Dangers of Caffeine, with References

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Caffeine Induced Anaphylaxis, A Progressive Toxic Dementia

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

author.

Email: _Tenpaisleypark_ (Tenpaisleypark)

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.

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