Are the salutogenic effects of social supports modified by income? A test of an "added value hypothesis".

Older adults (54 men, 113 women; M age = 69.5 years) were examined to test the hypothesis that social supports would be more salutogenic (health promoting) for persons with lower incomes than for persons with higher incomes. Interactions of income and social supports (mean of 3 emotional scales of the Interpersonal Support Evaluation List) at study entry predicted changes 15-18 months later in a cardiovascular composite (linear combination of high-density lipoproteins-mean arterial pressure; p < .05), and natural killer cell activity (p < .05). For both outcomes, emotional supports were salutogenic for persons with lower incomes (< or =$29,000/year), but not for persons with higher incomes (>$29,000/year). In contrast, interactions of the Tangible Support Scale with income did not occur. Persons with lower incomes may derive benefits from social supports that go beyond tangible assistance.

Sense of coherence buffers relationships of chronic stress with fasting glucose levels.

Sense of coherence (SOC) was examined as a buffer of the relationship of chronic stress with fasting glucose and insulin levels. Spouse caregivers of persons with diagnoses of Alzheimer's disease (AD) (n = 73) were compared to controls [spouses of nondemented persons (n = 69)], group-matched on age/gender. After controlling for anger and coronary heart disease (CHD), interactions of SOC and gender explained variance in glucose (but not insulin) at study entry (T1) and 15-18 months later (T2). However, this occurred only in caregivers. At both times SOC and glucose were negatively related in men caregivers but not in women caregivers or in controls. In caregivers (but not controls), SOC at T1 predicted glucose at T2, independent of gender, anger, and glucose at T1; and hassles at T1 appeared to mediate this relationship. Future research should examine SOC as a buffer of other chronic stressors and metabolic variables.

CD4 and CD8 counts are associated with interactions of gender and psychosocial stress.

OBJECTIVE: This study examined relationships of gender, psychosocial stress/distress (caregiving, hassles, depressed mood), and the relative percentage and absolute cell counts of CD4 and CD8 cells in two samples of older adults (mean age = 69.4)--spouse caregivers of persons with Alzheimer's disease (N = 78) and age- and gender-matched spouses of nondemented controls (N = 72). METHODS: Counts and percentages of CD4 and CD8 cells and psychosocial variables were assessed twice (Time 1, Time 2) over a 15- to 18-month period. Several covariates were examined in the analyses, including body mass index (BMI), medication use, alcohol use, exercise, and illness history. RESULTS: Caregiver men had fewer CD4 cell counts at Times 1 and 2 than did control men (p < .05). At Times 1 and 2, both CD8 cell counts and percentages were positively associated with hassles in men (p < .05), but not in women. Although interactions of hassles and gender were present for CD8 percentages at both times, interactions and main effects were not present for CD4 percentages at either time. When the ratio of CD4 to CD8 levels was analyzed, hassles by gender interactions were present at both Times 1 and 2-hassles were negatively associated with the CD4/CD8 ratio in men (p < .05), but unrelated in women. From Time 1 to Time 2, change analyses showed that increases in hassles scores were associated with decreases in CD4 counts (p < .05), whereas increases in Hamilton Depression Scores were related to increases in both CD8 counts and percentages (p < .05). CONCLUSION: Caregiver status, hassles, and depressed mood had cross-sectional and/or longitudinal associations with CD4 and CD8 counts, but such relationships occurred primarily in men. Moreover, absolute cell counts were more related to psychosocial factors than were percentages.

Sleep deprivation alters body temperature dynamics to mild cooling and heating not sweating threshold in women.

Sleep deprivation alters thermoregulatory responses. We used control of skin temperature to produce mild thermal challenge, both cool (32 degrees C) and warm (38 degrees C), and recorded esophageal and rectal temperatures, sweat rate and forearm blood flow in six healthy young women at rest. We discovered that after one night of sleep deprivation (1) both mean esophageal and rectal temperatures were reduced, (2) the mean threshold for sweating was not altered, and (3) there was no direct indication that skin blood flow was set at different levels with skin temperature neutral or cool. Peripheral vasodilation was attenuated when skin temperature was held at 38 degrees C. Following this period of mild hyperthermia, esophageal and rectal temperatures decreased much more rapidly in sleep-deprived subjects when skin temperature was cooled and held constant at 32 degrees C. We conclude that sleep-deprived women lose heat rapidly in response to a mild cooling stimulus. Sleep-deprived humans may be more vulnerable to heat loss with reduced ability to warm even at temperatures thought to be associated with thermal comfort.

Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression.

Circadian temperature, cortisol, and thyroid-stimulating hormone (TSH) rhythms during a constant routine were assessed in 6 female controls and 6 female patients with hypersomnic winter depression (seasonal affective disorder, SAD) before and after morning bright light treatment. After sleep was standardized for 6 days, the subjects were sleep-deprived and at bed rest for 27 hours while rectal temperature, cortisol, and TSH levels were assessed. The minimum of the fitted rectal temperature rhythm was phase-delayed in the SAD group compared to the controls 5:42 AM vs. 3:16 AM (p < .005); with bright light treatment, the minimum advanced from 5:42 AM to 3:36 AM (p = .06). The minimum of the cortisol rhythm was phase-delayed in the SAD group compared to the control group, 12:11 AM vs. 10:03 PM (P < .05); with bright light treatment, the minimum advanced from 12:11 AM to 10:38 PM (P = .06) [corrected]. The acrophase of the TSH rhythm was not significantly phase-delayed in SAD subjects compared to control, though the trend appeared to be toward a phase-delay (p = .07). After bright light therapy, the TSH acrophase was not significantly different in the SAD subjects; the trend was a phase-advance (p = .09). Overall, the data suggest that circadian rhythms are phase-delayed relative to sleep in SAD patients and that morning bright light phase-advances those rhythms.

Effect of facial cooling on tympanic temperature.

BACKGROUND: In clinical practice, tympanic temperature is used as an estimate of body temperature. Theoretically, temperature recorded directly from the tympanum reflects the temperature of arterial blood circulating to the brain. However, some studies do not support this connection. Ear-based thermometers in clinical use, commonly called tympanic thermometers, detect heat emission from the aural canal and tympanum. Dissociation of core body temperature and tympanic temperature would suggest that factors other than arterial blood perfusion affect tympanic temperature. METHODS: In a controlled laboratory experiment with four adult volunteers, esophageal and tympanic temperatures were recorded repeatedly at 2-minute intervals during whole-body heating and cooling. Facial cooling, produced by a small electrical fan, was used in three subjects. RESULTS: The gradient between tympanic and esophageal temperature was inconsistent across subjects, with tympanic temperature both higher and lower than esophageal temperature. Correlations between esophageal and tympanic temperature varied widely across subjects. Fanning the face produced a decrease in tympanic temperature without an accompanying decline in esophageal temperature. CONCLUSIONS: Facial cooling in the form of fanning altered the relationship between tympanic and esophageal temperature. This result suggests the possible lowering of tympanic temperature by cooled facial venous blood flow. Use of tympanic temperature in circumstances in which facial temperature may be different from that of other regions of the body deserves further study.

Control of skin blood flow in the neutral zone of human body temperature regulation.

In humans, matching of heat loss and heat production in the "neutral" zone, defined operationally in terms of a range of skin temperatures (Tsk), is accomplished by regulation of skin blood flow (SkBF). Our studies were designed to reveal the characteristics of control of SkBF [from measurements of forearm blood flow (FBF)] in this zone. We controlled the temperature of water sprayed on most of the body of supine men and women at 33 or 35 degrees C in a square-wave pattern (15 min at each temperature) or a step pattern (60 min at 33 degrees C separated by short periods at 35 degrees C). FBF followed Tsk (0.5 ml.min-1.degrees C-1). Esophageal temperature changed approximately 0.11 degrees C with each 2 degrees C change in Tsk, falling with Tsk increase and vice versa. Little influence on FBF, < 0.1 ml.min-1.100 ml-1. degrees C-1, was observed when only the forearm was sprayed with 33 and 35 degrees C water. We conclude that SkBF control in the 33-35 degree C range of Tsk is dominated by the feedforward reflex influence of Tsk on SkBF. The reflex response overcompensates for the effect of Tsk on thermal balance in the neutral zone, so that equilibrium core temperature has an inverse relationship to Tsk.

Reproducibility of core temperature threshold for sweating onset in humans.

The control of sweating in humans has been described quantitatively in terms of skin and core temperatures (Tsk and Tcore, respectively). However, the precision with which features of the relationship between sweat rate and Tcore at a given Tsk can be reproduced in the short term is not known. We focused on the threshold Tcore. We held Tsk at 38 degrees C until sweating began for two periods separated by a period of cooling with Tsk at 32 degrees C in six men and three women. The esophageal temperature (Tes) at which sweating began was invariably lower in the second period of heating (average difference 0.09 degree C; maximum 0.17 degree C). Also, the rate of rise in Tes was invariably higher (average 148%) during the second period of heating. Thus, although a threshold cannot be reproduced within the error of Tes measurement, the consistency and small magnitude of the downward shift recommend our protocol as a practical method for evaluating other influences on thermoregulation, provided that the effects are big enough to be seen against a background of an expected small decrease. From the fundamental point of view, the consistency of the downward displacement has provocative implications, e.g., the rate of change in Tcore influences sweating or thermosensitive units in slow-responding thermal compartments contribute to the Tcore input signal.

Maximal skin blood flow is decreased in elderly men.

When subjected to total body heating and exercise, skin blood flow does not increase as much in elderly as in young subjects. It is not known whether this age-related decline is due to the autonomic dysfunction that develops in the elderly or to changes at the level of the blood vessels of the skin. We used local heating of the forearm to quantify the intrinsic ability of the cutaneous vasculature to dilate in seven young men (avg age 31 yr) and seven elderly men (avg age 71 yr). A water spray was used to maintain a neutral skin temperature of 32-35 degrees C for > 10 min, followed by 60 min of a 42 degrees C skin temperature to induce maximal skin blood flow. Forearm blood flow was measured by venous occlusion plethysmography with a mercury-in-Silastic circumference gauge. At the neutral skin temperature, forearm blood flows in the elderly subjects were comparable to those in the young subjects: 3.0 +/- 0.5 vs. 2.8 +/- 1.0 ml.min-1 x 100 ml-1. During the last 10 min of heating, however, blood flows were much lower in the elderly than in the young subjects: 11.1 +/- 2.7 vs. 19.9 +/- 5.2 ml.min-1 x 100 ml-1 (P = 0.002). We conclude that aging results in a reduction of the maximal conductance of the cutaneous vasculature.

Reproducibility of the vascular response to heating in human skin.

Blood flow in human skin increases enormously in response to direct heating. If local skin temperature is held above 42 degrees C, blood flow eventually stabilizes at a level beyond which other influences, barring change in blood pressure, can produce no further increase. If this maximal level is a reproducible characteristic of an individual's cutaneous vasculature, it could be useful in comparing individuals; for example, in their response to hyperthermia. Our experiments were carried out to discover whether the maximal response of the vasculature of the skin of the forearm can be reproduced within reasonable limits and, also, to clarify the time course of the response. We used water sprayed over the surface of the forearms of 10 subjects to hold skin temperature above 42 degrees C for 60 min. During the last 10 min of heating, forearm blood flow (via venous occlusion plethysmography) was stable, at a level ranging from 16 to 38 ml.min-1.100 ml-1. This level, normalized to a blood pressure of 100 mmHg, was reproduced in a given individual on four or five occasions, with an average coefficient of variation of 10%. The response was 77 +/- 11% (SD) complete after 20 min of heating. Elapsed time at 90% of the final value was 35 +/- 9 (SD) min. We conclude that the maximal forearm blood flow response to local heating is a reproducible characteristic of the cutaneous vasculature with potential utility in the scaling of responses between and within individuals.

Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression.

The onset of melatonin secretion under dim light conditions (DLMO) and the circadian temperature rhythm during a constant routine were assessed in 6 female controls and 6 female patients with winter depression (seasonal affective disorder, SAD) before and after bright light treatment. After sleep was standardized for 6 days, the subjects were sleep-deprived and at bedrest for 27 h while core temperature and evening melatonin levels were determined. The DLMO of the SAD patients was phase-delayed compared with controls (2310 vs 2138); with bright light treatment, the DLMO advanced (2310 to 2135). The minimum of the fitted rectal temperature rhythm was phase-delayed in the SAD group compared with the controls (0542 vs 0316); with bright light treatment, the minimum advanced (0542 vs 0336).

Body temperature and diurnal type in women with seasonal affective disorder.

Body temperature rhythms and diurnal type were explored in female controls and women with seasonal affective disorder (SAD) before and after phototherapy. Women with SAD reported being more like evening types than did controls. Morning phototherapy advanced the body temperature rhythms of women with SAD, and shifted their morningness/eveningness scores toward the morning end of the continuum. The implications of these results for our understanding of both SAD and depression in women are discussed.

Cardiovascular responses to graded reductions in leg perfusion in exercising humans.

Our objective was to determine whether the chemoreflex from human muscle is elicited by small graded reductions in muscle blood flow (MBF) during mild exercise or whether this reflex has an obvious threshold associated with large changes in femoral venous lactate and H+ levels (i.e., as in dogs with high muscle oxidative capacity). Seven subjects exercised supine at 40, 87, and 142 W; lower body positive pressure (LBPP) was applied in 3-min steps at 25, 35, 45, and 50-60 mmHg with the lower body and the cycle ergometer in a sealed box. Estimated MBF (Fick) fell by 5.3 +/- 4.3 to 19.9 +/- 3.8% at four levels of LBPP over three work rates. Mean arterial pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) concentration rose with increasing LBPP. MAP was significantly correlated with femoral venous pH, lactate, O2 tension, and O2 content during moderate and heavy exercise, without an apparent threshold. Percentage decreases in muscle vascular conductance exceeded the decreases in MBF twofold, indicating significant opposition to reduction in MBF by the chemoreflex. Approximately 50% of the correction of MBF back toward control (i.e., at 0 LBPP) could be explained by increased cardiac output, calculated from the rise in HR; the remaining correction could be attributed to both sympathetic vasoconstriction (indicated by high NE levels) and to mechanical effects of partial occlusion. Results suggest that in humans stepwise reductions in MBF gradually elicit muscle chemoreflexes with no apparent threshold at these levels of exercise.

Cystic fibrosis, vasoactive intestinal polypeptide, and active cutaneous vasodilation.

The transmitter substance for the active cutaneous vasodilation that accompanies sweating during hyperthermia in humans is unknown. Hökfelt et al. (Nature Lond. 284: 515-521, 180) hypothesized that it is vasoactive intestinal polypeptide (VIP) that is cotransmitted with acetylcholine. Heinz-Erian et al. (Science Wash. DC 229: 1407-1408, 1985) reported that VIP innervation is sparse in the skin of persons with cystic fibrosis (CF). A corresponding attenuation of active vasodilation in these subjects would be evidence that VIP is involved in this effector mechanism of human thermor-regulation. Immunocytochemical analysis of skin biopsies from four men with CF confirmed that VIP innervation was sparse. We also analyzed immunoreactivity for calcitonin gene-related peptide (CGRP; normal), substance P (normal), and neuropeptide Y (low). VIP-immunoreactive Merkel cells were abnormal. Despite sparse VIP-immunoreactive innervation, our CF subjects' cutaneous vascular responses to hyperthermia were normal. Because VIP was not completely absent, this evidence is insufficient to rule out VIP as the vasodilator transmitter. However, the CGRP and substance P innervation we observed could mean that release of one or both of these peptides was the mechanism of the fully developed active cutaneous vasodilation.

Does acute hypoxemia blunt sympathetic activity in hyperthermia?

Sympathetic alpha-adrenergic function is depressed by hypoxemia per se; does addition of another sympathoexcitatory stimulus elicit normal responses in other sympathetic effector pathways? We activated by hyperthermia four sympathetic pathways: alpha-adrenergic [norepinephrine (NE) release], beta-adrenergic [plasma renin activity (PRA)], cholinergic (sweating), and peptidergic (active vasodilation). In the first test, five normothermic men were exposed to hypoxemia for 10 min (control), then hypoxemia plus heat for 30 min, and then heat with normoxia for 8-10 min over a continuous 48- to 50-min period. Heating was controlled with a water-perfused suit. Time courses and magnitudes of heat-induced increments in body temperature, forearm blood flow, and sweat rate were normal during hypoxemia and unaffected by switching to normoxia. Hypoxemia exaggerated increases in plasma NE, epinephrine, PRA, and heart rate but had no additional effects on blood pressure. In a second 50-min test (2 men) with normoxic control (10 min), heating plus normoxia (20 min), and heating plus hypoxemia (20 min), effects of hypoxemia on all variables were as in the first test. Thus, acute moderate hypoxemia did not blunt active cutaneous vasodilation or sweating and exaggerated increases in catecholamines and heart rate, indicating maintained peripheral autonomic function.

Effect of exercise on the development of salt-induced hypertension in Dahl-S rats.

Male Dahl-S rats were randomly assigned to either normal chow (NC) or high-salt (HS) diets to induce hypertension. Animals were further subdivided into trained (NCT, HST) and untrained (NCN, HSN) groups. Trained groups were exercised on a rodent treadmill 5 days per week for 12 weeks at a constant workload of 26.4 m/min, 5% grade, while duration progressed from 7.5 to 115 min/day. Arterial blood pressure was measured under anaesthesia by direct catheterization of femoral arteries after 4 and 8 weeks, and terminally via the carotid artery. Training resulted in significantly lower systolic and diastolic blood pressure in trained groups compared with untrained. The trained animals also had significantly lower body weights. Analysis of regressed organ weights adjusted for differences in final body weight revealed that the NCT animals had heavier hearts and kidneys than the NCN animals. The HST animals had heavier hearts and lighter kidneys than the HSN animals.