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Harmful Brain Effects of Interferons

Dr. Mercola's Comment:

Dr. Blaylock, a board-certified neurosurgeon and author of the

highly recommended books _Health and Nutrition Secrets That Can Save your Life_

(http://www.amazon.com/exec/obidos/ASIN/0929173422/optimalwellnessc) and

_Natural Strategies for Cancer Patients_

(http://www.amazon.com/exec/obidos/ASIN/0758202210/optimalwellnessc) ,

contributed this outstanding article about

interferons, which are used widely for the treatment of multiple sclerosis

(MS),

hepatitis, cancer and more. If you, or someone you know, are taking these

drugs, this article will help you decide if the benefits outweigh the many

risks.

____________________________________

By L. Blaylock, M.D.

_http://www.russellblaylockmd.com/_ (http://www.russellblaylockmd.com/)

Interferons are used in clinical medicine for a number of medical conditions

including:

* A wide range of cancers

* Chronic hepatitis

* Multiple sclerosis

* Chronic granulomatous disease

* AIDS-related disorders

Rarely considered are the effects of large doses of this immune cytokine on

brain function. For example, the conventional treatment of chronic hepatitis

is interferon-alpha-2b. Despite poor results in controlling the disease and

the existence of safer, more effective natural treatments, physicians continue

to use this toxic treatment. Of major concern are the neurologic effects of

the treatment.

Acute Problems

It is known that interferons have two patterns of injury to the brain. One

is acute and occurs within hours of treatment, often lasting for the first one

to three weeks of the treatment. This usually includes fever, chills,

headache and fatigue.

Chronic Problems

This is followed by a chronic phase in which more serious injuries to the

nervous system result. Chronic symptoms can include malaise, lethargy,

somnolence, headaches, low-grade fevers, anorexia (loss of appetite) and more

serious

symptoms such as psychomotor symptoms, cognitive problems, psychiatric

behaviors and even delirium and coma.

Brain Toxicity

The severity of symptoms depends on the dose of the interferon and manner of

administering the medication. Continuous infusion of high-dose interferons

is associated with more severe neurologic problems. It is known that chronic

brain toxicities occur at all doses but more so after doses higher than 18

million to 20 million units a day. Most common is severe fatigue.

Even lower doses have been associated with a lack of drive and disinterest

in participating in normal activities, a process called psychomotor

retardation. This occurs in anywhere from 47 percent to 80 percent of patients.

Changes

in the ability to think clearly (cognitive changes) are frequently seen in

patients treated with as little as 9 million units of interferon per week. The

difficulty with thinking reaches a peak at one to three months. This can

include a decreased attention span, difficulty concentrating, defective

short-term memory and mental clouding.

Studies have described frequent periods of silence and vacant staring,

occurring even in mid-sentence. Objective testing for recall and cognitive

function have shown an incidence of 17 percent to 50 percent in patients

receiving

standard doses of interferons. Most of these cognitive difficulties do

improve, yet there are reports of persistent impairments lasting up to two

years

following cessation of treatment.

In some patients the effect is so severe on the brain that patients sleep up

to 20 hours a day and during waking periods experience disorientation and

confusion. Speech difficulties (expressive dysphasia) and problems with balance

have also been reported. On rare instances, these neurological effects have

progressed to a demented state. Hallucinations have also been reported.

It is important to appreciate that the patients in the first two categories

to be described had no previous psychiatric history. Renault and co-workers,

who examined many of these patients, divided the neurobehavioral effects into

three syndromes: organic personality syndrome, organic affective syndrome

and delirium effects. Patients with organic personality syndrome frequently

experience uncontrollable overreaction to minor frustrations, are very

irritable

and have a short temper.

Depression Common

Those with the organic affective syndrome often describe feelings of

depression and hopelessness. They cry easily and have difficulty interacting

socially with others. Patients experiencing delirium have a clouding of their

thinking, have short-term memory problems and have frequent mood changes. Many

become severely agitated, abusive, withdrawn and may exhibit suicidal thoughts,

delusions of being persecuted and phobias. Patients having delirium symptoms

often had co-existing liver disease, history of psychiatric disorder or

previous brain injury.

Severe Reactions in Cancer Treatment

The most severe effects have been seen in patients treated for cancers. In

these patients death due to encephalopathy (widespread brain injury) and

associated seizures have been described. This may be a result of combined

toxicities of radiation, chemotherapy and interferon.

Interferon-gamma is less toxic than the alpha or beta-interferons. With

higher doses one can see chronic neurotoxicities, which can include dizziness,

slowed thinking, confusion, crying spells, and even symptoms resembling

Parkinson's disease.

How Interferon Ruins Your Brain

The mechanism of this injury to the brain appears to involve the brain's

special immune cell called the microglia. Normally, these cells remain dormant

in the brain. That is, they are sleeping. Microglia cells can be activated by

numerous factors, including mercury, aluminum, iron, overvaccination, and

brain trauma, strokes, infections (viruses, bacteria, rickettsia) and cytokines

such as interferons.

Once activated, microglia can move about the brain secreting very toxic

compounds, which include two excitotoxins (glutamate and quinolinic acid).

These

excitotoxins dramatically increase free radical generation in the brain as

well as oxidation of lipids (called lipid peroxidation). These radicals damage

synaptic connections, interfere with neurotransmitters and can even kill

neurons. In addition, these activated microglia generate other toxic compounds

such as prostaglandins (PGE2), which increase brain inflammation.

If the microglia activation is short lived, the damage to the brain is

minimal and recovery takes place. Yet, should the activation continue, which

would

occur with high-dose and long-term use of interferons, the damage could be

substantial and irreversible. Protecting the brain with high-dose and varied

antioxidants as well as certain metabolic stimulants can substantially reduce

this damage. Certain nutrients, such as malate, pyruvate, DHA, ascorbate,

magnesium and methylcobalamin inhibit excitotoxicity.

Physicians Frequently Miss Side Effects

Physicians often ignore patient complaints of neurological difficulties

during interferon treatments, assuming they are benign and reversible. As

stated

in the beginning, natural alternatives have been shown to be much more

effective and dramatically safer than interferon treatments.

____________________________________

Related Articles:

_MS Drugs 'a Waste of Money'_

(http://www.mercola.com/2003/mar/5/ms_drugs.htm)

_Hepatitis Drug Interferon Linked to Depression_

(http://www.mercola.com/2002/dec/21/interferon.htm)

_Amazing Recovery From Multiple Sclerosis_

(http://www.mercola.com/2003/oct/11/ms_success.htm)

_Is Glutamine Supplementation Helpful or Harmful?_

(http://www.mercola.com/2004/may/1/glutamine.htm)

_Is it Hepatitis C or Iron Toxicity?_

(http://www.mercola.com/2003/apr/2/iron.htm)

_Modified Interferon Reported to be Effective Against Hepatitis C_

(http://www.mercola.com/2000/dec/17/hepatitis_c.htm)

____________________________________

References:

Turowski RC, Triozzi PL. Central Nervous System Toxicities of Cytokine

Therapy. In, Plotnikoff NP, et al (eds): Cytokines: Stress and Immunity. CRC

Press, Boca Raton,1998. pp 93-114.

F, et al. Neuropsychiatric manifestations of human leukocyte

interferon therapy in patients with cancer. JAMA 252: 938, 1984.

Iaffaiolo RV, et al. Neurotxic effects of long-term treatment with low-dose

ab interferon. Current Therapy Research 48: 403, 1990.

Meyers CA, et al. Persistent neurotoxicity of systemically administered

interferon-a Neurology 41: 672, 1991.

Renault PF, et al. Psychiatrc complications of long-term interferon-a

therapy. Arch Internal Medicine 147: 1577, 1987.

Kurzock R, et al. Phase I study if IV administrated recombinant g interferon

in cancer patients. Cancer Treatment Reports 70: 1357, 1986.

Blaylock RL. Chronic Microglial activation and excitotoxicity secondary to

excessive immune stimulation: Possible factors in Gulf War Syndrome and

autism. Journal of American Physicians and Surgeons. 9: 46-51, 2004.

Thyroid autoimmunity disorders during interferon beta-1b treatment in

patients with multiple sclerosis: review and case report]

[Article in German]

Lange-Asschenfeldt C, Boor S, Kahaly GJ, Thomke F.

Klinik und Poliklinik fur Neurologie, Klinikum,

Johannes-Gutenberg-Universitat, Mainz, lange@...

Occurrence of thyroid autoimmunity and dysfunction following interferon

alpha treatment of viral hepatitis and other diseases are known adverse effects

and have been ascribed to the cytokine's general immunomodulatory and

-activating properties. However, in spite of its extensive application, there

have

been few reports of such incidents during interferon beta (IFN-beta-1a/b)

therapy, which is considered the standard treatment of relapsing-remitting

multiple sclerosis (MS), and prospective studies have been published only

recently.

Here we present the case of a 38-year-old woman with Graves' disease

including massive thyroid-associated ophthalmopathy appearing de novo following

IFN-beta-1b therapy for MS. A literature search revealed an 11% (5% clinically

overt) overall incidence of de novo thyroid dysfunction in IFN-beta-treated MS

patients, mostly autoimmune hyperthyroidism. (Large-scale comparative studies

for IFN-beta-1a are not available at present). Specific treatment but not

necessarily discontinuation of IFN-beta-1b therapy was required in most cases.

Female gender, pre-existing thyroid autoimmunity, and family history of

thyroid disorders are presumable risk factors for thyroid dysfunction de novo

during IFN-beta-1b treatment.

PMID: 15257382 [PubMed - in process]

____________________________________

Jeff el

_http://www.msprotocols.netfirms.com/_ (http://www.msprotocols.netfirms.com/)

_http://www.msprotocols.netfirms.com/Getting%20Started.htm_

(http://www.msprotocols.netfirms.com/Getting%20Started.htm)

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