Saturated Fats: A Perspective from Lactation and Milk Composition

For recommendations of specific targets for the absolute amount of saturated fat intake, we need to know what dietary intake is most appropriate? Changing agricultural production and processing to lower the relative quantities of macronutrients requires years to accomplish. Changes can have unintended consequences on diets and the health of subsets of the population. Hence, what are the appropriate absolute amounts of saturated fat in our diets? Is the scientific evidence consistent with an optimal intake of zero? If not, is it also possible that a finite intake of saturated fats is beneficial to overall health, at least to a subset of the population? Conclusive evidence from prospective human trials is not available, hence other sources of information must be considered. One approach is to examine the evolution of lactation, and the composition of milks that developed through millennia of natural selective pressure and natural selection processes. Mammalian milks, including human milk, contain 50% of their total fatty acids as saturated fatty acids. The biochemical formation of a single double bond converting a saturated to a monounsaturated fatty acid is a pathway that exists in all eukaryotic organisms and is active within the mammary gland. In the face of selective pressure, mammary lipid synthesis in all mammals continues to release a significant content of saturated fatty acids into milk. Is it possible that evolution of the mammary gland reveals benefits to saturated fatty acids that current recommendations do not consider

Relationship between arterial blood gas values, pulmonary function tests and treadmill exercise testing parameters in patients with COPD

WOS: 000224419300005PubMed: 15363002Objective: There have been controversial reports regarding the relationship between exercise tolerance and resting pulmonary function in patients with COPD. The aim of this study was to examine the relationship between resting pulmonary function tests (rPFT) and cardiopulmonary exercise testing parameters (CETP) and their value in estimating exercise tolerance of patients. Methodology: In total, 45 patients with COPD (nine females, 36 males; mean age 61.2 +/- 11.2) and 21 healthy subjects (four females, 17 males; mean age 60.3 +/- 9.7) as a control group were studied. COPD patients (group I) were divided into three subgroups according to their FEV1 (mild/group II: FEV1 60-79% of predicted; moderate/group III: FEV1 40-59%; severe/group IV. FEV1 < 40%). In controls FEV1 was greater than or equal to 80%. Results: There were significant correlations between FEV1 and CETP in group III (maximal O-2 consumption (mVO(2)), r = 0.35, P < 0.005; total treadmill time (TTT), r = 0.31, P < 0.01; total metabolic equivalent values (TMET), r = 0.29, P < 0. 01)) and in group IV (mVO(2), r = 0.49, P < 0.001; TTT, r = 0.45, P < 0.005; TMET, r = 0.31, P < 0.01; peak heart rate (pHR), r = 0.29, P < 0.02; frequency of ventricular extrasystole (fVES), r = -0.27, P < 0.05). Additionally, in group IV there were significant correlations between PaO2 and CETP (mVO(2), r = 0.41, P < 0.02; TTT, r = 0.38, P < 0.03; TMET, r = 0.31, P < 0.05; pHR, r = 0.29, P < 0.05; fVES, r = -0.28, P < 0.05). Conclusion: There are significant correlations of resting FEV1% predicted and PaO2 Values with CETP in patients with moderate and severe COPD and these parameters may also have a role as indicators of exercise tolerance in these COPD patients