Calorie restriction (CR) delays the development of age-associated disease and increases lifespan in rodents, but the effects in humans remain uncertain.
Purpose. Determine the effect of 6 months of CR with or without exercise on cardiovascular disease (CVD) risk factors and estimated 10-year CVD risk in healthy non-obese men and women.
Methods. Thirty-six individuals were randomized to one of three groups for 6 months: Control, 100% of energy requirements; CR, 25% calorie restriction; CR+EX, 12.5% CR + 12.5% increase in energy expenditure via aerobic exercise. CVD risk factors were assessed at baseline, 3 and 6 months.
Results. After 6 months, CR and CR+EX lost approximately 10% of body weight. CR significantly reduced triacylglycerol (-31 ± 15 mg/dL) and factor VIIc (-10.7 ± 2.3%). Similarly CR+EX reduced triacylglycerol (-22 ± 8 mg/dL) and additionally reduced LDL-C (-16.0 ± 5.1 mg/dL) and DBP (-4.0 ± 2.1 mmHg). In contrast, both triacylglycerol (24 ± 14 mg/dL) and factor VIIc (7.9 ± 2.3%) were increased in the control group. HDL-cholesterol was increased in all groups while hsCRP was lower in the Controls vs. CR+EX. Estimated 10-year CVD risk significantly declined from baseline by 29% in CR (P< 0.001) and 38% in the CR+EX (P<0.001) while remaining unchanged in the Control group.
Conclusions. Based on combined favorable changes in lipid and blood pressure, caloric restriction with or without exercise that induces weight loss favorably reduces risk for CVD even in already healthy non-obese individuals.
Coronary heart disease (CHD) risk factors and the risk of CHD increase with increased adiposity. Fat loss induced by negative energy balance improves all metabolic CHD risk factors.
To determine whether fat loss induced by long-term calorie restriction (CR) or increased energy expenditure induced by exercise (EX) has different effects on CHD risk factors in nonobese subjects, we conducted a 1-yr controlled trial involving 48 nonobese subjects who were randomly assigned to one of three groups: CR, 20% CR diet (n = 18); EX, 20% increase in energy expenditure through daily exercise with no increase in energy intake (n = 18); or HL, healthy lifestyle guidelines (n = 10). Subjects were 29 women and 17 men aged 57 ± 3 yr, with BMI 27.3 ± 2.0 kg/m2.
Assessments included total body fat by DEXA, lipoproteins, blood pressure, HOMA-IR, C-reactive protein (CRP), and estimated 10-yr CHD risk score. Body fat decreased by 6.3 ± 3.8 kg in CR, 5.6 ± 4.4 kg in EX, and 0.4 ± 1.7 kg in HL, which corresponded to reductions of 24.9, 22.3, and 1.2% of baseline body fat mass, respectively.
The energy deficits [induced by either caloric restriction or exercise] were accompanied by reductions in most of the major CHD risk factors, including plasma LDL-cholesterol, total cholesterol/HDL ratio, HOMA-IR index, and CRP concentrations that were similar in the two intervention groups.
Data from the present study provide evidence that [both calorie restriction and exercise-induced] negative energy balance result in substantial and similar improvements in the major risk factors for coronary heart disease in normal-weight and overweight middle-aged adults.
SOURCE: Am J Physiology
A chemical system in the brain, the cholinergic system, is primarily responsible for cognitive symptoms seen in people with dementia. It is not clear what role the cholinergic system (and a subset of receptors called the nicotinic system) plays in cognition during normal cognitive aging. This is critical because the ever-growing healthy aging population will show declines in cognition that fall short of dementia but still impact functional abilities and independence. Maintaining good nicotinic system functioning throughout adulthood might lessen the cognitive symptoms of aging.
This study will examine the role of the nicotinic system in the healthy aging brain, and examine its role in memory and thinking processes in older + younger adults.