Monday, July 16, 2012

Under-reporting of food intake and exercise

Discrepancy between Self-Reported and Actual Caloric Intake and Exercise in Obese Subjects
Steven W. Lichtman, Ed.D., Krystyna Pisarska, M.S., Ellen Raynes Berman, Psy.D., Michele Pestone, M.S., Hillary Dowling, Ph.D., Esther Offenbacher, Ed.D., Hope Weisel, M.S., R.D., Stanley Heshka, Ph.D., Dwight E. Matthews, Ph.D., and Steven B. Heymsfield, M.D.
N Engl J Med 1992; 327:1893-1898December 31, 1992
[Discussion Section] The main finding of this study is that failure to lose weight despite a self-reported low caloric intake can be explained by substantial misreporting of food intake and physical activity. The underreporting of food intake by the subjects in group 1 even occurred 24 hours after a test meal eaten under standardized conditions. In contrast, values for total energy expenditure, resting metabolic rate, thermic effect of food, and thermic response to exercise were comparable with those of obese subjects in group 2 who did not report a history of diet resistance.
In addition to their greater degree of misreporting, the subjects in group 1 used thyroid medication more often, had a stronger belief that their obesity was caused by genetic and metabolic factors and not by overeating, and reported less hunger and disinhibition and more cognitive restraint than did the subjects in group 2. Subjects presenting for weight-control therapy who had these findings in association with a history of self-reported diet resistance would clearly convey the impression that a low metabolic rate caused their obesity.
The results of the evaluation of all major aspects of energy metabolism in the subjects in group 1 confirmed that substantial misreporting of food intake and physical activity accounted for the diet resistance they reported. There are, however, physiologic explanations for short-term diet resistance that should be considered in subjects with unexpectedly slow weight loss. Under certain conditions, fluid retention can mask weight loss for up to 16 days in subjects who are actually losing fat through dieting.36 After several weeks of weight loss, energy expenditure decreases and adaptive changes in protein metabolism occur, reducing the degree of negative energy and nitrogen balance and slowing the weight loss until it is almost imperceptible. Also, subjects with undiagnosed or untreated thyroid disease and those taking medications that lower energy expenditure may lose weight slowly.
Misreporting by the subjects in group 1 does not appear to be a facile deception, for several reasons. First, underreporting of food intake has been noted in obese and nonobese subjects with no history of diet resistance.6 7 8 9 , 37 , 38 The mechanisms responsible for this phenomenon are not well understood. Second, the subjects in group 1 participated voluntarily in a complex, time-consuming protocol designed to evaluate the cause of their perceived diet resistance. Several had a history of up to 20 serious diet attempts, and most had had extensive medical evaluations for obesity. Third, the subjects in group 1 were distressed when they were given their study results. Thus, important basic psychological issues require elucidation before this form of diet resistance can be properly understood.
In conclusion, all the obese subjects we studied who had a history of self-reported diet resistance had appropriate energy expenditure, but they misreported their actual food intake and physical activity.
Supported by grants (P01-DK42618, DK-26687, and RR 00047) from the National Institutes of Health.
Presented in part at the annual meeting of the American Federation of Clinical Research, Seattle, May 4–7, 1991.
We are indebted to Mr. Charles Gilker, Ms. Susan Thomas, and Ms. Kathleen Buhl for assistance with the mass-spectroscopic analyses using doubly labeled water; to Dr. William Berman for advice on developing procedures for psychological testing; and to Ms. Judy Dickson for assistance in the preparation of the manuscript.

SOURCE INFORMATION

From the Obesity Research Center, Department of Medicine, St. Luke's–Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons (S.W.L., K.P., E.R.B., M.P., H.D., E.O., H.W., S.H., S.B.H.), and the Departments of Medicine and Surgery, New York Hospital—Cornell Medical Center (D.E.M.), all in New York. Address reprint requests to Dr. Heymsfield at the Weight Control Unit, 411 W. 114th St., New York, NY 10025.

Wednesday, July 11, 2012

Glycemic Load

Chang et al. (2012) have an interesting study showing that diets with a low glycemic load leave people feeling much more satiated.

[Abstract] Effective strategies for reducing food intake are needed to reduce risk of  obesity-related cancers. We investigated the effect of low and high glycemic load (GL) diets on satiety and whether satiety varied by body mass index (BMI), gender, and serum leptin. Eighty normal weight (BMI = 18.5-24.9 kg/m(2)) and overweight/ obese (BMI = 28.0-40.0 kg/m(2)) adults participated in a randomized, crossover controlled feeding study testing low GL vs. high GL diets. The 28-day diets were isocaloric with identical macronutrient distributions, differing only in GL and fiber. Participants completed visual analog satiety surveys and fasting serum leptin after each 28-day period. T-tests compared mean within- and between-person satiety scores and leptin values. Participants reported 7% greater satiation on the low GL vs. the high GL diet (P = 0.03) and fewer food cravings on the low GL vs. the high GL diet (P < 0.001). Compared to males, females  reported less hunger (P = 0.05) and more satiety on the low GL vs. the high GL diet (P < 0.01). Participants with low body fat (<25.0% for men; <32.0% for women) and BMI <25.0 kg/m(2) reported study food was tastier on the low GL vs. the high GL diet (P = 0.04 and P = 0.05, respectively). In summary, reducing GL, and/or increasing fiber, may be an effective way to lower calories consumed, improve energy balance, and ultimately reduce cancer risk.

Tuesday, July 3, 2012

Brachycardia/Bradycardia

    Types of Bradyarrhythmias

    A bradyarrhythmia is a slow heart rhythm that is usually caused by disease in the heart’s conduction system. Types of bradyarrhythmias include:
    • Sinus node dysfunction: Slow heart rhythms due to an abnormal SA node.
    • Heart block: A delay or complete block of the electrical impulse as it travels from the sinus node to the ventricles. The level of the block or delay may occur in the AV node or HIS-Purkinje system. The heartbeat may be irregular and slow.
[Abstract] The significance of sinus bradycardia (SB) in clinically healthy, non-endurance-trained, middle-aged and older persons is unknown. From 1,172 normal volunteers, aged 40 to 96 years, enrolled in the Baltimore Longitudinal Study of Aging, 47 subjects, aged 58 ± 13 years, with SB (less than 50 beats/min) were identified by rest electrocardiography and were compared with a group of control subjects matched for age and sex. The prevalence of unexplained SB was approximately 4% and was nearly identical in men and women. At the latest follow-up examination, after a mean follow-up of 5.4 years, the SB group had a higher prevalence of associated conduction abnormalities (first-degree atrioventricular [AV] block, left-axis deviation, and complete or incomplete right bundle branch block) than the control group (43% vs 19%, p <0.05). On maximal treadmill exercise testing, performed in 44 patients within 1 visit of their most recent examination showing SB, maximal heart rate (157 ± 18 beats/min) did not differ significantly from that of control subjects (163 ± 19 beats/min); exercise duration, however, was greater in the former group, 11.0 ± 2.8 vs 9.7 ± 3.1 minutes (p <0.05). No patients with SB had syncope, high-degree AV block or other manifestation of sick sinus syndrome during follow-up. Angina pectoris, myocardial infarction, congestive heart failure or cardiac death occurred in 8% of patients with SB and 11% of control subjects over the observation period (difference not significant). Thus, unexplained SB in apparently healthy, nonathletic subjects older than 40 years is associated with certain abnormalities of AV or intraventricular conduction, but does not signify chronotropic incompetence with exercise and does not appear to adversely influence long-term cardiovascular morbidity or mortality.

Research generally shows that caffeine increases blood pressure in some people (James, 1994; Nurminen, Nittynen, & Vapaatalo, 1999).

Bichler, Swenson and Harris (2006) found a link between caffeine+taurine, arterial blood pressure and brachycardia.

[Abstract] Red Bull energy drink has become extraordinarily popular amongst college students for use as a study aid. We investigated the combined effects of Red Bull’s two active ingredients, caffeine and taurine, on short term memory. Studies on the effects of these two neuromodulators on memory have yielded mixed results, and their combined actions have not yet been investigated. In this double-blind study, college student subjects consumed either caffeine and taurine pills or a placebo and then completed a memory assessment. Heart rate and blood pressure were monitored throughout the testing period. The combination of caffeine and taurine had no effect on short term memory, but did cause a significant decline in heart rate and an increase in mean arterial blood pressure. The heart rate decline may have been caused by pressure-induced bradycardia that was triggered by caffeine ingestion and perhaps enhanced by the actions of taurine.


[Abstract] The mechanisms by which caffeine typically elevates blood pressure (BP) in humans have not been previously examined using a placebo-controlled design. Accordingly, oral caffeine (3.3 mg/kg body weight, equivalent to 2 to 3 cups of coffee) was given on 2 days and a placebo was given on 1 day to 15 healthy young men using a double-blind, crossover procedure. All 3 test sessions were held during a week ofcaffeine abstinence. Multiple measurements were made on subjects at rest (baseline values) and over a 45-minute interval after ingestion of caffeine for BP, heart rate, systolic time intervals and thoracic impedance measures of ventricular function. Baseline measurements were highly reliable for each subject across all sessions and yielded means for placebo vs caffeine days that were not different. Caffeine increased systolic and diastolic BP (p < 0.01) and decreased heart rate (p < 0.05). The pressor effect was due to progressively increased systemic vascular resistance and resulted in greater stroke work (p < 0.01). There was no indication that caffeine increased cardiac output or contractility. These actions of caffeine were replicable when each caffeine day was tested separately against the placebo day. These results suggest that caffeine use by persons with cardiovascular diseases should be examined to determine whethercaffeine's enhancement of vascular resistance may contribute to systematic hypertension and/or create excessive demands for cardiac work.


Northcote et al. (1989) have a short description of two athletes with bradycardia.