The influence of a low-fat diet on incidence and severity of migraine headaches.

Migraine headaches are a common, debilitating syndrome causing untold suffering and loss of productivity. A review of the literature indicates that high levels of blood lipids and high levels of free fatty acids are among the important factors involved in triggering migraine headaches. Under these conditions, platelet aggregability, which is associated with decreased serotonin and heightened prostaglandin levels, is increased. This leads to vasodilation, the immediate precursor of migraine headache. A high-fat diet is one factor that may directly affect this process. This study, undertaken to evaluate the impact of dietary fat intake on incidence and severity of migraine headache, was conducted over a 12-week period on 54 previously diagnosed migraine headache patients. During the first 28 days, the study subjects recorded all food consumption in a diet diary and maintained a headache diary. At the conclusion of this 28-day baseline period, subjects were individually counseled to limit fat intake to no more than 20 g/day. A 28-day run-in period was allowed for adaptation to the low-fat diet. Results are reported on the final 28-day postintervention period. Subjects significantly decreased the ingestion of dietary fat in grams between baseline (mean 65.9 g/day, p < 0.0001) and the postintervention period (mean 27.8 g/day). The decreased dietary fat intervention was associated with statistically significant decreases in headache frequency, intensity, duration, and medication intake (all p < 0.0001). There was a significant positive correlation between baseline dietary fat intake and headache frequency (r = .44, p = 0.02). This study indicates that a low-fat diet can reduce headache frequency, intensity, and duration and medication intake.

In search of the ideal treatment for migraine headache.

Migraine headache is a common syndrome, afflicting millions, that has so far defied a definitive cure. Experimental research studies of the syndrome tend to describe the triggering factors separately. We propose a common denominator--namely, high levels of blood lipids and free fatty acids--as underlying factor in the development of migraine headaches. Biological states that may cause increases in free fatty acids and blood lipids include: high dietary fat intake, obesity, insulin resistance, vigorous exercise, hunger, consumption of alcohol, coffee, and other caffeinated beverages, oral contraceptives, smoking, and stress. Elevated blood lipids and free fatty acids are associated with increased platelet aggregability, decreased serotonin, and heightened prostaglandin levels. These changes lead to the vasodilatation that precedes migraine headache. We suggest that migraine headache should not be seen as an isolated symptom, but as a first signal of potential biochemical imbalances in the body, which can lead to development of chronic disease.

The role of exercise in weight loss.

Aerobic exercise has traditionally been viewed as a critical component of most weight-reduction programs. The resulting weight loss from the exercise alone, however, is often disappointing. Researchers too frequently fail to take into account the normal energy expenditure associated with living; the degree of obesity; the intensity and duration of the exercise itself; the activity during the recovery period; food intake before and after the exercise; and the age, gender, and training status of the individuals. Nor do they consider variations in baseline resting metabolic rates. In this article, the authors explore the effect of the intensity of aerobic exercise on weight loss, emphasizing the inability of many obese individuals to maintain an intensity level sufficient to produce significant weight loss. Aerobic exercise should be emphasized for its health benefits rather than as a short-term method of enhancing weight loss.

The effects of acute moderate exercise on lymphocyte function and serum immunoglobulin levels.

The extent and duration of changes on lymphocyte function and serum immunoglobulin (Ig) levels were examined in 12 women who walked 45 min at 60% VO2 max in a laboratory setting. A 2-factor, 2 x 6 design with repeated measures on both factors was utilized. The first factor was condition (exercise and rest), and the second factor was time (six times of measurement over a 24-h period), with treatment order counterbalanced. The 45-min walk, in comparison to rest in a seated position, was not associated with significant changes in circulating numbers of interleukin-2-activated T cells (CD5 and CD25) or on spontaneous or concanavalin-A-stimulated lymphocyte proliferation. A trend for decreased phytohemagglutinin-stimulated lymphocyte proliferation in comparison to the rest condition, however, was seen 1.5 h following the exercise bout (p = 0.047). The patterns of change for serum IgG, IgA, and IgM were significantly different (p = 0.001, p less than 0.001, p = 0.010, respectively) between conditions. IgG rose 7.2% immediately following exercise, and then returned to baseline 1.5 h later, which contrasted significantly with changes in the rest condition. These same patterns of change occurred also with IgA and IgM, but increases immediately following exercise were not significant, although a trend was seen for IgA (p = 0.03). The 45-min walk had no effect on plasma cortisol and epinephrine levels relative to the rest condition, but was associated with a significant 89% increase in norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)