The Constitutionality of Punitive Damages Under the Excessive Fines Clause of the Eighth Amendment

This Note explores whether courts should look beyond the broad language in Ingraham v. Wright and scrutinize punitive damages under the excessive fines clause. Part I sets out the intuitive argument that punitive damages are analogous to criminal fines. Part II analyzes the Supreme Court\u27s decision in Ingraham v. Wright and also reviews the few federal and state court decisions that have dealt with the excessive fines clause in civil cases, most of which have concluded that the clause has no application in a civil setting. This Part asserts that courts cannot rely solely on the Ingraham decision but must examine the history of the excessive fines clause and the penal character of punitive damages. Part III pursues the analysis that is lacking in those decisions which have relied on Ingraham. First, this Part sketches the history of the eighth amendment to determine whether the excessive fines clause should apply only to criminal fines and not civil punitive damages or whether the clause expresses a broader principle requiring proportionality in punishments of any form. Second, this Part questions whether punitive damages are sufficiently penal to implicate eighth amendment scrutiny. Part III suggests that courts apply the analysis outlined in Kennedy v. Mendoza-Martinez, rather than Ingraham. Finally, Part IV concludes that, since the excessive fines clause is historically linked to civil monetary penalties and since punitive damages are penal in nature, excessive awards violate the eighth amendment\u27s principle of proportionality in punishments. This Note contends that the eighth amendment, unlike other constitutional protections, functions as a restraint on the broader system of punishment rather than simply the process through which criminals are prosecuted. It argues that courts should determine whether punitive damages are sufficiently penal to warrant eighth amendment protection and not whether punitive damages are criminal or quasi-criminal sanctions

Altitude Acclimatization Alleviates the Hypoxia-Induced Suppression of Exogenous Glucose Oxidation During Steady-State Aerobic Exercise

This study investigated how high-altitude (HA, 4300 m) acclimatization affected exogenous glucose oxidation during aerobic exercise. Sea-level (SL) residents (n = 14 men) performed 80-min, metabolically matched exercise (V˙O2 ∼ 1.7 L/min) at SL and at HA < 5 h after arrival (acute HA, AHA) and following 22-d of HA acclimatization (chronic HA, CHA). During HA acclimatization, participants sustained a controlled negative energy balance (-40%) to simulate the “real world” conditions that lowlanders typically experience during HA sojourns. During exercise, participants consumed carbohydrate (CHO, n = 8, 65.25 g fructose + 79.75 g glucose, 1.8 g carbohydrate/min) or placebo (PLA, n = 6). Total carbohydrate oxidation was determined by indirect calorimetry and exogenous glucose oxidation by tracer technique with 13C. Participants lost (P ≤ 0.05, mean ± SD) 7.9 ± 1.9 kg body mass during the HA acclimatization and energy deficit period. In CHO, total exogenous glucose oxidized during the final 40 min of exercise was lower (P < 0.01) at AHA (7.4 ± 3.7 g) than SL (15.3 ± 2.2 g) and CHA (12.4 ± 2.3 g), but there were no differences between SL and CHA. Blood glucose and insulin increased (P ≤ 0.05) during the first 20 min of exercise in CHO, but not PLA. In CHO, glucose declined to pre-exercise concentrations as exercise continued at SL, but remained elevated (P ≤ 0.05) throughout exercise at AHA and CHA. Insulin increased during exercise in CHO, but the increase was greater (P ≤ 0.05) at AHA than at SL and CHA, which did not differ. Thus, while acute hypoxia suppressed exogenous glucose oxidation during steady-state aerobic exercise, that hypoxic suppression is alleviated following altitude acclimatization and concomitant negative energy balance

Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

The Constitutionality of Punitive Damages Under the Excessive Fines Clause of the Eighth Amendment

This Note explores whether courts should look beyond the broad language in Ingraham v. Wright and scrutinize punitive damages under the excessive fines clause. Part I sets out the intuitive argument that punitive damages are analogous to criminal fines. Part II analyzes the Supreme Court\u27s decision in Ingraham v. Wright and also reviews the few federal and state court decisions that have dealt with the excessive fines clause in civil cases, most of which have concluded that the clause has no application in a civil setting. This Part asserts that courts cannot rely solely on the Ingraham decision but must examine the history of the excessive fines clause and the penal character of punitive damages. Part III pursues the analysis that is lacking in those decisions which have relied on Ingraham. First, this Part sketches the history of the eighth amendment to determine whether the excessive fines clause should apply only to criminal fines and not civil punitive damages or whether the clause expresses a broader principle requiring proportionality in punishments of any form. Second, this Part questions whether punitive damages are sufficiently penal to implicate eighth amendment scrutiny. Part III suggests that courts apply the analysis outlined in Kennedy v. Mendoza-Martinez, rather than Ingraham. Finally, Part IV concludes that, since the excessive fines clause is historically linked to civil monetary penalties and since punitive damages are penal in nature, excessive awards violate the eighth amendment\u27s principle of proportionality in punishments. This Note contends that the eighth amendment, unlike other constitutional protections, functions as a restraint on the broader system of punishment rather than simply the process through which criminals are prosecuted. It argues that courts should determine whether punitive damages are sufficiently penal to warrant eighth amendment protection and not whether punitive damages are criminal or quasi-criminal sanctions

Effects of carbohydrate supplementation on aerobic exercise performance during acute high altitude exposure and after 22 days of acclimatization and energy deficit

Background The ergogenic effects of supplemental carbohydrate on aerobic exercise performance at high altitude (HA) may be modulated by acclimatization status. Longitudinal evaluation of potential performance benefits of carbohydrate supplementation in the same volunteers before and after acclimatization to HA have not been reported. Purpose This study examined how consuming carbohydrate affected 2-mile time trial performance in lowlanders at HA (4300 m) before and after acclimatization. Methods Fourteen unacclimatized men performed 80 min of metabolically-matched (~ 1.7 L/min) treadmill walking at sea level (SL), after ~ 5 h of acute HA exposure, and after 22 days of HA acclimatization and concomitant 40% energy deficit (chronic HA). Before, and every 20 min during walking, participants consumed either carbohydrate (CHO, n = 8; 65.25 g fructose + 79.75 g glucose, 1.8 g carbohydrate/min) or flavor-matched placebo (PLA, n = 6) beverages. A self-paced 2-mile treadmill time trial was performed immediately after completing the 80-min walk. Results There were no differences (P > 0.05) in time trial duration between CHO and PLA at SL, acute HA, or chronic HA. Time trial duration was longer (P < 0.05) at acute HA (mean ± SD; 27.3 ± 6.3 min) compared to chronic HA (23.6 ± 4.5 min) and SL (17.6 ± 3.6 min); however, time trial duration at chronic HA was still longer than SL (P < 0.05). Conclusion These data suggest that carbohydrate supplementation does not enhance aerobic exercise performance in lowlanders acutely exposed or acclimatized to HA. Trial registration NCT, NCT02731066, Registered March 292,01

Prolonged high altitude exposure exacerbates fat-free mass and fat mass loss during negative energy balance regardless of dietary protein intake

Protein intake above the recommended dietary allowance attenuates fat-free mass (FFM) loss during moderate negative energy balance ( 40% energy deficit) at sea level (SL). Sustained periods of strenuous physical activity at high altitude (HA) may exacerbate FFM loss, especially during energy deficit. However, increased dietary protein intake has not been evaluated as a countermeasure to FFM loss at HA. This study aimed to determine whether consuming dietary protein at amounts consistent with current recommendations for elevated physical activity (2.0 g protein/kg) attenuates FFM loss during prolonged energy deficit at HA. Seventeen healthy males (mean ± SD, 23.4 ± 5.6y, 81.9± 13.9 kg) participated in a 2-phase, 43-d study. During phase 1 (SL), participants were instructed to consume a weight maintenance diet with standard protein intake(1.0 g protein/kg, STD) for 21 d. During phase 2, participants resided at HA (4300 m, Pikes Peak, CO) for 22 d and were randomly assigned to either a STD or high (2.0 g protein/kg, HIGH) protein diet designed to elicit a 40% energy deficit (30% dietary restriction and 10% increase in physical activity, estimated energy deficit was 1074 ± 122 kcal/d based on the total energy requirements necessary to maintain body mass during phase 1) and 3 kg total body mass loss. Diet and physical activity were highly controlled. Total body mass, FFM, and fat mass (FM) were assessed by dual energy x-ray absorptiometry and resting metabolic rate (RMR) by indirect calorimetry. Volunteers were weight stable during SL and lost −7.9 ± 1.9 kg(P\u3c0.01)during HA, regardless of protein group (P\u3e0.05). Decrements in FFM (−4.0 ± 3.3 vs. −3.2 ± 1.5 kg) and FM (−3.3 ± 1.8 vs. −3.9 ± 0.8 kg) were not statistically different between STD and HIGH (P\u3e0.05). The overall energy deficit was 2306 ± 444kcal/d when calculated based on changes in FFM and FM. The additional energy deficit was attributable, in part, to an increase in RMR, which peaked at 58%above SL on HA day 1 and remained ≥ 25% higher than SL throughout HA(P\u3c0.05), accounting for 27% (634 ± 273 kcal/d) of the total energy deficit at HA. The remaining 598 kcal/d (26% of total deficit) could not be accounted for by estimated energy expenditure of prescribed daily physical activity and measured energy intake, suggesting the energy cost of physical activity may be greater at HA than SL. Prolonged HA exposure exacerbated the catabolic effects of negative energy balance. In this context, consuming a higher versus standard protein diet was equally ineffective at sparing FFM with weight loss. The opinions or assertions contained herein are the private views of the author(s)and are not to be construed as official or reflecting the views of the Army or the Department of Defense. Support or Funding InformationSupported by USAMRMC

Severe negative energy balance during 21 d at high altitude decreases fat-free mass regardless of dietary protein intake: A randomized controlled trial

In this 2-phase randomized controlled study, we examined whether consuming a higher-protein (HP) diet would attenuate fat-free mass (FFM) loss during energy deficit (ED) at high altitude (HA) in 17 healthy males (mean ± SD: 23 ± 6 yr; 82 ± 14 kg). During phase 1 at sea level (SL, 55 m), participants consumed a eucaloric diet providing standard protein (SP; 1.0 g protein/kg,) for 21 d. During phase 2, participants resided at HA (4300 m) for 22d andwere randomly assigned to either an SP or HP (2.0 g protein/kg) diet designed to elicit a 40% ED. Body composition, substrate oxidation, and postabsorptive whole-body protein kinetics were measured. Participants were weight stable during SL and lost 7.9 ± 1.9 kg (P\u3c0.01) during HA, regardless of dietary protein in take. Decrements in whole body FFM (3.662.4 kg) and fat mass (3.661.3 kg) were not different between SP and HP. HP oxidized 0.95 ± 0.32 g protein/kg per day more than SP and whole-body net protein balance was more negative for HP than for SP (P\u3c0.01). Based on changes in body energy stores, the overall ED was 70% (-1849 ± 511 kcal/d, no group differences). Consuming an HP diet did not protect FFM during severe ED at HA

Altitude Acclimatization Alleviates the Hypoxia-Induced Suppression of Exogenous Glucose Oxidation During Steady-State Aerobic Exercise

This study investigated how high-altitude (HA, 4300 m) acclimatization affected exogenous glucose oxidation during aerobic exercise. Sea-level (SL) residents (n = 14 men) performed 80-min, metabolically matched exercise (V·O2 ~ 1.7 L/min) at SL and at HA \u3c 5 h after arrival (acute HA, AHA) and following 22-d of HA acclimatization (chronic HA, CHA). During HA acclimatization, participants sustained a controlled negative energy balance (-40%) to simulate the real world conditions that lowlanders typically experience during HA sojourns. During exercise, participants consumed carbohydrate (CHO, n = 8, 65.25 g fructose + 79.75 g glucose, 1.8 g carbohydrate/min) or placebo (PLA, n = 6). Total carbohydrate oxidation was determined by indirect calorimetry and exogenous glucose oxidation by tracer technique with 13C. Participants lost (P ≤ 0.05, mean ± SD) 7.9 ± 1.9 kg body mass during the HA acclimatization and energy deficit period. In CHO, total exogenous glucose oxidized during the final 40 min of exercise was lower (P \u3c 0.01) at AHA (7.4 ± 3.7 g) than SL (15.3 ± 2.2 g) and CHA (12.4 ± 2.3 g), but there were no differences between SL and CHA. Blood glucose and insulin increased (P ≤ 0.05) during the first 20 min of exercise in CHO, but not PLA. In CHO, glucose declined to pre-exercise concentrations as exercise continued at SL, but remained elevated (P ≤ 0.05) throughout exercise at AHA and CHA. Insulin increased during exercise in CHO, but the increase was greater (P ≤ 0.05) at AHA than at SL and CHA, which did not differ. Thus, while acute hypoxia suppressed exogenous glucose oxidation during steady-state aerobic exercise, that hypoxic suppression is alleviated following altitude acclimatization and concomitant negative energy balance