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Caffeine allergy, cerebral vasculitis, leads to breakdown of blood brain barrier


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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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