Caffeine Induced Anaphylaxis: A Progressive Toxic Dementia

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THE DANGERS OF CAFFEINE

is such a popular topic at

http://www.doctoryourself.com that we are publishing a new paper, below, in its

entirety.

 

Caffeine Induced Anaphylaxis, A Progressive Toxic Dementia

by Ruth Whalen, MLT, ASCP

 

Cerebral allergy is an allergy to a substance, which targets vulnerable brain

tissue and alters brain function. Masked cerebral allergy can cause symptoms of

mental illness (Walker, 1996; Rippere, 1984; Sheinken et al., 1979).

 

Symptoms

range from minimal reactions to severe psychotic states, which may include

irrational behavior, disruptions in attention, lack of focus and comprehension,

mood changes, lack of organizational skills, abrupt shifting of activities,

delusions, hallucinations, and paranoia (Sheinken et al., 1979; McManamy et al.,

1936).

 

An allergic reaction to caffeine manifests as anaphylaxis (Przybilla et al.,

1983).

 

During a state of caffeine anaphylaxis, the body enters the fight

or flight mode, which may be mistaken as hyperactivity, anxiety, or panic

disorder.

 

Caffeine anaphylaxis causes cerebral vasculitis, leads to the

breakdown of the blood brain barrier, and generates toxic dementia.

 

Toxic dementia induced by a stimulant or other toxin affects function of

all brain areas (Jacques, 1992). Several signs of toxic dementia are

memory impairment, deterioration of social and intellectual behavior,

and attention deficits (Allen et al., 2001; Jacques, 1992; Headlee, 1948).

 

Attention Deficit Disorder (ADD), assumed to affect children, (though of late,

adult onset ADD is grabbing a slice of the pie of psychiatric disorders),

is indistinguishable from caffeine allergy.

 

Claudia Miller, M.D. stresses that a chemical sensitivity, which includes

caffeine as a chemical capable of

inducing sensitivity, can induce attention deficits with hyperactivity

(Miller, 1997).

 

Deteriorating intellect, the first stage of caffeine induced allergic

toxicity masquerades as ADD.

 

Inability to concentrate, lack of comprehension, lack of focus, hyperactivity,

delusions, and disorganized

thought processes are hallmark signs of caffeine allergy.

 

An allergic reaction to caffeine results in poisoning of the prefrontal cortex.

Damage

to the underside area on the prefrontal cortex, above the eye sockets,

generally renders a person absent minded and interferes with the ability

to monitor personal activities (Carter, 1998). Injury results in loss

of verbal and social inhibition, interferes with focus and memory

(Eliot, 1999), and suppresses math skills (Carter, 1998).

 

In studies involving comprehension skills, as in mathematics and logical

reasoning, caffeine has either exhibited no change, or has actually depleted

performance (Braun, 1997). Caffeine may jeopardize math skills and detailed

projects, which require additional thought (Serafin, 1996; NTP Chemical,

1991).

 

Caffeine anaphylaxis interferes with the ability to focus.

 

Sitting still becomes a project. Raising the catecholamine level, caffeine

produces

additional dopamine, which increases locomotive movement.

 

Agitation is associated with excess dopamine (Carter, 1998).

 

Caffeine causes faster speech and mobility in children (Nehlig et al.,

1992). With 80% of the world’s population consuming caffeine, most

persons have remained stimulated since childhood.

 

Stimulated adults

can’t detect caffeine-induced changes in themselves or in children.

Misjudging a child’s natural state, adults assume children should speak

and act at the same rate as stimulated adults. People forget that we

are born relaxed. Acceleration of speech and action indicates mania

(Victor et al., 2001; Restak, 1984), associated with bipolar

affective disorder. Manic symptoms affect children. Psychiatrically

hospitalized manic children display symptoms of ADD (Carlson et al., 1998).

 

Complaints of lack of focus, failing memory, and other mental

abnormalities, signify hypomania, a lesser degree of mania

(Victor, 2001), which accompanies the first stage of

ongoing-caffeine-induced-anaphylaxis-induced fight or flight

dementia. Unable to correlate the patient’s complaints with a

textbook disorder, physicians assume ADD.

 

According to the American Psychiatric Association, which classifies

caffeine as a substance, substance intoxication can present with

disturbance in thinking, judgment, perception, attention, motor

activity, and social functioning (1994).

 

Caffeine toxicity can induce restlessness, agitation, irritability, confusion,

and delerium

(Steinman, 2001; Fisher Scientific, 1997; Turkington, 1994; Shen et al.,

1979). In addition, anaphylaxis can induce delerium (Kaplan, 2000).

 

Unlike Stephen Cherniske, aware of instinct warning him that caffeine

was affecting his behavior (Cherniske, 1998), a child does not know.

 

A youngster can’t feel the mild stimulant rush because the

underdeveloped body has developed a tolerance. Similarly, a toxic

adult loses natural insight and can’t recognize caffeine induced

intellect and personality changes (Shen, 1979; McManamy, 1936; Crothers, 1902).

 

During partial withdrawal, the body metabolizes some caffeine,

saturating cells. Clarity struggles to return. Symptoms of partial

withdrawal can overlap traits of poisoning (Strain et al., 1997)

and can mimic depression (Hirsch, 1984). As the noradrenaline level

diminishes, symptoms of depression set in (Restak, 1994, Ackerman,

1992). Caffeine induced withdrawal depression can manifest as

hyperactivity, lethargy, irritability, confusion, and lack of

focus.

 

The glucose level, which rises along with adrenaline

(Davidson et al., 1969) and remains elevated during the body’s

struggle to maintain homeostasis, drops. A decrease in glucose

encourages lack of motivation, which may also mimic depression.

 

As Allbutt and Dixon stressed, in 1909, regarding caffeine,

another “dose of the poison” provides minor relief, but continues

to jeopardize organs (1909). A return to caffeine intake increases

noradrenaline, heightening the fight or flight response. In turn,

adrenaline, dopamine, and glucose increase, thus lifting

depression. With continued substance exposure, toxins accumulate

(Van Winkle, 2000).

 

Caffeine allergy is a deceptive allergy. Ongoing caffeine

anaphylaxis reduces allergic inflammation and maintains organ

stimulation. Endogenous glucocorticoids (including cortisol)

inhibit inflammation (Claman, 1983). Theophylline is the principle

therapy for asthma. All forms of theophylline maintain open

bronchial passages, allowing for easier breathing. During ongoing

caffeine anaphylaxis, airways remain open. Adrenaline, the drug of

choice for anaphylaxis, is always present in a caffeine consumer.

By suppressing phosphodiesterase release, caffeine (Davidson, 1969)

increases cyclic AMP. Excess amounts of cyclic AMP inhibit histamine

production (Dykewicz, 2001; Ernst et al., 1999). Phosphodiesterase

inhibitors inhibit histamine release (Raderer et al., 1995).

 

Cyclic AMP is increased in patients diagnosed as schizophrenic and

many individuals diagnosed with affective disorders (Nishino et al.,

1993; Erban et al., 1980; Biederman et al., 1977). Histamine is

reduced in persons diagnosed with schizophrenia, a late stage of

ongoing caffeine anaphylaxis.

 

Although the histamine level is low in schizophrenics (Malek-Ahmadi

et al., 1976; Hoffer et al., 1967), schizophrenic patients exhibit

a marked tolerance to histamine (Lea, 1955). This suggests, in the

case of caffeine anaphylaxis, that during the onset stage of

schizophrenia, when anaphylaxis induced hyperactivity,

or anaphylaxis induced panic symptoms were mistaken as ADD, anxiety,

or panic, (before continued cerebral poisoning), histamine was

increased but the allergy went undetected.

 

Symptoms of allergic anxiety (Bonner, 2000; Kaplan, 2000; Walsh,

2000) may be mistaken as anxiety neurosis, considered an onset

symptom of schizophrenia. When a young person experiencing a first

anxiety episode arrives in an emergency room, doctors suspect a

developing schizophrenia (Victor, 2001).

 

Attention and memory deficits accompany schizophrenia (Zuffante et

al., 2001; Goldberg et al., 1993). Researchers theorize that prior

to the onset of schizophrenia changes in a person’s cognition may

be subtle (Goldberg, 1993).

 

Chlorpromazine (Thorazine) and other phenothiazine drugs exhibit

an anti-histamine effect (Sifton, 1994; Malek-Ahmadi, 1976),

similar to diphenhydramine (Benadryl). A person allergic to caffeine,

taking a phenothiazine medication, will experience relief of the

physical manifestations of ongoing caffeine anaphylaxis. In addition,

phenothiazine medications reduce allergic induced abnormal psychological

symptoms, including a reduction in paranoia, hallucinations, and

delusions, and generate a return of partial insight, focus, and

comprehension.

 

Ongoing caffeine allergy induces a progressive toxic dementia (McManamy, 1936).

 

In a caffeine allergic person, each caffeine or theophylline

dose increases toxin accumulation. A buildup of caffeine, which may

exceed tolerance level, saturates the ability of metabolism

(Carrillo et al., 2000; Nehlig, 1999); rate of drug accumulation

exceeds rate of elimination. Introducing a stimulant into a

caffeine allergic individual’s system will further poison the frontal

cortex and hypothalamus and continue to mask allergic symptoms of

caffeine anaphylaxis. Continued stimulant use increases toxic psychosis,

which results in decreased affect and deterioration of mental abilities.

 

(I have posted all the references cited in the paper above at

http://www.doctoryourself.com/caffeine2.html

To read another of Ruth’s excellent caffeine articles, please go to

http://www.doctoryourself.com/caffeine_allergy.html )

 

Copyright 2002 Ruth Whalen, MLT, ASCP. Reprinted with permission of the author.

Email Ms Whalen at

Tenpaisleypark

 

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