Plasma Caffeine Concentrations in Outpatients

Smith, JanetM.; Pearson, S; Marks, Vincent

doi:10.1016/s0140-6736(82)90182-9

Cited by 45 publications

(15 citation statements)

References 10 publications

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“…In our pregnant rats, 0.04 and 0.02% caffeine intakes were calculated to correspond approximately to less than 50 and 25 mg caffcine/kg body weight/day, re spectively, because the consumed volume measurements were rough [5,6], When the maternal and fetal caffeine levels in the morning on gestational day 21 in the present study were compared with those in the eve ning on gestational day 20 in the previous study [5], it was considered that these levels were maintained at least during middle to late pregnancy. Therefore, an adverse effect of maternal caffeine on the fetal cerebrum is possible with a level of 1.5-3.0 jig caffeine/ml in maternal plasma, this concentra tion coinciding with that found on random plasma caffeine measurement in 600 adult outpatients [10].…”

Section: Discussionsupporting

confidence: 72%

Effects of Maternal Caffeine Ingestion on the Perinatal Cerebrum

Tanaka¹,

Nakazawa²,

Arima³

1987

Neonatology

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The cerebra of fetal rats from dams given 0.04 or 0.02% caffeine in drinking water ad libitum before and/or during pregnancy were examined on gestational day 21. A low placental weight was induced by caffeine ingestion for a long time throughout premating and pregnancy. A greater reduction in the fetal weight of the cerebrum than that of the body was observed with caffeine ingestion during pregnancy of levels of 1.5–3.0 μg caffeine/ml or g wet weight in dams and fetuses. In the cerebra of offspring, the levels of caffeine and theophylline did not change for 4 h after birth, and theophylline was not detected at all after intraperitoneal injection of caffeine. Thus, maternal caffeine should be warned against the fetal cerebral function.

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Section: Discussionsupporting

confidence: 72%

Effects of Maternal Caffeine Ingestion on the Perinatal Cerebrum

Tanaka¹,

Nakazawa²,

Arima³

1987

Neonatology

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“…It is also interesting that caffeine is detected in habitual caffeine-consuming humans at concentrations capable of antagonizing A2AR, 10 -50 M in moderate to heavy caffeine consumers (43,44). Other studies showed that when humans acutely ingested 2-2.5 mg/kg caffeine (corresponding to the amount in two cups of coffee), blood caffeine concentration was ϳ20 M (41,45,46). In contrast, amounts of caffeine much higher than what people usually consume will be required for the immunosuppressive effects of caffeine.…”

Section: Discussionmentioning

confidence: 99%

1,3,7-Trimethylxanthine (Caffeine) May Exacerbate Acute Inflammatory Liver Injury by Weakening the Physiological Immunosuppressive Mechanism

Ohta

Lukashev

Jackson

et al. 2007

The Journal of Immunology

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The genetic elimination of A2A adenosine receptors (A2AR) was shown to disengage the critical immunosuppressive mechanism and cause the dramatic exacerbation of acute inflammatory tissue damage by T cells and myeloid cells. This prompted the evaluation of the proinflammatory vs the anti-inflammatory effects of the widely consumed behavioral drug caffeine, as the psychoactive effects of caffeine are mediated largely by its antagonistic action on A2AR in the brain. Because caffeine has other biochemical targets besides A2AR, it was important to test whether the consumption of caffeine during an acute inflammation episode would lead to the exacerbation of immune-mediated tissue damage. We examined acute and chronic treatment with caffeine for its effects on acute liver inflammation. It is shown that caffeine at lower doses (10 and 20 mg/kg) strongly exacerbated acute liver damage and increased levels of proinflammatory cytokines. Because caffeine did not enhance liver damage in A2AR-deficient mice, we suggest that the potentiation of liver inflammation was mediated by interference with the A2AR-mediated tissue-protecting mechanism. In contrast, a high dose of caffeine (100 mg/kg) completely blocked both liver damage and proinflammatory cytokine responses through an A2AR-independent mechanism. Furthermore, caffeine administration exacerbated liver damage even when mice consumed caffeine chronically, although the extent of exacerbation was less than in “naive” mice that did not consume caffeine before. This study suggests an unappreciated “man-made” immunological pathogenesis whereby consumption of the food-, beverage-, and medication-derived adenosine receptor antagonists may modify an individual’s inflammatory status and lead to excessive organ damage during acute inflammation.

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“…Only one other study has evaluated caffeine plasma concentration in a naturalistic setting. In that study, general medical outpatients were found to have caffeine concentrations between 0.2 and 13.1 mg/l, with a mean of 2.1 mg/l (Smith et al, 1982).…”

Section: Introductionmentioning

confidence: 93%