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Effect of caffeine on circadian excretion of urinary calcium and magnesium

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Abstract

To determine if later renal conservation occurs in calcium (Ca) and magnesium (Mg) excretion after morning caffeine-induced increases in urinary Ca and Mg excretion. Before-after trial of caffeine abstinance and consumption was conducted on two consecutive days in a metabolic ward while subjects ate a controlled diet containing 11.3 mmol Ca and 12.7 mmol Mg. 17 healthy males and females, ages 17-41 yr volunteered. Two caffeine doses of 3 mg/kg lean body mass caffeine were consumed at 7 and 10 a.m. on second day. Salivary caffeine concentrations and urinary Ca, Mg, sodium and creatinine excretion were measured. Salivary caffeine peaked at 4.7 umol/mL at 11:30 a.m. and declined with a half-life of 7.3 hours. Urinary Ca and Mg were elevated significantly (p = 0.01 and p = 0.04) for six h after the second caffeine dose. Caffeine had no significant effect on urinary calcium or magnesium excretion between 4 p.m. and 1 a.m. Between 1 and 4 a.m., urinary Ca and Mg excretion was decreased after caffeine (p = 0.04 and p = 0.01). Creatinine excretion was not different at any time. Nighttime compensatory renal conservation was insufficient to offset morning caffeine-induced mineral losses, resulting in net 24-hour urinary increases of 0.32 mmol Ca and 0.16 mmol Mg.

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... Although it is not known how caffeine may affect bone density, several potential mechanisms exist, including caffeine-associated inhibition of secretion and mineralization of the extracellular matrix of bone, 24 calcium resorption from bone, 25,26 and calciuria. [27][28][29][30][31][32][33][34] Oral caffeine increases urinary excretion of calcium, magnesium, sodium, and chloride in human beings [27][28][29][30][31] and may increase parathyroid hormone (PTH) levels 34 ; caffeine-associated calciuria may be blocked by an adenosine receptor agonist in an animal model. 32 However, most human studies indicate that these changes are not statistically significant in premenopausal women 27,28 and are limited to postmenopausal women ingesting a relatively low calcium diet (600 mg daily) 30 and to persons with hypertension ingesting a low calcium diet (700 mg daily). ...
... Although it is not known how caffeine may affect bone density, several potential mechanisms exist, including caffeine-associated inhibition of secretion and mineralization of the extracellular matrix of bone, 24 calcium resorption from bone, 25,26 and calciuria. [27][28][29][30][31][32][33][34] Oral caffeine increases urinary excretion of calcium, magnesium, sodium, and chloride in human beings [27][28][29][30][31] and may increase parathyroid hormone (PTH) levels 34 ; caffeine-associated calciuria may be blocked by an adenosine receptor agonist in an animal model. 32 However, most human studies indicate that these changes are not statistically significant in premenopausal women 27,28 and are limited to postmenopausal women ingesting a relatively low calcium diet (600 mg daily) 30 and to persons with hypertension ingesting a low calcium diet (700 mg daily). ...
... The following paragraphs address this issue because a better understanding of this relationship may lead to new recommendations for prevention and treatment of skin atrophy and ated increase in 24-hour urinary calcium excretion of 0.32 mmol/L (12.8 mg). 29 Whether such a small daily loss during a lifetime might be clinically significant is not known. ...
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The decline in skin thickness that occurs with aging interests many different groups. Among these are pharmaceutical, cosmeceutical, and cosmetic companies promoting antiaging or antiwrinkling products, geriatricians and rheumatologists treating elderly and steroid-dependent patients who are "outliving" their skin, cosmetic surgeons, and dermatologists. Dermatologists are frequently asked how to prevent or slow aging of the skin. The answer regarding "photoaging" of sun-exposed skin is obvious; the answer regarding aging of photoprotected skin is not. Although the bulk of epidemiologic literature about aging and thinning of photoprotected skin is from the 1970s, literature regarding risk factors for and treatment of aging and thinning of the bony skeleton is more recent. Because both skin and bone are composed of more than 70% type I collagen, it may be hypothesized that the pathophysiologic processes involved in chronological atrophy of both tissues may overlap, thereby providing a foundation for further investigation of the skin. A better understanding of skin and bone loss may motivate the "appearance-conscious" public to modify risk factors (e.g., begin exercising) or select hormonal therapies (e.g., postmenopausal hormone replacement) to reduce aging of the skin. These measures may provide additional benefits, such as decreasing the risk of osteoporosis.
... In addition to its recognized stimulatory effect on the central nervous system, caffeine affects several other tissues and organs, including the kidney, where it increases water and mineral urinary excretion (2). Acute ingestion of caffeine in amounts such as those found in two to three cups of coffee (ϳ300 mg caffeine) increases the urinary excretion of calcium, magnesium and sodium for at least 3 h after consumption (3)(4)(5)(6)(7). Renal conservation over 24 h after a caffeine load appears insufficient to offset the caffeine-induced calcium and magnesium losses (6). ...
... Acute ingestion of caffeine in amounts such as those found in two to three cups of coffee (ϳ300 mg caffeine) increases the urinary excretion of calcium, magnesium and sodium for at least 3 h after consumption (3)(4)(5)(6)(7). Renal conservation over 24 h after a caffeine load appears insufficient to offset the caffeine-induced calcium and magnesium losses (6). These increased urinary losses may potentially affect bone mass by increasing bone mineral release to maintain balance (8). ...
... The present study indicates that use of oral hormonal contraceptives does not prevent the diuretic effect of caffeine. Many studies in adult women show that a caffeine load acutely increases urinary excretion of calcium, magnesium and sodium (3)(4)(5)(6)(7). A caffeine load also increased urinary potassium (4) but not urinary phosphorous (5,45). ...
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Caffeine consumption increases the urinary excretion of calcium and other minerals. Factors that affect caffeine metabolism such as steroid hormones may modify this effect. The purpose of this study was to evaluate the influence of oral contraceptive (OC) use on the 4-h urinary excretion of calcium, phosphorus, magnesium, zinc, sodium, potassium and caffeine metabolites in response to a high caffeine dose given as coffee beverage. Adult women, 20-29 y, users (+OC, n = 15) and nonusers (-OC, n = 15) of oral contraceptives, with calcium intake approximately 500 mg/d, participated in two tests, caffeine load (5 mg/kg body weight) and no-caffeine control, in a randomized crossover design. The net increase (caffeine load corrected by no caffeine) in urinary excretion of most minerals was significantly higher in -OC than in +OC (P < 0.05), with the larger group difference for calcium (ninefold) followed by magnesium (twofold), zinc (onefold) and potassium (onefold). Net increases in urinary excretion of 1-methylurate and paraxanthine were about three- and fivefold higher, respectively, in -OC than in +OC (P < 0.05) whereas net increases in urinary excretion of 5-acetylamino-6-formylamino-3-methyluracil (AFMU) and 1,7-dimethylurate were over twofold higher in the +OC than in -OC (P < 0.05). Following the caffeine load, most urinary minerals showed negative correlation with urinary 1-methylurate in -OC (R </= -0.78, P < 0.01), and with urinary AFMU and 1,7-dimethylurate in +OC (R </= -0.84, P < 0.01). Oral contraceptives appear to limit the renal effect of caffeine on mineral excretion possibly by reducing paraxanthine excretion, the most active caffeine metabolite.
... Altered gastrointestinal absorption due to medications such as proton-pump inhibitors, malabsorptive conditions, or vomiting, can contribute to a negative body magnesium balance (31,39). An increase in renal excretion of magnesium can occur with renal disease, poorly controlled diabetes mellitus, numerous medications (most notably loop diuretics and caffeine), alcohol use, and stress (31,38,(40)(41)(42). ...
... Although there is a strong body of correlational data demonstrating a relationship between magnesium and migraine, the studies fail to account for additional migraine risk factors such as obesity, metabolic syn- drome, or caffeine overuse (6-21). Dietary magnesium intake has been shown to be inversely associated with metabolic syndrome and obesity, and caffeine has been demonstrated to increase magnesium excretion (40,41,(67)(68)(69)(70). The possibility that obesity, metabolic syndrome, or caffeine overuse are influencing the strength of the correlation between magnesium and migraine is worth considering. ...
Article
Migraine is an incompletely understood, debilitating disorder that lacks a universally effective treatment. Magnesium participates in a variety of biochemical processes related to migraine pathophysiology, and a deficiency could contribute to migraine development. A review of the literature from 1990 to the present on magnesium and migraine was conducted. The authors identified 16 studies aimed at magnesium status assessment in migraine, and four intervention trials assessing the efficacy of oral magnesium supplementation, independent of other therapies, in the prevention of migraine. The strength of evidence supporting oral magnesium supplementation is limited at this time. With such limited evidence, a more advantageous alternative to magnesium supplementation, in patients willing to make lifestyle changes, may be to focus on increasing dietary magnesium intake. © International Headache Society 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
... In addition, fluoride, found in 74% of the American population's drinking water, with ~50% of drinking water having a concentration of 0.7 mg/L, prevents magnesium absorption through binding and production of insoluble complexes [46][47][48]. Ingestion of caffeine and alcohol increase renal excretion of magnesium causing an increase in the body's demand [49,50]. Common medications can also have a deleterious effect on magnesium absorption such as antacids (e.g., omeprazole), due to the increase in gastrointestinal (GI) tract pH (see Section 2.5) [51,52], antibiotics (e.g., ciprofloxacin) [53], and oral contraceptives due to complexation [54,55], and diuretics (e.g., furosemide and bumetanide), due to an increase in renal excretion (see Section 2.6) [56,57]. ...
... In addition, fluoride, found in 74% of the American population's drinking water, with~50% of drinking water having a concentration of 0.7 mg/L, prevents magnesium absorption through binding and production of insoluble complexes [46][47][48]. Ingestion of caffeine and alcohol increase renal excretion of magnesium causing an increase in the body's demand [49,50]. Common medications can also have a deleterious effect on magnesium absorption such as antacids (e.g., omeprazole), due to the increase in gastrointestinal (GI) tract pH (see Section 2.5) [51,52], antibiotics (e.g., ciprofloxacin) [53], and oral contraceptives due to complexation [54,55], and diuretics (e.g., furosemide and bumetanide), due to an increase in renal excretion (see Section 2.6) [56,57]. ...
Article
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Magnesium is a critical mineral in the human body and is involved in ~80% of known metabolic functions. It is currently estimated that 60% of adults do not achieve the average dietary intake (ADI) and 45% of Americans are magnesium deficient, a condition associated with disease states like hypertension, diabetes, and neurological disorders, to name a few. Magnesium deficiency can be attributed to common dietary practices, medications, and farming techniques, along with estimates that the mineral content of vegetables has declined by as much as 80–90% in the last 100 years. However, despite this mineral’s importance, it is poorly understood from several standpoints, not the least of which is its unique mechanism of absorption and sensitive compartmental handling in the body, making the determination of magnesium status difficult. The reliance on several popular sample assays has contributed to a great deal of confusion in the literature. This review will discuss causes of magnesium deficiency, absorption, handling, and compartmentalization in the body, highlighting the challenges this creates in determining magnesium status in both clinical and research settings.
... For most of these factors, the effect is usually attributed to increased urinary calcium loss. Individually, phosphorus and caffeine were shown to have little or no net effect (6)(7)(8)(9)(10)(11), but concern remains about the acid load (12). The combination of all 3 factors, as would be found in many colas, has not been directly tested. ...
... At the same time it must be noted that the calciuric effect of caffeine is biphasic. Massey et al previously showed a compensatory drop in overnight calciuria in caffeine consumers (11), and no net effect on 24-h excretion (10). Similarly, Barger-Lux et al (21) found no effect of caffeine on 24-h urinary calcium at caffeine doses 5-6 times those used in this study. ...
Article
Intake of carbonated beverages has been associated with increased fracture risk in observational studies. The usual explanation given is that one or more of the beverage constituents increase urinary calcium. We assessed the short-term effects on urinary calcium excretion of carbonated beverages of various compositions. An incomplete random block design was used to study 20-40-y-old women who customarily consumed > or =680 mL carbonated beverages daily. Four carbonated beverages were tested: 2 with caffeine and 2 without. Two contained phosphoric acid as the acidulant and 2 contained citric acid. The study included one neutral control (water) and one positive control (skim or chocolate milk). Serving size was 567 mL for the carbonated beverages and water and 340 mL for the milks. Beverages were consumed with a light breakfast after an overnight fast; no other foods were ingested until urine collection was complete. pH, titratable and total acidity, sodium, creatinine, and calcium were measured in 2-h (morning) fasting and 5-h postbeverage urine specimens. Relative to water, urinary calcium rose significantly only with the milks and the 2 caffeine-containing beverages. The excess calciuria was approximately 0.25 mmol, about the same as previously reported for caffeine alone. Phosphoric acid without caffeine produced no excess calciuria; nor did it augment the calciuria of caffeine. The excess calciuria associated with consumption of carbonated beverages is confined to caffeinated beverages. Acidulant type has no acute effect. Because the caffeine effect is known to be compensated for by reduced calciuria later in the day, we conclude that the net effect of carbonated beverage constituents on calcium economy is negligible. The skeletal effects of carbonated beverage consumption are likely due primarily to milk displacement.
... This may be due to the displacement of milk consumption or to a direct effect of soft drink components. Caffeine has been shown to increase the excretion of calcium in the urine, and phosphoric acid may interfere with calcium absorption (Fernando et al 1999, Kynast-Gales and Massey 1994). ...
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High consumption of soft drinks and other sugary drinks are associated with a number of health problems, including overweight and obesity, type 2 diabetes, osteoporosis and dental caries. In Australia, soft drinks are the most commonly consumed sugary beverage and have been singled out for specific attention as a target of obesity prevention programs. Soft drinks are well-known, readily available and marketed extensively, especially to adolescents. They have no nutritional value other than sugar and fluid, and are identified in the Australian Guide to Healthy Eating as an ‘extra’ food – one that should be consumed only occasionally and in small amounts.
... In another research project by the same authors, an identical effect of caffeine was noticed in 15 healthy men [100]. A study from 1994 (Kynast-Gales et al. [101]) assessed the effect of caffeine alone on urinary magnesium excretion. The consumption of two doses of caffeine at 3 mg/kg of lean body mass increased the excretion of magnesium. ...
Article
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Coffee brews, made by pouring water on coffee grounds or brewing in an espresso machine, are among the most popular beverages. The aim of this study was to summarize data on the content of macroelements (sodium, potassium, calcium, magnesium, and phosphorus) in coffee brews prepared with different methods, as well as to review the factors influencing the content of the elements. Studies from 2000 to 2020, published in the PubMed and Google Scholar databases, were reviewed. Taking into account the results presented by the authors, we calculated that one portion of coffee brew can cover 7.5% or 6.4% (for women and men) and 6.6% of the daily requirement for magnesium and potassium, respectively. Coffee provides slightly lower amounts of phosphorus (up to 2.2%), sodium (up to 2.2%), and calcium (up to 0.7% of the daily requirement for women and 0.6% for men). If coffee is drunk in the quantity of three to four cups, it can be an important source of magnesium, considering the risk of magnesium deficiency in modern societies.
... It is presently unknown how caffeine may influence the bone quality in our body. Some early studies have shown that caffeine intake caused acute increase of urinary cal- cium excretion (12,13) and reduced calcium absorption in the gut (14,15). Cell and animal studies have found that caffeine directly inhibits osteoblast cell function (4) or in- duces calcium release from bone (26). ...
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Context and Objective: Caffeine is a highly consumed psychoactive substance present in our daily drinks. Independent studies have reported associations between caffeine consumption, low bone mineral density, and urinary calcium loss, as well as impaired bone development in vitro and in vivo. Calcium (Ca2+), vitamin D, and PTH are critical regulators of bone remodeling. A possible association between caffeine and parathyroid gland function has been suggested in the literature. Design, Setting, and Patients: Effects of caffeine on PTH secretion and Ca2+ levels were determined by batch incubation and Fura-2, respectively, in pathological parathyroid cells. Protein expressions were studied by Western blot and immunohistochemistry in normal and parathyroid adenoma tissues. Alterations in gene expressions of adenosine receptor A1 (ADORA1) and A2 (ADORA2A) and PTH were quantified by PCR; intracellular cAMP levels and protein kinase A activity were analyzed by an antibody-based assay. Results: We studied physiological concentrations of caffeine ranging from 1 to 50 μm and found that 50 μm caffeine caused a significant decrease of PTH secretion and PTH gene expression. This decrease occurred in parallel with a decrease of the intracellular cAMP level, protein kinase A activity, and ADORA1 gene expression, indicating a possible causal relationship. The intracellular level of Ca2+ was unaffected even by high concentrations of caffeine. Protein expressions demonstrated two main targets for caffeine—ADORA1 and ADORA2A. Conclusion: A physiological high dose of caffeine inhibits PTH secretion in human parathyroid cells, possibly due to a decrease of the intracellular level of cAMP. The observation demonstrates a functional link between caffeine and parathyroid cell function.
... As opposed to other minerals such as calcium and iron, Mg homeostasis is not known to be regulated by hormones but depends mostly on gastrointestinal absorption and reuptake by the kidney. Unlike Mg intestinal absorption, however, Mg re-absorption by the renal tubes has been shown to be influenced by hormones such as parathormone and norepinephrine [19][20][21], the presence of other salts and proteins [22], diuretic compounds such as caffeine [23] or alcohol [24], and many other factors. Due to the limited scope of the present review, renal handling of Mg is not discussed here, and the reader is referred to comprehensive reviews [25][26][27]. ...
Article
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Decreased Mg intake and low Mg status have been associated with a number ot major health concerns such as diabetes mellitus type II, coronary heart disease, and osteoporosis. While information on Mg-intake is available, relatively little is known on dietary factors influencing Mg bioavailability. While it is established that Mg absorption is based on a combination of a non-saturable and a saturable pathway, the nature of especially the latter mechahism is not well understood. Recently, stable isotopes have improved techniques available for the determination of Mg absorption from single test meals or supplements. Some inorganic Mg forms such as MgO seem of limited solubility in the intestine, suggesting low bioavailability. Recent studies have further added evidence that some commonly consumed dietary compounds, such as phytate and oxalate, can inhibit Mg absorption, presumably via complexation, preventing absorption from the small intestine. Phytate for example has been shown to decrease Mg absorption by up to 60%, in a dose dependent manner. On the other hand, fermentable dietary fibre, such is fructo-oligosaccharides, have been demonstrated to increase Mg absorption in humans by 10-25%, even though the underlying mechanisms remain to be elucidated. Future studies to investigate factors impacting Mg absorption are warranted.
... increase in 24 hourly urinary calcium and magnesium loss in healthy volunteers (17-41y) (Kynast-Gales & Massey, 1994) stanlg 9/ 2/ 2011 500mg increase unfavourable subjective (tension, nervousness, anxiety, excitement, irritability) and somatic effects (nausea, palpitations, restlessness) and performance disruption in healthy volunteers greater increase in BP and HR than 100mg dose in healthy non-smoking habitual coffee drinkers 547mg increased vigor and mean arterial BP, decreased fatigue and headache in chronic caffeine consumers following single dose after half day abstinence (Lane, 1997) ...
... Also, the intake of cola, but not other carbonated soft drinks, has been associated with low bone mineral density in women, suggesting caffeine as the cause (Tucker et al. 2006). Caffeine has been shown to increase the excretion of calcium in the urine (Gales and Massey 1994), a potential contributor to osteoporosis. An epidemiological study in Mexico found that consumption of soft drinks with phosphoric acid, included in many soft drinks to give them " bite " , was an independent risk factor for developing hypocalcemia (low serum calcium) in postmenopausal women (Fernando et al. 1999). ...
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The prevention of overweight and obesity, particularly among children, is a public health priority. A range of initiatives to address this problem have already been developed and implemented in NSW. However, a broader range of additional strategies are needed to effectively address this complex issue. The high consumption of soft drinks, i.e. sugarsweetened carbonated beverages, and other sugary drinks is one of an array of dietary behaviours which has been identified by a number of policy documents as an important, specific behaviour to address in the prevention and management of obesity.
... From the measurements thus carried out, it was possible to highlight a net increase in urinary Ca and Mg after the second dose of caffeine administered, but caffeine had no significant effect on the urinary excretion of calcium or magnesium between 16:00 and 1:00 in the morning, while between 1:00 and 4:00 in the morning, the urinary excretion of Ca and Mg decreased after intake. It emerged, therefore, that nocturnal compensatory renal conservation was insufficient to compensate for the mineral losses induced by morning caffeine, with a consequent net urinary increase in the 24 h of excretion of 0.32 mmol Ca and 0.16 mmol Mg [264]. ...
Article
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Bone is a nutritionally modulated tissue. Given this background, aim of this review is to evaluate the latest data regarding ideal dietary approach in order to reduce bone mineral density loss and to construct a food pyramid that allows osteopenia/osteoporosis patients to easily figure out what to eat. The pyramid shows that carbohydrates should be consumed every day (3 portions of whole grains), together with fruits and vegetables (5 portions; orange-colored fruits and vegetables and green leafy vegetables are to be preferred), light yogurt (125 mL), skim milk (200 mL,) extra virgin olive oil (almost 20 mg/day), and calcium water (almost 1 l/day); weekly portions should include fish (4 portions), white meat (3 portions), legumes (2 portions), eggs (2 portions), cheeses (2 portions), and red or processed meats (once/week). At the top of the pyramid, there are two pennants: one green means that osteopenia/osteoporosis subjects need some personalized supplementation (if daily requirements cannot be satisfied through diet, calcium, vitamin D, boron, omega 3, and isoflavones supplementation could be an effective strategy with a great benefit/cost ratio), and one red means that there are some foods that are banned (salt, sugar, inorganic phosphate additives). Finally, three to four times per week of 30–40 min of aerobic and resistance exercises must be performed.
... ISN'T IT GENERALLY THOUGHT IT WAS SHORTER -~ 6 HRS? GARY? This prediction, however, is in line with other studies that show that the half-life of the effect of caffeine is shorter than the half-life of its concentration in the blood (Kynastgales and Massey, 1994;Ammar et al, 2001;Robertson et al, 1978;Whitsett et al, 1984;Myers, 1988). This common finding of the abbreviated effect of caffeine is consistent with the possibility of competitive inhibition. ...
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Sleep loss, as well as concomitant fatigue and risk, is ubiquitous in today's fast-paced society. A biomathematical model that succeeds in describing performance during extended wakefulness would have practical utility in operational environments and could help elucidate the physiological basis of sleep loss effects. Eighteen subjects (14 males, 4 females; age 25.8 +/- 4.3 years) with low levels of habitual caffeine consumption (<300 mg/day) participated. On night 1, subjects slept for 8 h (2300-0700 h), followed by 77 h of continuous wakefulness. They were assigned randomly to receive placebo or caffeine (200 mg, i.e., two sticks of Stay Alert gum) at 0100, 0300, 0500, and 0700 during nights 2, 3, and 4. The psychomotor vigilance test (PVT) was administered periodically over the 77-h period of continuous wakefulness. Statistical analysis reveals lognormality in each PVT, allowing for closed-form median calculation. An iterative parameter estimation algorithm, which takes advantage of MatLab's (R2007a) least-squares nonlinear regression, is used to estimate model parameters from subjects' PVT medians over time awake. In the model, daily periodicity is accounted for with a four-component Fourier series, and a simplified binding function describes asymptotic fatigue. The model highlights patterns in data that suggest (1) the presence of a performance inhibitor that increases and saturates over the period of continuous wakefulness, (2) competitive inhibition of this inhibitor by caffeine, (3) the persistence of an internally driven circadian rhythm of alertness, and (4) a multiplicative relationship between circadian rhythm and performance inhibition. The present inhibitor-based minimal model describes performance data in a manner consistent with known biochemical processes.
... claimed that increased phosphorus intake or acid load due to consuming these drinks or the caffeine in caffeine-containing drinks are contributing factors to this correlation. Though no studies have proved the net correlation between phosphorus intake, caffeine and these effects [32][33][34] there is still concern about the acid load [35]. ...
Article
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Objective: The aim of this animal study was to evaluate the possible effects of Carbonated Soft Drink consumption on the rate of orthodontic tooth movement in rats. Materials and Methods: Thirty-six adult male Sprague-Dawley rats were randomly divided into two experimental groups and one control group. In the experimental groups (A&B), the water in the dietary regimen was replaced with soft drinks (Fanta® in group A and Cola® in group B) two weeks before placement of orthodontic appliances. Then 5-mm nickel-titanium closed-coil springs were placed between the maxillary right first molars and first incisors under general anesthesia. This regimen continued for two weeks more and animals drank soft drink ad libitum. At the end of the experimental period, the rats were sacrificed, and interproximal tooth movements were measured. Results: The mean amounts of tooth movement were 0.19mm in group A, 0.22mm in group B and 0.37mm in group C. Statistical analysis with analysis of variance (ANOVA) test showed significant differences between all groups. The least movement occurred in group A that had received Fanta® drink. Conclusion: CSDs consumption decreases the rate of orthodontic tooth movement. The role of soft drinks in decreasing tooth movement might be related to its effects on bone metabolism.
... Dietary caffeine acutely increases urinary calcium loss (1), and these losses are not entirely compensated for in the 24 h after caffeine consumption (2). Overall, the evidence indicates that younger individuals can increase their calcium absorption to compensate for the urinary losses, whereas the elderly are less adaptable (3). ...
... Massey and Wise, 1984; Massey and Hollingbery, 1988; Bergman et al., 1990), showing that caffeine induced a significant acute calcium diuresis. However, subsequent studies showed that this renal effect was biphasic (Gales and Massey, 1994); that is, the acute increase was followed by a later fall in urinary calcium. While this late fall did not completely obliterate the acute increase reported by the investigators, earlier estimates of the net negative effect of caffeine consumption had to be lowered substantially. ...
Article
Caffeine-containing beverage consumption has been reported to be associated with reduced bone mass and increased fracture risk in some, but not most, observational studies. Human physiological studies and controlled balance studies show a clear but only a very small depressant effect of caffeine itself on intestinal calcium absorption, and no effect on total 24-h urinary calcium excretion. The epidemiologic studies showing a negative effect may be explained in part by an inverse relationship between consumption of milk and caffeine-containing beverages. Low calcium intake is clearly linked to skeletal fragility, and it is likely that a high caffeine intake is often a marker for a low calcium intake. The negative effect of caffeine on calcium absorption is small enough to be fully offset by as little as 1-2 tablespoons of milk. All of the observations implicating caffeine-containing beverages as a risk factor for osteoporosis have been made in populations consuming substantially less than optimal calcium intakes. There is no evidence that caffeine has any harmful effect on bone status or on the calcium economy in individuals who ingest the currently recommended daily allowances of calcium.
... The higher fracture rate might have been simply due to the higher risk of falling experienced by women drinking Ն2 drinks/day. Caffeine, as a mild diuretic, temporarily increases urinary Ca excretion [9], and some evidence shows that there is no compensation for the losses after 2 to 24 hours [37,38], while there is little evidence showing higher Ca losses over a longer period. The negative effect of caffeine, at least on Ca balance, and presumably indirectly on bones, might also be due to the impaired endogenous Ca absorption [10] and, therefore, particularly present in women with low Ca intake [17,18]. ...
Article
To determine relationship between alcohol, caffeine, past smoking and bone mineral density of different skeletal sites in elderly women, accounting for other biological and life-style variables. A cross-sectional study in 136 Caucasian women, mean +/- SD age 68.6 +/- 7.1 years, all healthy and free of medications affecting bones, including estrogen. Bone mineral density (BMD) of multiple skeletal regions and body composition were measured by dual X-ray absorptiometry. Serum vitamin D (25-OHD) and parathyroid hormone (PTH) were analyzed and used as confounders. Calcium (Ca) intake was assessed by food frequency questionnaire. Alcohol and caffeine consumption was assessed by questionnaires determining frequency, amount and source of each. There were no current smokers, but the history of smoking was recorded, including number of years and packages smoked/day. Past physical activity was assessed by Allied Dunbar National Fitness Survey and used as confounder. Statistical significance was considered at p <or= 0.05. In the correlational analysis, alcohol was positively associated with spine BMD (r = 0.197, p = 0.02), 25-OHD and negatively with PTH. Smoking was negatively related to Ca intake, 25(OH)D and number of reproductive years. In subgroup (stratified by Ca intake) and multiple regression analyses, alcohol (average approximately 0.5-1 drinks/day or approximately 8 g alcohol/day) was favorably associated with BMD of spine and total body. Caffeine (average approximately 2.5 6-fl oz cups/day or 200-300 mg caffeine/day) had negative association with most of the skeletal sites, which was attenuated with higher Ca intake (>or=median, 750 mg/day). The past smokers who smoked on average 24 years of approximately 1 pack cigarettes/day had lower BMD in total body, spine and femur than never-smokers when evaluated in subgroup analyses, and the association was attenuated in participants with >or=median Ca intake. There was no significant association between past smoking and BMD of any skeletal site in multiple regression analyses. The results support the notion that consumption of small/moderate amount of alcohol is positively, while caffeine and past smoking are negatively associated with most of the skeletal sites, which might be attenuated with Ca intake above 750 mg/day.
... This study included 30 women aged 20-40 years and demonstrated an association between 5-h urinary excess calcium excretion and caffeine-containing carbonated beverages. Beverages without caffeine including those containing phosphoric acid did not affect urinary calcium excretion, but the available evidence concerning caffeine and bone health is conflicting [27,28,29]. Nonetheless, this study was not designed to reach conclusions about the role of caffeine in relation to cola consumption. ...
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In the Western world, increased consumption of carbonated soft drinks combined with a decreasing intake of milk may increase the risk of osteoporosis. This study was designed to reflect the trend of replacing milk with carbonated beverages in a group of young men on a low-calcium diet and studies the effects of this replacement on calcium homeostasis and bone turnover. This controlled crossover intervention study included 11 healthy men (22-29 years) who were given a low-calcium basic diet in two 10-day intervention periods with an intervening 10-day washout. During one period, they drank 2.5 l of Coca Cola per day and during the other period 2.5 l of semi-skimmed milk. Serum concentrations of calcium, phosphate, 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol (1,25(OH)2D), osteocalcin, bone-specific alkaline phosphatase (B-ALP) and cross-linked C-telopeptides (CTX), plasma intact parathyroid hormone (PTH) and urinary cross-linked N-telopeptides (NTX) were determined at baseline and endpoint of each intervention period. An increase in serum phosphate (P<0.001), 1,25(OH)2D (P<0.001), PTH (P=0.046) and osteocalcin (P<0.001) was observed in the cola period compared to the milk period. Also, bone resorption was significantly increased following the cola period, seen as increased serum CTX (P<0.001) and urinary NTX (P<0.001) compared to the milk period. No changes were observed in serum concentrations of calcium or B-ALP. This study demonstrates that over a 10-day period high intake of cola with a low-calcium diet induces increased bone turnover compared to a high intake of milk with a low-calcium diet. Thus, the trend towards a replacement of milk with cola and other soft drinks, which results in a low calcium intake, may negatively affect bone health as indicated by this short-term study.
... All these studies demonstrated that caffeine-induced diuresis generates a rapid increase in the loss of calcium via urine. Though this effect was shown to be affected by night-time compensatory renal calcium conservation, the overall result was net increase in renal excretion of calcium [50]. On the other hand, other investigators [8, 51, 52] could not detect any significant increase in calcium excretion after a high caffeine intake. ...
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Consumption of coffee and tea, and total intake of caffeine has been claimed to be associated with osteoporotic fracture risk. However, results of earlier studies lack consistency. We examined this relation in a cohort of 31,527 Swedish women aged 40-76 years at baseline in 1988. The consumption of coffee, caffeinated tea and the intake of caffeine were estimated from a self-administered food frequency questionnaire (FFQ). Multivariate-adjusted hazards ratios (HRs) of fractures with 95% confidence intervals (95% CIs) were estimated by Cox proportional hazards models. During a mean follow-up of 10.3 years, we observed 3,279 cases with osteoporotic fractures. The highest (>330 mg/day) compared with the lowest (<200 mg/day) quintile of caffeine intake was associated with a modestly increased risk of fracture: HR 1.20 (95% CI: 1.07-1.35). A high coffee consumption significantly increased the risk of fracture (p for trend 0.002), whereas tea drinking was not associated with risk. The increased risk of fracture with both a high caffeine intake and coffee consumption was confined to women with a low calcium intake (<700 mg/day): HR 1.33 (95% CI: 1.07-1.65) with > or =4 cups (600 ml)/day of coffee compared to <1 cup (150 ml)/day. The same comparison but risk estimated for women with a high propensity for fractures (> or =2 fracture types) revealed a HR of 1.88 (95% CI: 1.17-3.00). In conclusion, our results indicate that a daily intake of 330 mg of caffeine, equivalent to 4 cups (600 ml) of coffee, or more may be associated with a modestly increased risk of osteoporotic fractures, especially in women with a low intake of calcium.
... Authors of relevant articles state that cola drinks generally lead to a more marked decrease in bone density compared to other carbonated drinks. Hypotheses related to this observed effect generally focus on phosphoric acid and caffeine, but it has been shown that the phosphorus/ phosphoric acid and caffeine found in greater amounts in cola drinks has very little or no effect on calcium metabolism [10][11][12][13][14][15]. However, some studies report that phosphoric acid has an effect on calcium metabolism, further that caffeine can cause increased fractures and decreased bone mineral density, and that acid load due to consumption of cola drinks may have a negative influence on the calcium and bone metabolism [4]. ...
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The aim of the study was to determine bone mineral density changes caused by consumption of cola drinks and the associated factors. Thirty Sprague-Dawley rats were divided into four groups. Groups 1 and 2, consisting of 10 male and 10 female rats, respectively, were provided with as much food, water and cola drinks as they wanted. Groups 3 and 4, consisting of five rats each, received only rat chow and water. The bone mineral density of the rats was measured using dual energy X-ray absorptiometry at the end of 30 days. The blood values and weights of the animals were also determined. The oesophagus and kidneys were removed for histopathological examination. The weight gain was higher in the groups consuming cola drinks than the control group rats (P < 0.05). Water consumption decreased 5.9 times while total fluid consumption increased 1.6 –1.9 times in the group consuming cola drinks. No significant change was detected in the blood calcium levels. There was a significant decrease in the bone mineral density of test groups when compared to the control groups (P < 0.05). While we did not detect any pathological oesophageal changes in the rats consuming cola drinks, examination of the kidneys revealed general glomerular congestion and intertubular bleeding. We suggest that the decrease in bone mineral density might be related to the renal damage caused by cola drinks in addition to other related factors.
... This may be due to the displacement of milk consumption or to a direct effect of soft drink components. Caffeine has been shown to increase the excretion of calcium in the urine, and phosphoric acid may interfere with calcium absorption (Fernando et al 1999, Kynast-Gales and Massey 1994). ...
... Other reports indicated that caffeine induces a significant acute calcium diuersis (Massey and Wise, 1984;Debry 1994;Heaney, 1998). However, subsequent investigation suggested that the increase in calcium excretion was followed by reduction in excretion, resulting in a net negative effect on calcium balance lower than previously thought (Kynast-Gales and Massey, 1994). ...
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Coffee, consumed for its refreshing and stimulating effect, belongs to the tribe Coffea of the subfamily Cinchonoidea of Rubiaceae family. Coffee is a complex chemical mixture composed of several chemicals. It is responsible for a number of bioactivities and a number of compounds accounting for these effects. Few of the significant bioactivities documented are antioxidant activity, anticarcinogenic activity, antimutagenic activity etc. Various compounds responsible for the chemoprotective effects of coffee are mainly polyphenols including chlorogenic acids and their degradation products. Others include caffeine, kahweol, cafestol, and other phenolics. Coffee also shows protective or adverse effects on various systems like the skeletal (bone) system, the reproductive system, the nervous system, the cardiovascular system, the homocysteine levels, the cholesterol levels etc. Harmful effects of coffee are associated with people who are sensitive to stimulants. Overall, with the available information, it can be concluded that the moderate consumption, corresponding to 3 to 4 cups/day with average strength is safer to human health.
... Renal calculi were induced in group II to VI by ethylene glycol for 30 days. [9] After administration for 15 days, group III treated with cystone 750mg/kg [10][11][12][13] and group IV were treated with aqueous extract of Amarathus viridis 200 mg/kg. ...
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INTRODUCTION Urinary stone disease is a common disorder estimated to occur in approximately 12% of the population, with a recurrence rate of 70-81% in males and 47-60% in females. Urolithiasis, one of the oldest, painfull aliments of the urinary tract disorder, wide spread among men. Calcium oxalate (CaOx) is the primary constituent of the majority of stones in the urinary system of patients with urolithiasis. [1] Approximately 80% of stones are composed of calcium oxalate (Caox) and calcium phosphate (CaP); 10% of struvite, 9% of uric acid (UA) and remaining 1% are composed of cystine. [2] The incidence of urolithiasis in world – wide is quite high and there is no satisfactory mode of treatment. Combinations of surgical and medical approach using percutaneous nephrolithotomy (PCNL), extracorporeal shock wave lithotripsy (ESWL) are employed to manage urolithiasis. All these treatments are relatively costly, painful and cause undesirable side effects such as hemorrhage, hypertension, tubular necrosis and subsequent fibrosis of the kidney leading to cell injury and recurrence of renal stone formation. [1] So it is worthwhile to look for an alternative for the management of urolithasis, and hence medicinal plants are adopted. Amarathus viridis linn, [3] is an annual herb, erect, 10 to 75 cm stem, slender, branched, angular, glabrous, long petiolate, lamina deltoidovate to rhomboid-oblong, flowers are green, axillary or terminal, often paniculate spikes. Amarathus viridis contains chemical constituents, [4-6] like carbohydrates, proteins, calcium, phosphorus, iron, magnesium, sodium, potassium and zinc, thiamine, riboflavin, niacin, flavonoids like rutin and quercetin. The Amarathus viridis roots contain sterol, used in snake bite; the leaves contain fatty acid like palmitic acid, carotenoids, amino acids. Traditionally [7, 8] Amarathus viridis is used as anti-inflammatory agent, vermifuge, diuretic, antirheumatic, antiulcer, analgesic, antiemetic, laxative, antilerotic, respiratory problems, eye treatment and for asthma and antiviral activity. The whole plant is used for the treatment of pain and fever. MATERIALS AND METHODS Drugs/Chemicals/Reagents All the chemicals (Ethylene glycol, Cystone, Creatinine estimation kit, Uric acid estimation kit, Electrolyte estimation kit) used were of analytical grade purchased from S. D. fine chemicals Pvt. Ltd. Bangalore. All the biochemical kit used in the study was purchased from span Diagnostics Pvt. Ltd, Surat, India. Plant Material The roots of plant Amarathus viridis was collected from Vellore and authenticated. The plant part was shade dried and crushed at room temperature. The powder obtained was extracted with distilled water. The extract obtained was stored in an air tight container for future use.
... The effects of caffeine on the kidney have been investigated in a number of studies (6,(15)(16)(17)(18)(19)(20)(21)(22)(23). Massey and Wise (24) published a pooled analysis of the experiments performed by their research group on the renal effects of an acute caffeine load in relatively small samples of healthy volunteers. ...
Article
Although caffeine intake may increase urine calcium excretion, caffeine-containing beverages have been associated with a lower risk of nephrolithiasis. We sought to determine the association between caffeine intake and the risk of incident kidney stones in 3 large prospective cohorts. We prospectively analyzed the association between intake of caffeine and incidence of kidney stones in 3 large ongoing cohort studies, the Health Professionals Follow-Up Study (HPFS) and the Nurses' Health Studies (NHS) I and II. Information on the consumption of caffeine and the incidence of kidney stones was collected by validated questionnaires. The analysis included 217,883 participants; over a median follow-up of >8 y, 4982 incident cases occurred. After multivariate adjustment for age, BMI, fluid intake, and other factors, participants in the highest quintile of caffeine intake had a 26% (95% CI: 12%, 38%) lower risk of developing stones in the HPFS cohort, a 29% lower risk (95% CI: 15%, 41%) in the NHS I cohort, and a 31% lower risk (95% CI: 18%, 42%) in the NHS II cohort (P-trend < 0.001 for all cohorts). The association remained significant in the subgroup of participants with a low or no intake of caffeinated coffee in the HPFS cohort. Among 6033 participants with 24-h urine data, the intake of caffeine was associated with higher urine volume, calcium, and potassium and with lower urine oxalate and supersaturation for calcium oxalate and uric acid. Caffeine intake is independently associated with a lower risk of incident kidney stones. © 2014 American Society for Nutrition.
... Magnesium is now relevant to maintenance of peripheral hepatic amyloid beta metabolism with magnesium levels critical to the prevention of high-cell cholesterol-induced amyloid beta formation. In NAFLD (Figure 4), caffeine consumption should be carefully controlled to prevent magnesium deficiency [117] and to assist with the reduction in hepatic fibrosis in NAFLD [118]. ...
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Nutritional diets are essential to prevent nonalcoholic fatty liver disease (NAFLD) in the global obesity and diabetes epidemic. The ingestion of palmitic acid-rich diets induces NAFLD in animal and human studies. The beneficial properties of olive oil (oleic acid) may be superseded by ingestion of palmitic acid-rich diets. Hepatic caffeine metabolism is regulated by palmitic and oleic acid with effects of these fats on amyloid beta metabolism. Healthy fats such as olive oil may facilitate rapid amyloid beta clearance in the periphery to maintain drug therapy in diabetes and various neurological diseases. Repression of the anti-aging gene sirtuin 1 (Sirt 1) prevents the beneficial properties of olive oil. Brain disorders induce NAFLD and supersede caffeine’s therapeutic effects in the prevention of NAFLD. Delayed hepatic caffeine metabolism in NAFLD and increased caffeine transport to the brain with aging-induced mitophagy in neurons with induction of type 3 diabetes and neurodegenerative disease.
... Dietary caffeine acutely increases urinary calcium loss [62], and these losses are not entirely compensated for in the 24 h after caffeine consumption [63]. In an overview on the literature of osteoporosis, a high consumption of caffeine was suggested as a risk factor for loss of bone mass and fragility fractures [64].The interaction of caffeine intake with calcium on bone loss was reported by Harris and Dawson-Hughes [65].These investigators found that bone loss from the spine and total-body bone mineral density occurred only in postmenopausal women who had both low calcium intakes (440-744 mg/d) and high caffeine intakes (450-1120 mg/d). ...
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As peace and harmony is the priority in life. This also lies in the hands of our border security. In recent years due to poor border security, the terrorist gained their access into our country and has cost many damages to life and property. If these scenario continues then the peace in the country will become no more. And therefore a well organized and stringent security has to be made sure. Here this paper comprises of a multi level security system using biometrics, Fingerprint scanning along with Iris reorganization. Therefore this implementation promises (a) Faster immigration (b) Criminals or Terrorist can be easily identified Iris and Fingerprint inputs are given by the citizens who emigrate from one country to other country. In control room identifications takes place by fusing inputs then passes the decision signal automatically. The most common unimodal biometric system, it can be seen in most of the places due to its popularity. Its reliability has decreased because it requires larger memory footprint, higher operational cost and it have slower processing speed. So by introducing Multimodal Biometric Identification System 1-3 this uses Iris and Fingerprint for security purpose4. The major advantage of this multimodal approach is that since both modalities utilized the same matcher module the memory footprint of the system is reduced 11. Integrating multiple modalities in user verification and identification leads to high performance, high reliability and high accuracy. So this technique enhances high security in border control and thus saves lives and property.
... Magnesium is now relevant to maintenance of peripheral hepatic amyloid beta metabolism with magnesium levels critical to the prevention of high-cell cholesterol-induced amyloid beta formation. In NAFLD (Figure 4), caffeine consumption should be carefully controlled to prevent magnesium deficiency [117] and to assist with the reduction in hepatic fibrosis in NAFLD [118]. ...
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Nutritional diets are essential to prevent nonalcoholic fatty liver disease (NAFLD) in the global obesity and diabetes epidemic. The ingestion of palmitic acid-rich diets induces NAFLD in animal and human studies. The beneficial properties of olive oil (oleic acid) may be superseded by ingestion of palmitic acid-rich diets. Hepatic caffeine metabolism is regulated by palmitic and oleic acid with effects of these fats on amyloid beta metabolism. Healthy fats such as olive oil may facilitate rapid amyloid beta clearance in the periphery to maintain drug therapy in diabetes and various neurological diseases. Repression of the anti-aging gene sirtuin 1 (Sirt 1) prevents the beneficial properties of olive oil. Brain disorders induce NAFLD and supersede caffeine’s therapeutic effects in the prevention of NAFLD. Delayed hepatic caffeine metabolism in NAFLD and increased caffeine transport to the brain with aging-induced mitophagy in neurons with induction of type 3 diabetes and neurodegenerative disease.
... Saturation of albumin by caffeine or theophylline interferes with plasma magnesium and calcium corrections [95,96] that are related to plasma albumin contents ( Figure 3). Caffeine excess with aging is relevant to magnesium deficiency [97][98][99] and relevant to neuron calcium dyshomeostasis [17,100] that is connected to SCN dysynchrony critical to the maintainance of circadian rhythms [7]. Disturbances in neurons by caffeine involve neuron calcium disturbances that involve the adenosine receptors, synapses and neuron networks [101,102] with detrimental effects on the central nervous system with irreversible T3D [36,37]. ...
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In the developed and developing world nutritional interventions have become essential to prevent global Non Alcoholic Fatty Liver Disease (NAFLD) and to maintain the metabolism of glucose, fatty acids, cholesterol, amyloid beta, bile acids and xenobiotics. The World Health Organization (WHO) has reported that cardiovascular disease is the most prevalent global chronic disease that may be connected to NAFLD and the alarming death rate in various communities. Caffeine (appetite suppressant) may improve the adipose tissue- liver cross talk with the prevention of NAFLD in obese and Type 2 diabetic populations. Overeating may accelerate chronic diseases with repression of anti-aging genes linked to NAFLD and delayed caffeine clearance linked to the induction of Type 3 diabetes in global populations. Nutritional interventions to reverse NAFLD in the developing world are associated with accelerated caffeine clearance rates with prevention of caffeine induced mitochondrial apoptosis that is linked to early neuron loss and the development of Type 3 diabetes in these populations.
... После приема второй дозы кофеина содержание магния в моче резко возрастало до 16:00; в период с 16:00 до 1:00 следующих суток не было отмечено достоверного повышения экскреции магния. В целом было показано, что потребление кофеина усиливало суточные потери магния с мочой [33]. ...
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Высокое содержание магния в тех или иных продуктах питания не находится в прямой взаимосвязи с уровнем усвоения магния. Продукты питания могут содержать такие компоненты, как фитиновая кислота, щавелевая кислота, кальций, которые существенно затрудняют всасывание магния из этих продуктов питания. Ксантины (в составе кофе или крепкого чая), синтетические пищевые добавки и алкоголь приводят к усилению потерь магния с мочой. В то же время, например, ину- линовые олигосахариды повышают всасывание магния из продуктов питания. Прием пищи, не содержащей упоминаемых выше ингибиторов всасывания магния, улучшает всасывание магния из раствора (например, из минеральной воды).
... The major side effects of caffeine overconsumption (Figure 1) leads to magnesium and calcium deficiency [47] with relevance to insulin resistance and corruption of the peripheral sink Aβ clearance pathways [48] . Magnesium is a Sirt 1 activator with caffeine responsible for low brain magnesium levels and induction of Type 3 diabetes [5,6,43] . ...
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EDITORIAL The main constituent of plaques in the brain of Alzheimer's disease (AD) individuals namely amyloid beta (Aβ) [1] is a pro-teolytic product of a larger protein, the amyloid precursor protein (APP) protein. Carriers of the apo E4 allele are at greater risk of developing AD with increased deposition of amyloid beta plaques in Western countries. Apo E4 is also a major risk factor for cardiovascular disease linked to defective cholesterol metabolism [2,3]. Protein and Aβ homeostasis is now crucial to the lifespan of organisms and is an important feature that determines the aging process in obesity, diabetes and neurodegenerative diseases [4]. The scientific understanding of the maintenance of peripheral blood plasma Aβ metabolism has now become essential to prevent neurodegeneration and is now linked to Type 3 diabetes [5,6]. The concentration of Aβ within the brain is determined by hepatic Aβ clearance and interest in the liver has increased markedly since in Western countries the incidence of non-alcoholic fatty liver disease (NAFLD) has reached approx. 20% of the developed world and by the year 2050 it may reach to approx. 40% of the global population [7]. Induction of Type 3 diabetes disease progression now involves unhealthy diets that corrupts neuron calcium flux and the circadian rhythm of the neuron Aβ peptide [8-13] connected to defective peripheral hepatic glucose and Aβ metabolism [4] in individuals with NAFLD [4]. The liver is of principal importance and the mechanisms for the clearance of Aβ by the liver involve lipoproteins (5%) and albumin (90%) which bind and sequester Aβ for clearance to the liver, preventing the toxic effects of Aβ to the heart and brain [4]. Caffeine is hydrophobic and increased consumption can rapidly allow distribution to the liver and adipose tissue with rapid transport across the blood brain barrier to neurons [14-17]. In adipose tissue caffeine has been shown to increase adinopectin levels with relevance to anti-aging gene activation [18-20] and the adipose tissue-liver crosstalk [21]. Caffeine has become important to peripheral Aβ metabolism with suppression of plasma and brain Aβ in AD transgenic mice [22,23] and beneficial effects involve prevention of bacterial lipopolysaccharides (LPS) induction of inflammation and Aβ aggregation [24,25]. In the developing world increased plasma LPS levels may override caffeine effects with spontaneous Aβ aggregation [26,27]. Caffeine consumption over many years' effects cerebrospinal fluid production (CSF) and increased caffeine binding to albumin may displace Aβ from CSF albumin and mediate toxic effects on Aβ oligomer generation relevant to the development of Type 3 diabetes and various neurological diseases [28-31]. In global NAFLD epidemic caffeine metabolism is markedly reduced and metabolism of caffeine (4-6 hr) delayed (Figure 1) with increased transport of caffeine to the brain with effects on altered neuron calcium signalling relevant to the induction of Type 3 diabetes and circadian rhythm abnormalities [14-16,32-36]. Caffeine is metabolized mostly by the P450 enzyme system in the body and specifically the CYP1A enzymes (CYP1A1, 1A2) [37,38]. The metabolism by hepatic CYP1A enzymes of caffeine follows first-order kinetics and is the rate-limiting step of plasma clearance [37,38]. Interest in the anti-aging gene Sirtuin 1 (Sirt 1) in neuron transcrip-tional responses has accelerated with relevance to Type 3 diabetes [5,6] and the gene Sirt 1 is now connected to the development of NAFLD [39,40] with its deacetylation of nuclear pregnane X receptor (PXR) relevant to drug metabolism [39]. Sirt 1/PXR interactions are now important to the regulation of the CYP1A enzymes [37,38] with rapid metabolism of caffeine in individuals without NAFLD. Caffeine consumption (coffee, coca cola, chocolate, tea, other sources) that was previously recommended to be approx. 200 mg
Chapter
This chapter examines the evidence that caffeine consumption increases the risk of hip fracture, decreases bone mineral density, and negatively influences calcium retention. Among adults living in the United States, coffee is by far the most important source of caffeine (Fig. 17.1). A cup of coffee contains approximately 103 mg of caffeine, although this amount is highly variable, and average servings of tea and cola beverages contain about 36 mg and 46 mg, respectively. Many of the results in this chapter are presented in terms of “cup of coffee equivalents” equal to 103 mg of caffeine, regardless of the source.
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The purpose of this study was to explore the association of serum caffeine concentrations with serum glucose levels in caffeine-drug users and non-users, aiming at the chronic effects of caffeine on glucose metabolism in comparison with known acute effects of caffeine. Eight hundred and fourteen caffeine-drug users and 623 non-users were identified from German National Health Surveys. Their serum caffeine concentrations and glucose levels were measured. The associations of caffeine concentrations with glucose levels were established by correlation analysis and multivariable regression analysis in caffeine-drug users and non-users separately. Antidiabetic therapy was considered. Caffeine concentrations were closely positively correlated to serum glucose levels in caffeine-drug users (Spearman r = 0.117, p = 0.001; partial r = 0.102, p = 0.020) particularly in women (Spearman r = 0.155, p < 0.001; partial r = 0.150, p = 0.005) although the correlation was weak as shown by multivariable regression analysis. The serum glucose levels were significantly higher (5.403 +/- 0.033 vs. 5.306 +/- 0.037 mmol/l) whereas the magnesium level was significantly lower (0.8941 +/- 0.0026 vs. 0.9024 +/- 0.0030 mmol/l) in caffeine-drug users than in non-users. No associations of caffeine concentrations with serum glucose levels were found in any groups of caffeine-drug non-users in our study. Whereas acute intake of caffeine-drugs may impair glucose metabolism, chronic intake of caffeine exclusively from diet has little effects on glucose metabolism and therefore may not contribute to the risk reduction of type 2 diabetes that was found in recent coffee consumption studies.
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The consumption of caffeine has been linked to osteoporosis, believed to be due to enhanced bone resorption as a result of increased calcium excretion in the urine. However, the amount of calcium in the urine may not necessarily reflect the true effect of caffeine on calcium clearance. This study therefore examined the impact of high‐dose, short‐term caffeine intake on renal clearance of calcium, sodium and creatinine in healthy adults. In a double‐blind clinical study, participants chewed caffeine (n=12) or placebo (n=12) gum for 5 min at 2‐hour intervals over a 6‐hour treatment period (800mg total caffeine). Caffeine increased renal calcium clearance by 77%. Furthermore, the effect was positively correlated with sodium clearance and urine volume, suggesting that caffeine may act through inhibition of sodium reabsorption in the proximal convoluted tubule. This study confirmed that caffeine does increase renal calcium clearance and fosters the further investigation into safe consumption of caffeine.
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Caffeine increases urinary calcium (ca) excretion in nonstone formers. We designed a study to determine the effect of caffeine consumption on urinary composition in stone formers. A total of 39 normocalcemic patients with calcium stones consumed caffeine (6 mg/kg lean body mass) after 14 hours of fasting. Urinary composition was compared 2 hours before and 2 hours after caffeine consumption. Control subjects included 9 nonstone formers studied contemporaneously with patients plus data from 39 nonstone formers from previous studies matched to each patient by level of fasting calcium/creatinine (Cr), gender and age. Caffeine increased urinary Ca/Cr, magnesium/Cr, citrate/Cr and sodium/Cr but not oxalate/Cr in stone formers and controls. The Tiselius stone risk index for calcium oxalate precipitation increased from 2.4 to 3.1 in stone formers and from 1.7 to 2.5 in nonstone formers. Of the 39 stone formers 32 had an increased Tiselius risk index after caffeine. Post-caffeine increases in Ca/Cr and Na/Cr were highly correlated. Caffeine consumption may modestly increase risk of calcium oxalate stone formation.
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This 6-week study was designed to determine the effects of graded doses of caffeine intake (3, 25 or 100 mg/kg per day) on the metabolic balance and tissue concentrations of fluoride, calcium and phosphorus in Sprague-Dawley rats. Caffeine intake did not affect the absorption, urinary excretion or balance of fluoride, the plasma, bone or enamel concentrations of fluoride, nor the occurrence of incisor enamel fluorosis. Neither did it affect the metabolism of calcium or phosphorus except that the urinary excretion of calcium was increased. This effect, however, was not sufficient to influence significantly calcium balance. The ash content of the femur epiphysis and bone mineral content of the tibia were significantly reduced only in the group exposed to the highest dose of caffeine. These effects on bone were not significantly related to the balance of calcium or phosphorus. It was concluded that caffeine, even at an extremely high level of intake, has no detectable effect on the balance or tissue concentrations of fluoride, calcium or phosphorus in the rat.
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Coffee is widely consumed and appreciated all over the world, both for their stimulating effect and organoleptic characteristics. Due to its complex chemical composition and the factors involving brews preparation, the consumer is exposed to a wide range of chemical compounds. Several investigations aimed to clarify and understand coffee health effects. There is no evidence that moderate consumption could be harmful. On the contrary, some benefits and possible protective effects against several pathologies have been suggested. This review compiles the main conclusions related with the "coffee and health" topic, reporting, when possible, the chemicals involved.
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The per capita consumption of carbonated soft drink has increased over the years especially among the pediatric population. This review attempts to give an insight of the impact of soft drinks on child's health and suggests some alternative for a healthy life style. Various research studies have shown that children consuming soft drinks have developed various acute and chronic ill effects such as nutritional deficiency, obesity, dental diseases, bone pathologies & psychological illness. As rightly said "an ounce of prevention is better than a pound cure", Government, parents, teachers, health professionals & mainly manufacturing companies should play a crucial role in solving the problems related to soft drink consumption.
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IntroductionObjectives and ScopeCoffee ConsumptionCoffee and CancerCoffee and Cardiovascular DiseaseCoffee and Bone HealthReproductive and Developmental Potentials of Coffee and CaffeineEmerging Benefical Health EffectsCoffee Consumption - Safety ConsiderationsConclusions References
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Purpose: The popularity of bottled water products (BWPs) is growing in Canada. Concentrations of minerals with important implications for health were compared in different types of BWPs. Methods: One sample of each brand and type of plain BWP (purified, remineralized, spring, mineral, and artesian), flavoured BWP, and nutrient-enriched BWP sold in major stores in Ottawa, Ontario, was purchased to allow determination of mineral concentrations by flame atomic absorption or emission spectroscopy. A total of 124 BWPs representing 37 brands were analyzed. Results: In general, spring and mineral water contained higher amounts of magnesium and calcium than did purified, remineralized, artesian, flavoured, or nutrient-enriched water. Most plain BWPs contained little sodium and potassium, whereas 15% to 35% of flavoured and nutrient-enriched products had considerably higher concentrations. Only magnesium and calcium concentrations were highly correlated (r=0.76, p<0.001). Calculation of the percentage of Dietary Reference Intakes that could be supplied by each product revealed that, if they are consumed habitually, many products can contribute substantially to recommended intakes of these minerals. Conclusions: Mineral concentrations in most types of BWP varied, but distinct differences between types of products were identified. Consumers should be aware of the mineral content of BWPs because some could influence intakes of certain minerals significantly.
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Background Maternal mortality remains a challenge in India. The current maternal mortality rate in India is 254 (India statistics, WHO, 2005). In Andhra Pradesh, the maternal mortality rate is 154 (2009) and the 2015 target is to reach below 100. The Each One save One (EOSO) program believes that no mother and child should lose their life in the natural process of childbirth. EOSO aims to reduce the incidence of maternal mortality in Andhra Pradesh by training student nurses on safe birthing practices. Aims The goals of the program are 1) to increase knowledge on safe birth practices among student nurses in Andhra Pradesh, India. 2) To improve the ability of nurses to identify complications during labor and to take quick action. And the objectives were that at the end of the program, 80% of the nurse participants at Modern Government Maternity Hospital will have an increase in knowledge about safe childbirth practices and complications. Material and Methods The program was run from 1st July 2010 to 30th August 2010. The program was targeted to the final year Bsc students of NIMS College and Laxmi College of nursing. The classes were conducted at the Modern Government Maternity Hospital, Hyderabad. There were a total of 61 nurses who attended the training modules. The program includes four educational training modules. Result The mean score on pretests was 7, and the mean score on post test was 10. A paired t-test conducted on participants who took both pre and post test, showed the result to be statistically significant (p < 0.05). By the end of the program, 91% of the nurses had increase in knowledge, when compared with the pretest. Conclusion The Each One Save One program can be used to educate more student nurses throughout Andhra Pradesh and the other states of India, where there is a lack of instructors. Our study shows that there was significant increase in knowledge among the nurses following the intervention program. This knowledge when converted to action will help in reducing maternal mortality rates.
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The determination of calcium in biologic fluids by atomic absorption spectrophotometry is interfered with by the presence of protein, cations, and those anions that form complexes with calcium. Such interference was overcome when lanthanum was included in a 1:50 dilution of serum or urine. Recovery of calcium added to calcium-free serum was 100%. The S.D. based on double-blind duplicates was 0.22 mg./lOO ml. Excellent statistical agreement was found between the test method and each of the 2 reference methods.
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Oral doses of caffeine increase the urinary excretion of calcium, magnesium, sodium and chloride for at least 3 h after consumption. The hypercalciuric effect can be blocked by adenosine receptor agonists. The effect is proportional to dose per lean body mass and no adaptation to the urinary losses occurs with continuing consumption of caffeine. Uncompensated losses of calcium would be a risk factor for development of osteoporosis. Risks of osteoporosis due to caffeine consumption are reviewed. Comparison of data from epidemiological surveys and animal and human studies suggests that for younger adult women consuming adequate calcium, moderate caffeine intakes may have little or no deleterious effects. Increased urinary and intestinal losses may be compensated for by increased intestinal calcium absorption. However older women do not seem to compensate adequately to maintain their former calcium balance, especially when calcium intakes are below recommendations.
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We propose a parametric pharmacokinetic-pharmacodynamic model for caffeine that quantifies the development of tolerance to the pressor effect of the drug and characterizes the mean behavior and inter-individual variation of both pharmacokinetics and pressor effect. Our study in a small group of subjects indicates that acute tolerance develops to the pressor effect of caffeine and that both the pressor effect and tolerance occur after some time delay relative to changes in plasma caffeine concentration. The half-life of equilibration of effect with plasma caffeine concentration is about 20 minutes. The half-life of development and regression of tolerance is estimated to be about 1 hour, and the model suggests that tolerance, at its fullest, causes more than a 90% reduction of initial (nontolerant) effect. Whereas tolerance to the pressor effect of caffeine develops in habitual coffee drinkers, the pressor response is regained after relatively brief periods of abstinence. Because of the rapid development and regression of tolerance, the pressor response to caffeine depends on how much caffeine is consumed, the schedule of consumption, and the elimination half-life of caffeine.
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A rapid method for simultaneous determination of caffeine and theophylline from the serum, saliva, or spinal fluid of neonates was developed. Fifty-microliter samples were extracted and analyzed by high-pressure liquid chromatography (HPLC) at a low accurately detectable limit of 0.1 mg/liter. The sample preparation time was about 40 minutes. Instrumental analysis was performed in less than 10 minutes. Extraction efficiency from repeated analyses was determined to be 95 ± A precolumn was used to increase the life of the analytical column. The EMIT-aad® method was compared to HPLC analysis and found to be less efficient.
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Twelve female college students drank decaffeinated coffee or tea to which 0, 150 or 300 mg caffeine had been added. Each subject had fasted at least ten hours before drinking each of the three test beverages. Urine samples were collected at one, two and three hours after caffeine consumption. Total urinary three hour excretion of calcium, magnesium and sodium, but not potassium, increased significantly after caffeine intake. The increased output of calcium and sodium was mainly due to significantly increased urinary calcium and sodium concentrations, while the increased output of magnesium appeared to be due to the combination of both a slightly increased urinary magnesium concentration and volume. Total urine volume correlated significantly with dose of caffeine per body weight when 300 mg of caffeine was consumed. The effects of caffeine on mineral excretion were primarily due to changes in mineral concentration and increased urinary volume at one and two hours.
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Urinary excretion of water, calcium, magnesium, potassium, sodium and chloride are increased for two hours after caffeine consumption in several different human populations of differing age and gender. The results of six previous studies were combined in order to investigate possible differences in response to caffeine-induced water and mineral excretion due to age or gender. 144 subjects were included: 92 females and 52 males, mean age 43 year, range 13–78. Each fasting subject drank a beverage on two separate mornings, one without caffeine and a second to which 6 mg/kg lean body mass caffeine was added, then urine was collected for two hours afterwards. Preload fasting total mineral and creatinine excretion was lower in women than men and increased with age. Urinary excretion of creatinine and phosphorus was not affected by caffeine. When mineral excretion was expressed as ratios to creatinine or increments above preload excretions, both genders had similar, significant caffeine-induced increases in water, calcium, magnesium, potassium, sodium and chloride excretion. Neither gender or age impacted urinary mineral excretion response to acute caffeine doses when expressed per creatinine excretion or incremental excretion.
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Seventeen young women aged 24.4±3.8 years abstained from dietary methylxanthines for 3 weeks. Two urine collections were made on day 7 of each week: 1 hour after drinking 120 ml water, then 2 hours after 240 ml decaffeinated beverage. During the control week subjects had no caffeine during the week or day 7. For the “abstention” week no caffeine was consumed during the week then 6 mg caffeine per kg lean body mass (LBM) was consumed on day 7 in the second beverage. During an “adaptation” week subjects consumed 300 mg caffeine daily, then on day 7, 6 mg caffeine/kg LBM was consumed. After both abstention and adaptation weeks, addition of caffeine significantly increased excretion from 2.9 to 6.7 mg Ca/hr (p<.0001). Caffeine similarly affected urinary magnesium (p<.0001) and sodium (p<.005). Basal fasting excretion rates for the hour before the second beverage were similar for each mineral for all periods. There were no differences for post-caffeine urinary calcium, magnesium and sodium excretion rates between caffeine-naive and caffeine-adapted weeks. Young women chronically consuming 300 mg caffeine/day continued to excrete increased calcium, magnesium and sodium after a caffeine challenge when compared to a caffeine-free week. Thus, there is no indication of conservation of urinary calcium excretion with continuing caffeine use after short-term adaptation.
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Fifteen males drank decaffeinated coffee to which 0, 150 or 300 mg caffeine had been added. Each subject had fasted at least ten hours before drinking each of the three test beverages. Urine samples were collected at one, two and three hours after caffeine consumption. Total urinary three hour excretion of calcium, magnesium, sodium and chloride increased significantly after caffeine intake, while zinc, phosphorus, potassium, creatinine and volume were unchanged. The increased outputs were due to increased urinary mineral concentrations.
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The rate of bone loss with age and the incidence of osteoporosis are greater in women than men, which led us to question whether subtle sex differences may occur in the circadian variation of serum ionized calcium (iCa) and PTH. We measured iCa hourly and intact PTH every 2 h for 26 h in 25 women (21-69 yr) and 24 men (20-67 yr) consuming self-selected diets. Urine was collected at 0800-1600, 1600-2400, and 2400-0800 h. Serum iCa levels followed a circadian rhythm in both sexes (P less than or equal to 0.01), and the patterns differed between sexes, notably during early morning, when serum iCa levels were lower in women (P = 0.02). Urinary calcium excretion and fractional excretion of calcium declined in both sexes at night (2400-0800 h), but the decline in men was significantly greater (P = 0.02). Similarly, the percent reduction in urinary calcium excretion at night was greater in men than in women (34% vs. 17%; P less than or equal to 0.05). In women, 26-h mean serum iCa values correlated significantly with total daily calcium intake (r = 0.44; P = 0.03). Serum intact PTH levels showed a significant circadian pattern in both sexes (P less than or equal to 0.001). The patterns of serum intact PTH differed between the sexes (P = 0.05), with an earlier and greater increase at night in men. This blunted nocturnal rise in PTH in women may explain the poor nocturnal adaptation to fasting found in women who, despite lower calcium intake, did not reduce urinary calcium loss at night as effectively as men.
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Serum osteocalcin varies in a diurnal rhythm, with peak values during the night and minimum levels before noon, but the factors controlling this rhythm are unknown. In this study, we evaluated the temporal relations between the osteocalcin rhythm and variations in serum concentrations of cortisol, intact parathyroid hormone (PTH(1-84)), and ionized calcium (Ca2+) in 15 normal volunteers, aged 22-46 years. Serum cortisol varied in a typical way preceding inverse changes in serum osteocalcin by about 4 h (r = 0.78, p less than 0.0001). Changes in serum osteocalcin following the early morning increase in serum cortisol were statistically indistinguishable from the changes seen after oral administration of 2.5 or 10 mg of prednisone. Serum PTH (1-84) showed a diurnal rhythm (p less than 0.01) with peak values (4.06 +/- 0.42 pmol/l) at 20.30 h and nadir (2.81 +/- 0.10 pmol/l) around 10.30 h, preceding changes in serum osteocalcin in the same direction by 5 h (r = 0.55, p less than 0.02). Prednisone at a dose of 10 mg did not change the time course significantly. Serum Ca2+ varied in an almost bi-phasic pattern (p less than 0.01) with maximal mean levels around 16.30 and 09.30 h and minimal levels around 05.30 and 14.30 h. Serum Ca2+ correlated inversely with PTH (1-84) (r = 0.53, p less than 0.01), and serum osteocalcin was inversely related to Ca2+ at concurrent time points (r = 0.59, p less than 0.005). Prednisone caused a 2-3 h lasting increase in serum Ca2+ 3-5 h after ingestion (p less than 0.001). In conclusion, our results suggest that cortisol is strongly associated to the diurnal rhythm in serum osteocalcin. The biological relevance of the reported relation between serum osteocalcin and PTH (1-84) and serum Ca2+ is uncertain.
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Hepatic microsomal function was assessed by a caffeine clearance test at night and during the day using saliva and serum samples obtained simultaneously. In 26 patients with cirrhosis, 21 patients with noncirrhotic liver disease and 15 control subjects caffeine elimination correlated well during the day and at night (r = 0.915 for serum and 0.917 for saliva). The correlation coefficients for caffeine clearance in saliva and serum were 0.940 during the day and 0.963 overnight. In the cirrhotic patients, clearance differed significantly from noncirrhotic liver disease and controls in saliva samples overnight: 0.51 +/- 0.45 ml/min per kg versus 0.91 +/- 0.44 and 1.41 +/- 0.56, respectively. Comparable results were obtained for serum clearance overnight and clearances during the day. Serum and saliva clearances at night correlated well with the aminopyrine breath test (rs = 0.884 and 0.907, respectively). Overnight caffeine clearance in saliva might be a simple useful method for assessing progression and prognosis of liver disease.
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Thirty-seven women, aged 31-78 years, on two separate mornings consumed a decaffeinated beverage to which 6 mg caffeine/kg lean body mass or no caffeine were added. Total urine output of water, calcium, magnesium, sodium, chloride, potassium and creatinine increased in the two hours following caffeine ingestion when compared to the control beverage. Increased urinary mineral (mg)/urinary creatinine (g) ratios were seen for calcium (120 to 200), magnesium (70 to 110), sodium (3,800 to 6,200) and chloride (9,200 to 14,800), following the caffeinated beverage. Creatinine clearance did not change significantly. The percent reabsorption of calcium (98.6% to 97.5%, p less than .001) and magnesium (97.0% to 94.2%, p less than .0001) decreased significantly during the post-caffeine period. The calcium and magnesium filtered loads did not differ significantly between the caffeine and no caffeine beverages. Therefore, caffeine-induced urinary loss of calcium and magnesium is largely attributable to a reduction in calcium and magnesium renal reabsorption, although the physiological mechanism and tubular segment affected remain to be established.
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We examined directly the effects of a moderate dosage of caffeine (400 mg/d) on the calcium economy in 16 healthy premenopausal women in a double-blind, placebo-controlled crossover design. The subjects took divided doses of caffeine (100 mg/tablet) or identical-appearing placebos with decaffeinated coffee on personalized schedules for treatment periods lasting 19 d each and with 37-d interstudy intervals. We randomized the treatment sequence among subjects and studied them as inpatients under metabolic-balance conditions. We found no significant effects of caffeine on fractional calcium absorption, endogenous fecal calcium, or urine calcium, whether examined day by day or cumulatively. Although the mean balance shift was negative, the change was not significantly different from zero. There was evidence of altered bone remodeling, with slight decreases in bone accretion, bone resorption, and calcium pool turnover.
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A highly selective and specific method for determining caffeine levels in plasma and saliva is described. The method is a microscale procedure that requires only 25 microliters of specimen, although the assay can be performed with as little as 10 microliters of the specimen and is therefore, particularly suitable for monitoring caffeine levels in the neonates. The method is sensitive to 0.5 microgram/ml and is specific for caffeine as none of the other xanthines shows any interference. The method is also fast as treatment of specimen requires only precipitation of proteins and thus is ideal for use in hospital and clinical laboratories.
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The temporal relationships between the circadian rhythms of serum PTH, total calcium (Cat), and phosphate (Pi) and plasma ionized calcium (Cai) concentrations were determined in 9 normal men. Blood samples were collected every half hour for 24 h. Serum PTH was measured by an RIA specific for the midregion of the molecule. The mean circadian pattern for each variable was derived by calculating the average value across all men at concurrent time points. After the data were smoothed by the method of running means, the correlations between PTH and mineral values from concurrent time points were calculated, as were cross-correlations to 12 lag periods (6 h). Spectral and cross-spectral analyses were performed on the same data set. Both statistical methods yielded consistent results: 1) at concurrent time points (0 lag), high correlations were found between serum PTH and Cat (r = -0.74), PTH and Pi (r = 0.79), and PTH and Cai (r = -0.53); and 2) when the PTH series was lagged by 2 h, the PTH/Cai correlation improved to -0.70. A direct PTH/Cai correlation of 0.50 was found when the Cai series was lagged about 4.5 h. No improvement in the correlations were found when the other series were lagged. Spectral analyses also detected significant interrelations between PTH and Cai at 2 and 3.5 h. These data describe the timing of the bidirectional interaction between serum PTH and plasma Cai under steady state conditions in normal adult men; changes in Cai concentrations precede inverse changes in PTH levels by 2 h, whereas changes in PTH precede similar directional alterations in Cai by about 4 h.
Article
A circadian variation in serum calcium, albumin and PTH concentration in normal subjects has been demonstrated. The levels of the three blood constituents were remarkably constant during the day, but striking night and early morning changes occurred. Serum calcium levels were highest at 8:00 p.m. and reached a nadir between 2:00 and 4:00 a.m. Serum albumin levels were parallel to those of serum calcium. PTH levels began to rise after 8:00 p.m., reached the highest levels between 2:00 and 4:00 a.m., and fell to baseline values by 8:00 a.m. The nocturnal fall in serum calcium levels appears to be secondary to dilution of serum proteins by increasing blood volume. The nocturnal rise in PTH levels appears to be independent of serum calcium levels within the normal range but it can be abolished by induced hypercalcemia. Serum phosphate levels were lowest between 8:00 a.m. and 10:00 a.m. and highest between 2:00 a.m. and 4:00 a.m. The data presented suggest that circadian changes in serum phosphate levels are not mediated in toto by parathyroid hormone but they are exaggerated when the secretion of this hormone is inhibited. They are independent of growth hormone levels and activity but they are greatly modified during a prolonged fast.
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Diurnal variations in calcium and magnesium excretion have been demonstrated in patients in a metabolism ward whose meals were eaten between 8 a.m. and 5:30 p.m. except for a light snack at 10 p.m. A reduction in the excretion of calcium, magnesium, sodium, and creatinine at night was observed, the decrease in calcium being proportionately greater than in other constituents. A diurnal rhythm in phosphaturia was variable being greater at night in some and less in others. Slight but consistent diurnal variations were observed in the blood serum concentrations of calcium and magnesium with lower values in the morning than in the evening. It is concluded that diet and physical activity play the dominant roles in this diurnal fluctuation, but it is suggested that there may possibly be a rhythmicity in parathyroid function as well.
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Blood volume was measured in 66 healthy subjects (38 males, 28 females), and extracellular fluid volume in 54 subjects (31 males, 23 females). Volumes were normalized against body weight, height, body surface area, leanness index, and lean body mass (estimated from body weight and height). The regression lines of body fluid volumes against lean body mass passed through the origin on extrapolation and were not different for males and females. None of the other indices fulfilled these criteria. It is concluded that estimated lean body mass is a suitable index for normalization of body fluid volumes. A single set of normal reference values can be used for males and females.
Article
The effects of different levels of nitrogen, phosphorus, and caffeine intake on calcium balance and on certain of its components were assessed in 170 studies in normal middle-aged, but still premenopausal women. Statistically significant negative associations with calcium balance were found for nitrogen and for caffeine, but no effect could be found for phosphorus. Higher nitrogen intakes were associated with proportionately higher levels of urinary calcium; higher phosphorus intake was associated with slightly lower levels of urinary calcium but also with slightly more intestinal secretion of calcium. Since these two effects were opposite in direction, there was no net association of different phosphorus intakes with calcium balance. Caffeine intake was associated with higher levels of both urinary calcium and intestinal calcium secretion. None of the three intake variables was associated with differences in calcium absorption efficiency. Both the nitrogen and the caffeine effects were proportional to intake. The magnitude of the effects observed was such that a 50% increase in intake of nitrogen above the group mean intake value would be predicted to result in calcium balance shift of -0.032 gm/day. For caffeine, the corresponding calcium balance shift would be predicted to be -0.006 gm/day.
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The primary objective of this study was to test the hypothesis that endogenous adenosine/A1 receptor interactions participate in the normal regulation of the cardiovascular system and kidneys. In anesthetized rats, we examined the effects of pharmacologically equivalent doses of DPCPX and FK453 (two structurally dissimilar A1 receptor antagonists) and the effects of FR113452 (the less active enantiomer of FK453) on 20 hemodynamic and renal function parameters. After baseline measurements, animals were randomized to an intravenous infusion of either vehicle or DPCPX, FK453, or FR113452 (10, 30, and 30 micrograms/kg/min, respectively), and all measurements were repeated. Neither DPCPX, FK453, nor FR113452 affected significantly the heart rate; cardiac output; stroke volume; arterial blood pressure; total vascular resistance; regional blood flows to and regional vascular resistances of the carotid, mesenteric, renal, and hindquarter vascular beds; glomerular filtration rate; filtration fraction; or potassium excretion. However, DPCPX and FK453, but not FR113452, caused a pronounced diuresis (from 194 +/- 30 to 696 +/- 144 microliters/30 min for DPCPX, and from 386 +/- 76 to 814 +/- 156 microliters/30 min for FK453) and natriuresis (from 0.88 +/- 0.30 to 5.09 +/- 1.28 mumol/min for DPCPX, and from 1.58 +/- 0.56 to 5.09 +/- 1.02 mumol/min for FK453). These results firmly establish that (a) endogenous adenosine/A1 receptor interactions regulate renal excretory function, (b) this regulation is via a renal tubular, rather than hemodynamic, mechanism, and (c) A1 receptor antagonists caused diuresis without disturbing potassium homeostasis.
Article
The diurnal variations in blood and urine calcium and phosphate were measured in five normal individuals under standardized conditions of calcium intake. A remarkably constant plasma calcium level was observed in all subjects, urinary calcium excretion rates rose during the day and fell during the night. The plasma phosphate showed greater diurnal variation; typically, there was a morning fall in plasma phosphate followed by an afternoon and evening rise. The diurnal pattern of urinary phosphate was one of a low morning excretion rate followed by an afternoon and evening rise. An increase in dietary calcium was followed by a corresponding increase in urinary calcium within 3 to 5 days and a minimal rise in plasma calcium, the significance of which varied from patient to patient.