The Bahadori Leanness Program (BLP) is a multi-step strategy for weight control, the most innovative feature of which is “mini-fast with exercise” – every 24 h includes a fast of 12–14 h duration within which is nested a session of aerobic exercise. Low-fat, low-glycemic-index foods choices help to insure that diurnal levels of glucose and insulin remain relatively low. Clinical experience demonstrates that clients can achieve good compliance with this protocol, and the long term impact on body weight is gratifying. Rodent studies demonstrate that alternate-day feeding is even more effective than caloric restriction for promoting neuroprotection, suggesting that intermittent periods of mild metabolic stress induce protective adaptations in the brain; exercise training is also neuroprotective in these models. Mattson has raised the possibility that regular meal-skipping might be a feasible strategy for achieving similar – though perhaps less potent – protection in humans. Thus, it is suggested that exercise superimposed on regular short-term fasts, as in the BLP, might provide meaningful neuroprotection. Studies assessing CSF levels of brain neurotrophic hormones might be useful for evaluating the impact of such a strategy on brain neurochemistry. It should not be overlooked that leanness, good insulin sensitivity, and regular exercise are likely to be neuroprotective in their own right. The episodic metabolic stress associated with BLP may also have potential for prevention and therapy of cancer, inasmuch as down-regulation of systemic IGF-I activity during the mini-fasts would be expected to boost the rate of apoptosis in IGF-I-responsive neoplastic or pre-neoplastic tissues. Moreover, the relatively low-diurnal insulin levels and exercise training associated with BLP would be expected to down-regulate sympathetic activity while boosting cardiac parasympathetic tone – effects that should decrease risk for hypertension and sudden-death arrhythmias. Thus, it is conceivable that BLP will provide a range of health benefits extending beyond those attributable to its favorable impact on body composition.

Young adult males who cannot produce or respond to estrogen (E) are osteopenic, suggesting that E may regulate bone turnover in men, as well as in women. Both bioavailable E and testosterone (T) decrease substantially in aging men, but it is unclear which deficiency is the more important factor contributing to the increased bone resorption and impaired bone formation that leads to their bone loss. Thus, we addressed this issue directly by eliminating endogenous T and E production in 59 elderly men (mean age 68 years), studying them first under conditions of physiologic T and E replacement and then assessing the impact on bone turnover of withdrawing both T and E, withdrawing only T, or only E, or continuing both. Bone resorption markers increased significantly in the absence of both hormones and were unchanged in men receiving both hormones. By two-factor ANOVA, E played the major role in preventing the increase in the bone resorption markers, whereas T had no significant effect. By contrast, serum osteocalcin, a bone formation marker, decreased in the absence of both hormones, and both E and T maintained osteocalcin levels. We conclude that in aging men, E is the dominant sex steroid regulating bone resorption, whereas both E and T are important in maintaining bone formation.