adrenergic antagonists and parasympathetic drugs.

Almost all cases of seizures have been reported in people with multiple sclerosis; seizures have not been reported in anyone with a spinal injury. People with multiple sclerosis have a higher risk of seizures because the disease also affects the brain. People with a history of seizures, epilepsy and head injury should take 4-AP with caution.

Other side effects include restlessness, parasthesias and increased frequency of bowel movements. Most of these side effects can be avoided by ramping up the dose of 4-AP over several weeks.

What are the long-term effects of 4-AP?

The long-term effects of 4-AP have not been systematically studied. Some people, particularly in the multiple sclerosis community, have taken the drug for many years. The drug does not have carcinogenic activity in animal studies, and there has been no report of long-term deleterious consequences of the drug on the heart, liver or kidney.

How does 4-AP work?

First, it improves conduction in demyelinated and dysmyelinated (abnormally myelinated) axons. It does so by blocking the fast voltage-sensitive potassium channels in cells, including neurons, muscle and other excitable tissues. This increases both the speed and reliability of conduction, including the amount of neurotransmitter released per action potential.

What are the dangerous interactions 4-AP has with other drugs?

4-AP is not an innocuous drug. It has powerful effects on the nervous system and interacts with many drugs, including alcohol. I recommend not drinking alcohol while taking 4-AP. Ethanol depresses neuronal excitability. 4-AP may antagonize many of the effects of ethanol and vice versa. Depending on the dose, 4-AP may mask alcohol so that you do not feel the effects of alcohol as much.

Likewise, alcohol may oppose the effects of 4-AP and reduce its efficacy. Ethanol withdrawal (the hangover stage), moreover, may be associated with irritability and hyperexcitability of the brain and spinal cord, which may increase the risk of 4-AP-induced seizures. Ethanol may also change the balance of excitability and inhibitory systems that have accommodated to 4-AP.

Many other drugs may interact with 4-AP, as it antagonizes most drugs that depress the neural activity. These include tetrahydrocannabinol, anesthetic agents, neuromuscular blockers, baclofen-induced anti-nociception, and sympathetic and parasympathetic drugs that are used to treat bladder plasticity, intestinal motility, blood pressure and other conditions. Unfortunately, most of these effects of 4-AP and interactions with drugs have not been systematically studied.

How do I get 4-AP?

The drug has not yet been approved by the FDA but nonetheless can be prescribed by doctors. It is dispensed by compounding pharmacies. Note that the FDA is attempting to regulate the compounding pharmacies, and 4-AP may be one of the first drugs that the FDA may withdraw from the compounding formulary because of concerns over variable formulation.

Because many doctors have not heard of 4-aminopyridine or do not know the drug well, they are often reluctant to prescribe it. It is important that you find a doctor who is willing to read some of the literature on the drug, learn about its use and limitations, and prescribe it for you. 4-AP must be taken under a doctor's supervision.

I do not personally know doctors who are prescribing the drug in each region of the country. I am sure, however, that there are people on the interactive SpineWire forum <http://www.cando.com/cgi-bin/templates/ /templates/cd_forums.html?section=123> who know doctors in each region who are experienced with 4-AP treatment.

How much does 4-AP cost?

The cost of 4-AP will depend on the amount of the drug that is taken. The prices range from $50 to $150 per month for the immediate-release formulation.

Do I need to take 4-AP under a doctor's supervision?

Many people are now experimenting with 4-AP without adequate medical supervision. More important, the information is not sufficient for many doctors to supervise the use of 4-AP. The main reason why doctors should and must be involved is that they can take care of complications if they should arise.

Is 4-AP for me?

The drug does not work for everybody. In clinical trials to date, the drug appears to improve the function of 30 to 40 percent of people with spinal cord injury. People with some preserved function below the injury tend to benefit more.

How much should I take?

The effective dose of 4-AP varies substantially from person to person, with the recommended dose at 40 milligrams per day in divided doses for safety reasons. Many factors influence a drug's effect. The compounded drug is variable in potency, and because it has a short half-life, it tends to have lower potency, especially when it is kept on the shelves for a long time.

Different people absorb different amounts of the drug when it is ingested, and its penetration into the nervous system is probably quite variable. The drugs that people are taking for spasticity and pain also affect 4-AP. Hence, the dose of the drug therefore must be carefully and individually titrated.

Some people have gone up to 60 milligrams per day, while others have success with 20. Again, 4-AP must be taken under medical supervision. Please don't keep pushing the dose higher if you get any significant side effect of the drug.

One of the reasons 4-AP is still going through clinical trials is to find out more about the optimal dose, including whether the dose should be related to body weight and if it needs to be different for men and women.

With the immediate-release formulation, 10 milligrams taken three to four times a day is the currently recommended approach. Some people are taking more, such as 15 milligrams four times per day. I do not recommend higher doses until more is known.

What are the chances that 4-AP will have any effect on me?

About a third of people with spinal cord injury show neurologically measurable beneficial effects from 4-AP. Although 4-AP is believed to have more effects on people with "incomplete" spinal cord injury, I think that it may have some effects on people with so-called "complete" spinal cord injury for the following reasons.
1. Most people have some preserved motor and sensory function below the injury site even though they have complete spinal cord injury. 4-AP should improve such function.
2. Demyelination may be the major reason why some people with spinal cord injury have functional loss. Many people with multiple sclerosis are paralyzed and have sensory loss from demyelination.
3. 4-AP does more than improve the function of demyelinated axons. It increases the amount of neurotransmitters released by axonal activity.
4. It should increase reflexes in the spinal cord. Despite this, 4-AP has beneficial effects on spasticity.

What formulations of 4-AP are available, and what effects does each have?

4-AP is available in two kinds of formulations: immediate release and timed release.
Most compounding pharmacies provide the immediate-release version, which is just the chemical 4-aminopyridine mixed with some filler material in gel caps. 4-AP reacts with many different kinds of fillers, leading to a shortened shelf life and lower potency.

For example, some formulations of 4-AP may lose as much as 10 to 20 percent of their potency per week. It is likely that many of the 4-AP pills out there do not have the potency that they are said to have.
In addition, the immediate-release formulation results in a peak plasma dose within 30 minutes. Plasma levels fall by about one-half within three to four hours. Immediate-release formulations therefore tend to produce higher peak levels and greater variations in plasma levels. Peak levels determine side effects -- one of the reasons why a sustained or timed-release formulation of the drug is desirable. In fact, with sustained-release formulations where the drug is released slowly over time, it may be possible to give two times higher doses of 4-AP with fewer side effects.

A company called Acorda Therapeutics (Note: I am a founder and a member of the scientific advisory board and board of directors of Acorda Therapeutics. Please take this into consideration when you read what I say about Acorda Therapeutics and its drugs.) is developing a time-release version of the drug.

This formulation has not yet been approved by the FDA and therefore is not available. That version of the drug is currently undergoing phase 2 clinical trials. Click here <http://www.cando.com/cgi-bin/templates/forum.html?thread=9953&stack=2,1,1> for more information.

It may take two years, depending on the current trial, for the FDA to approve Acorda’s drug. And once these trials are completed, there will be a lot of data associated with the drug to enable researchers to determine how to reduce side effects while improving efficacy.

The FDA has not, to my knowledge, decided whether it will withdraw the compounded version and replace it with the time-release version. It is difficult to predict because there is no precedent for this situation.

4-AP: All You Need to Know, Part Two

By Wise Young, M.D., Ph.D.

Is 4-AP for any certain injury level?

4-AP should work for any level of spinal cord injury, ranging from cervical to lumbar. For example, 4-AP may help somebody with a C2 injury recover respiratory function (C3), somebody with a C5 injury recover triceps and wrist extension (C6/7) or somebody with a T12 injury get bowel, bladder and sexual function. These improvements would be worthwhile.

What is ramping, and should I ramp my 4-AP dosing?

Ramping is a way to allow the body to get used to a dose, which typically takes two weeks. The goal is to reach 40 milligrams per day in four 10-milligram doses, spread four to five hours apart. I have been reluctant to give direct recommendations of dosing on a Web site, since you should work with your doctors. However, I will suggest a ramp-up schedule for the immediate-release formulation:
· 5 mg. t.i.d. (3 times a day; every 5-6 hours while awake) for 4 days = 15 mg./day
· 5 mg. q.i.d. (4 times a day; every 4-5 hours while awake) for 5 days = 20 mg./day
· 10 mg. t.i.d. (3 times a day; every 5-6 hours while awake) for 6 days = 30 mg./day
· 10 mg. q.i.d. (4 times a day; every 4-5 hours while awake) = 40 mg./day

Such an approach will get you to the 40-milligrams-per-kilogram dose in about two weeks. The approach assumes that the person does not have any side effects such as tingling, nervousness, insomnia and dizziness at any stage along the way. If there are side effects, wait until they subside before going up to the next step. It is probably a good idea for doctors prescribing 4-AP to initially order 5-milligram capsules for the ramping-up phase.

What is the most effective way to take 4-AP?

Ways to take your dose can vary. For example, I have a friend with MS who takes a 10-milligram capsule in the morning when he wakes up. He then takes one capsule just before lunch. He takes one before dinner. Depending on how late he stays up, he takes one at 10 p.m.

When are side effects most likely to occur?

The side effects should come mostly at the peak of plasma levels, which should occur within an hour of ingesting a capsule. The half-life of the drug is about three hours (the plasma drug levels fall by one-half every three to four hours). Therefore, within three hours, the effect should be waning. If you take the drug every six hours, there will be some waxing and waning of its levels. If you take it every four hours, it should maintain the plasma levels and perhaps even build up a bit during the day.

Please note that 4-AP from compounding pharmacies has a short shelf life. The drug may lose as much as 20 percent or more potency per month after it has been mixed with standard filler materials.

I find I am having trouble sleeping since I've started taking 4-AP. What can I do?

Sleeping problems are a common complaint of first-time 4-AP users. You might escape this side effect by avoiding 4-AP before sleep. Since the immediate-release version of 4-AP probably has a plasma half-life of about three hours, you should avoid taking 4-AP at least three hours before intending to sleep.

What happens if I stop taking 4-AP?

Most people who have stopped the drug show increased spasticity and pain (if they have pain). Ramp down in the same way as the ramp up. People should taper the dose over a period of a week or more to reduce the chance of effects. Interestingly, improvement in function can be subtle and difficult to appreciate until you go off the drug.

When will the FDA approve 4-AP?

It still needs to undergo pivotal trials, which may require one to two years to complete. It is not a cure, but it may help some people regain some function.

My friend lives in Russia, and he wants 4-AP. Can I buy it in the United States for him?

I believe that several compounding pharmacies will send 4-AP overseas if they get a physician's prescription for the drug. Call the compounding pharmacies and see whether or not they send overseas.

I had my injury eight months ago. Is it OK for me to take 4-AP?

There is very little experience with 4-AP in people who are less than a year after injury. In the clinical trial setting, to ensure that whatever improvements happen are due to 4-AP, most investigators have recommended waiting. I don't know of any evidence of deleterious effects of 4-AP started at eight months after injury.

Can 4-AP prevent re-myelination of the spinal cord if I undergo a re-myelination therapy?

To my knowledge, 4-AP should not prevent re-myelination of the spinal cord. However, this is something that could be tested in animal studies.

What are other uses for 4-AP?

The Russian army has been using 4-aminopyridine since the 1980s as an antidote against botulinum toxin and possibly other nerve gases. It was part of their battle kits. In fact, after 4-AP was first tested in clinical trials in Europe during the mid-1980s, when word spread in the United States that it might be beneficial in multiple sclerosis, there was no source of pharmacological grade 4-AP. I heard rumors that people were using ampules of 4-AP from Russian army kits brought in through the Czechoslovakian embassy.

You should also know that 4-AP is also the main active ingredient of poison that they use to kill pigeons in New York City.

I am noticing increased spasticity after taking 4-AP. What could this be?

4-AP has two known mechanisms of action on neural activity. First, it improves conduction in demyelinated and dysmyelinated (abnormally myelinated) axons. It does so by blocking the fast voltage-sensitive potassium channel, which normally limits the duration of action potentials that propagate in axons. This increases both the speed and reliability of conduction.

Second, it increases the duration of action potentials that reach the end of the axons. This causes more neurotransmitter release per action potential. The effects of 4-AP therefore depend on which axons are demyelinated and what remaining connections you have. If you have imbalance of excitatory and inhibitory connections to your legs, for example, 4-AP may enhance spasms.

Some drugs interact with 4-AP to produce more spasticity. If you are taking baclofen, tizanidine, clonidine and other anti-spasticity drugs, 4-AP may interact with these drugs to produce more spasticity. Interaction information is not sufficient to predict these effects. Also, individual reactions may differ.

How does 4-AP affect motor function?

Many studies have documented the effects of 4-AP on motor function in animals and humans after spinal cord injury. Besides Hansebout's trials, several other small trials have documented effects of 4-AP on motor function in spinal cord injury in humans; none has reported an increase in extensor spasms, although several subjects have reported reduced plasticity.

Qiao and colleagues, in 1997, studied the effects of 4-AP on motor-evoked potentials of subjects with chronic spinal cord injury. He showed a significant reduction in conduction latency (the time it took for the signal to go from the brain to the leg) but little change in the spinal reflex amplitudes. They concluded that the primary effect of the dose of 4-AP they used was on the conduction of signals from the brain to the spinal cord, as opposed to increased neurotransmitter release (which should be reflected in the reflex changes). Note that the doses of 4-AP used in this study were relatively low.

Dubuc and colleagues, in a 1986 study, showed that 4-AP increased rhythmic discharges from the spinal cord of cats below complete transection sites. This strongly suggests that 4-AP synchronizes the discharges of neuronal activity in the spinal cord, an effect that can override other spontaneous activity that may be occurring in the spinal cord. This may lead to spasms at rest.

Hatch and colleagues had an interesting observation that is potentially relevant. They showed that 4-AP and other excitatory drugs can reverse anesthesia in dogs. What was most fascinating was the fact that they observed opisthotonus, or extensor rigidity, in several dogs that were given combinations of excitatory drugs and were also receiving atropine.

In an early study, we found that 4-AP increases extracellular potassium levels and sensory conduction in rats that are genetically myelin deficient. Direct application of high doses of 4-AP to the rat spinal cord can cause tremors or shaking of the legs (personal observation). Very high doses (millimolar concentrations -- hundreds of times greater than therapeutic dose) can cause conduction failure in the spinal cord. So, the effects of 4-AP are very dose dependent.

goodshape.net/4AP.html

[Art]

New Year Resolutions

1. I resolve to be less cranky with my children at the end of the day when I'm too tired to cope with the mess they've made.

2. I resolve to never say "no" to my children when they ask me to read to them or tuck them into bed.

3. I resolve to be more appreciative of my spouse, who has a heavier load to bear because of my disease.

4. I resolve to be less neurotic about new symptoms that might not be caused by MS.

5. I resolve to keep exercising for as long as I can to extend my health.

6. I resolve to do everything in my power to keep my job for as long as possible.

6. I resolve to bite my tongue when people around me say stupid things about health-related issues.

7. I resolve to be more compassionate with other people's illnesses, and never to say "Welcome to my life" when somebody else is sick.

8. I resolve to be realistic about MS, to make plans that are practical about my illness without passing up opportunities to be all that I can be.

9. I resolve not to bite the heads off people who say "But you look so great", but instead to say "Thank you".

10. I resolve to complain less and laugh more.

11. I resolve to find a twentysomething supermodel girlfriend who has a big chest, a flat stomach, long legs, and several million dollars in the bank; who owns a Lamborgini, an apartment in Paris, and a chain of microbreweries; who is absolutely crazy about me and who doesn't like to wear clothing if she doesn't have to.

Hey, a man's gotta have a DREAM.

[Art]

LDN should only be given once per day and never be given before 9pm when we're off Daylight saving time(fall and winter) and never give LDN before 10pm during daylight saving time(spring and summer). This will insure that the LDN is in the system during peak endorphin production time of between 2am and 4am(the most endorphins are produced during this time and it is very important to take advantage of this to stop disease progression). Never give LDN twice within 24 hours. Read the LDN website and read the Further Q and A page while there, it's an important page and understanding how LDN works and why we take LDN in this manner is vital. LDN should not be given any later than 3am.

(above explanation borrowed from one of Brenda's posts)

[Art]

Check yourself for Candida(yeast overgrowth)...
tinyurl.com/48ds6l


It can easily take several months to completely stop a yeast infection and re-establish good bacteria. Do not get impatient.


Eight or more yes answers are typically found in someone who has a Candida overgrowth condition. Often times when suffering from the effects of chemotherapy, radiation and/or surgery, massive antibiotic loads will jump start yeast infection problems.

Do you crave sugar, bread, foods made with white flour, or alcoholic drinks?

Do you repeatedly notice any of these symptoms: rashes, cold hands and feet, feel chilly, numbness, burning, tingling, nasal or sinus congestion, post-nasal drip, bad breath, bothersome or persistent vaginal itching, burning, or discharge, constipation, diarrhea, bloating, gas, or belching, dry mouth, urinary frequency?

Have you taken birth control pills for over two years?

Do you have uncontrollable weight loss or a problem gaining weight?

Do you repeatedly notice any of these symptoms: tired or lethargic, mood swings, depression, headaches, poor memory or concentration, mentally foggy, feel drained, depleted or exhausted, anxiety

Have you taken prednisone or other cortisone steroid drugs for over two weeks?

Do your symptoms worsen when you are exposed to perfume, paint fumes, cigarette smoke, insecticides, or other chemicals?

Do your symptoms worsen on damp, muggy, humid days or when you are in a moldy place?

Have you ever been troubled with stubborn or recurring vaginitis, yeast infections, prostatitis, or other problems affecting your reproductive organs?

Have you had a persistent or severe case of athlete's foot, ringworm, jock itch or other chronic fungal infection of the skin or nails?

Have you taken tetracyclines or other antibiotics for one month or longer?

Have you taken broad spectrum antibiotics for two months total? They are used for respiratory, urinary, and other infections, and kill good bacteria while they kill the bacteria responsible for the infection. This group includes Keflex, ampicillin, amoxicillin, Bactrim, Sepra, and Ceclor.



Candida Yeast Die Off symptoms

Candida die off, also known as the Herxheimer response, occurs when you take an antifungal and the yeast is killed off too quickly and overwhelms the body with toxins. The Herxheimer response gets it's name from Austrian Dermatolist brothers Jarisch Adolf Herxheimer and Karl Herxheimer who discovered the phenomenon back in 1895. It was originally discovered as a healing crises that occurred in people with syphilis, but was then found to be a reaction that occurs in a variety of illnesses in response to treatment. The reaction presents itself as an intensification or extension of symptoms immediately preceding a period of time when the patients health then improves. With Candida overgrowth this phenomenon is called, die off. When the yeast dies, it releases a massive amount of toxins. You may experience a worsening of symptoms, new symptoms or flu-like symptoms. It can be quite severe for some people...

tinyurl.com/adk7y5

[Art]

Why the Silence About LDN?

Pharmaceutical News by Press Release? (OR: Low Dose Naltrexone Study
Doesn't Make the News)

In the article, "Statins (Crestor) for Everyone?", I wrote about how
the AstraZeneca-funded JUPITER study (JUPITER stands
for "Justification for the Use of Statins in Primary Prevention: an
Intervention Trial Evaluating Rosuvastatin") made a case for putting
many more people on statins, especially on AstraZeneca's own Crestor.
In the article, I pointed out several troubling facts, including that
studies funded by pharmaceutical companies are much more likely to
have positive results than those that are not industry-funded, and
that many of the "news stories" about the JUPITER study reported "the
facts" of this study, almost word for word, as they appeared in
AstraZeneca's press release.

In her November 14, 2008 Columbia Journalism Review article, "Science
Reporting by Press Release," Cristine Russell calls this kind
of "reporting" the "dirty little secret of journalism."

The subject came up recently in a conversation I had with Burt
Berkson, MD, PhD, pioneer in the use of alpha lipoic acid, and more
recently, of low dose naltrexone (LDN), as well, for treating some
very serious diseases and conditions -- without the side effects of
more toxic pharmaceuticals. Dr. Berkson was telling me that, at one
of the conferences he spoke at, LDN researcher Dr. Maira Gironi told
about the wonderful results she was having in Italy, reversing
multiple sclerosis with LDN. (You may read about Dr. Gironi's work
with LDN here, here and here.)

Dr. Berkson noted: "But you hear nothing about it because there are
no very wealthy corporations promoting it."

His words brought to mind the fact that Dr. Gironi had presented a
paper on this study at the 60th annual meeting of the American
Academy of Neurology in Chicago, in April, 2008, around the same time
that I was interviewing several of the LDN patient and physician
advocates for my article, "Four Lifesaving Medical Treatments: Not
So `Anecdotal,' After All." Everyone I spoke with was excited about
the very positive results Dr. Gironi was getting in Italy with LDN
for MS. They were eager for her paper to be presented at the AAN
meeting in Chicago.

Indeed, Dr. Gironi did present the paper on LDN. But, as Dr. Berkson
noted in our conversation, there were no big press announcements
about her paper.

So, I went online to see what had happened –- and why there was such
silence.

What I found was that, while there had been silence surrounding the
LDN study (which had no pharmaceutical company backing), at the same
conference one of Dr. Gironi's LDN co-investigators, Dr. Giancarlo
Comi, had also presented a paper on another MS drug, FTY720
(fingolimod). The research on this drug had been funded by the
pharmaceutical company, Novartis.

News stories about this pharmaceutical-company-funded
study/presentation abounded. The drug was called a "novel oral
therapy."

But then, I began to notice something very curious: ALL the "news
stories" about fingolimod had the same identical wording, from
beginning to end.

I knew exactly where to go to learn where the wording had come from.
There it was, in the April 15, 2008 Novartis company press release,
titled "FTY720, a novel oral therapy in development for MS, shows
sustained benefits for the majority of patients after three years of
treatment."

Then, I went to medicalnewstoday.com, which boasts that it is "the
largest independent health and medical news website on the Internet."
Well, not so independent, after all -- because there it was, on the
very same date (April 15, 2008), a news "article," titled -–
Surprise! -- "FTY720, a novel oral therapy in development for MS,
shows sustained benefits for the majority of patients after three
years of treatment," with the same exact wording as the Novartis
press release.

And the same day, on www.bio-medicine.org, which purports to
contain "the latest biology and medical news," this identically
titled article ran: "FTY720, a novel oral therapy in development for
MS, shows sustained benefits for the majority of patients after three
years of treatment."

And again, it ran (same title, same wording) on biospace.com and on
World Pharma News -- and so it went, on many other "scientific"
sites, too.

Is this why the "big news" to come out of the AAN meeting was NOT
about low dose naltrexone, but rather, about a pharmaceutical company-
funded drug? What do you think?

To learn about how Big Pharma also writes (or commissions to have
written) the "scientific" medical journal articles about the
pharmaceuticals they "study" and manufacture, read Dr. John
Abramson's Overdosed America and Melody Petersen's Our Daily Meds. In
addition, there is a wonderful PBS interview with Ms. Petersen, in
which she talks about this phenomenon (she says the pharmaceutical
industry calls it "publication planning").

tinyurl.com/the-silence-about-ldn

www.honestmedicine.com/2009/02/pharmaceutical-news-by-press-
release-or-low-dose-naltrexone-study-doesnt-make-the-news.html

[Art]

Burt Berkson, M.D., Ph.D., has gotten amazing results in his medical practice treating various conditions (including cancer, MS, and terminal liver disease) with alpha lipoic acid and/or Low Dose Naltrexone. The site below features a transcript of an interview with Dr. Berkson in which he discusses some of his most notable cases:

tinyurl.com/berkson-on-ala-and-ldn

The site also reveals how incredibly difficult it has been for him to interest mainstream medicine in his discoveries.

Antioxidants, Metabolic Maintenance-Alpha-Lipoic Acid 100mg and 300mg
store.metabolicmaintenance.com/category.aspx?categoryID=2
store.metabolicmaintenance.com/

Professional Supplement Center :: for Bio-Tech products click brand, scroll down
to Bio-Tech and click, then click L for lipoic Acid
www.professionalsupplementcenter.com/Default.aspx
www.professionalsupplementcenter.com/




ALA is best absorbed on an empty stomach, one to two hours before eating.

Read more: www.livestrong.com/article/426855-should-alpha-lipoic-acid-be-taken-with-food-or-on-a-empty-stomach/#ixzz1cwDVUObm

[Art]

4.5mg LDN soon to be available over the counter

International Antiaging Systems will soon sell 4.5mg LDN capsules without a Rx with a phone call or on the Internet at a slight premium but over time they may get some competition.

www.antiaging-systems.com/iasstore/acatalog/naltrexone.html

Phone orders: 1-866-800-4677