24-01-2016, 08:57 PM
blood serum FFA (free fatty acids) contribute to disease states, (insulin resistance , diabiates, cancer, ischemia, immune response, etc). Only 2-5% of fatty acids are unbound from albumin, the rest is bound causing these disease states. I think (imo) the FFA in blood serum (fat in our our NBE diet) makes us sluggish, like arthritic conditions (think RA). Freeing these fatty acids is a big deal, least not we forgot, hormones are tightly bound in albumin with similar binding percentage.
A few ways to fix this, e.g. fast for 12-14 hours, low dose aspirin........exercise. And it looks like FFA's reduces calcium.........PM also reduces calcium, I'm guessing because manufacturers knew that PM lowers the parathyroid. But, would they have known about FFA's causing these disease states?. dunno. That fact is, the same could be said for PUFA's, n6's, the ratio (imo) should be 1:3 n6 to n3.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656504/
FREE, I.E., NONESTERIFIED, fatty acids (FFA) are major substrates for energy metabolism, and consequently large quantities of FFA have to be supplied to peripheral cells. Since FFA are highly insoluble in the aqueous phase, their major proportion is transported in blood bound to albumin, thereby keeping the concentration of unbound FFA extremely low (1)⇓. However, the efficient binding of FFA to albumin not only mediates their solubility, but also prevents direct effects of unbound FFA on various cellular functions. Activation, degranulation, and cytolytic functions of lymphocytes in particular are inhibited in vitro by the naturally prevailing cis-unsaturated species of unbound FFA (2⇓3⇓4⇓5⇓6)⇓. Accordingly, diseases with increased serum FFA concentrations such as diabetes mellitus (7)⇓, cancer (8⇓, 9)⇓, and states of ischemia (10⇓, 11)⇓ are often associated with disturbances in immune function (12⇓, 13)⇓. Since activation of T lymphocytes plays a pivotal role for initiating immune response and cell-mediated cytotoxic activity, inhibition of lymphocyte activation by elevated serum FFA levels could evoke a clinically relevant immunosuppressive effect.
http://www.fasebj.org/content/14/7/939.full
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binding: a cause for misinterpretation of serum calcium values and hypocalcemia in critical illness.
Zaloga GP, Willey S, Tomasic P, Chernow B.
Abstract
FFAs are bound with calcium on the albumin molecule. We hypothesized that changes in circulating FFA levels during critical illness altered calcium-albumin binding. We found that serum from both normal subjects and critically ill patients contained an ether-extractable factor which lowered ionized calcium concentrations and increased albumin-calcium binding. This factor was found in higher concentrations in serum from ill patients. Oleic acid and palmitic acid increased albumin-calcium binding from 2-28% in a dose-dependent manner when added in vitro to calcium-albumin solutions. Scatchard analysis demonstrated that 0.1 mM oleic acid increased the number of calcium-binding sites on the albumin molecule (from three to five sites per molecule) without altering binding affinity. A similar effect was found when we performed Scatchard analyses of ether extracts in serum from three critically ill patients (number of calcium-binding sites increased from three to six). We also found that lipid infusions (during parenteral nutrition) lowered mean serum ionized calcium values in six critically ill patients [4.6 +/- 0.2 (+/- SEM) to 4.1 +/- 0.2 mg/dL; P less than 0.05]. These data support the concept that FFAs increase calcium binding to the albumin molecule. Alterations in FFA concentrations during critical illness may contribute to the poor correlation between corrected total serum calcium and ionized calcium concentrations in critically ill patients. In addition, acute elevations in circulating FFA concentrations may contribute to hypocalcemia in patients with defects in bone calcium mobilization.
Btw, nice pics Pino.
A few ways to fix this, e.g. fast for 12-14 hours, low dose aspirin........exercise. And it looks like FFA's reduces calcium.........PM also reduces calcium, I'm guessing because manufacturers knew that PM lowers the parathyroid. But, would they have known about FFA's causing these disease states?. dunno. That fact is, the same could be said for PUFA's, n6's, the ratio (imo) should be 1:3 n6 to n3.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656504/
FREE, I.E., NONESTERIFIED, fatty acids (FFA) are major substrates for energy metabolism, and consequently large quantities of FFA have to be supplied to peripheral cells. Since FFA are highly insoluble in the aqueous phase, their major proportion is transported in blood bound to albumin, thereby keeping the concentration of unbound FFA extremely low (1)⇓. However, the efficient binding of FFA to albumin not only mediates their solubility, but also prevents direct effects of unbound FFA on various cellular functions. Activation, degranulation, and cytolytic functions of lymphocytes in particular are inhibited in vitro by the naturally prevailing cis-unsaturated species of unbound FFA (2⇓3⇓4⇓5⇓6)⇓. Accordingly, diseases with increased serum FFA concentrations such as diabetes mellitus (7)⇓, cancer (8⇓, 9)⇓, and states of ischemia (10⇓, 11)⇓ are often associated with disturbances in immune function (12⇓, 13)⇓. Since activation of T lymphocytes plays a pivotal role for initiating immune response and cell-mediated cytotoxic activity, inhibition of lymphocyte activation by elevated serum FFA levels could evoke a clinically relevant immunosuppressive effect.
http://www.fasebj.org/content/14/7/939.full
-----------------------
binding: a cause for misinterpretation of serum calcium values and hypocalcemia in critical illness.
Zaloga GP, Willey S, Tomasic P, Chernow B.
Abstract
FFAs are bound with calcium on the albumin molecule. We hypothesized that changes in circulating FFA levels during critical illness altered calcium-albumin binding. We found that serum from both normal subjects and critically ill patients contained an ether-extractable factor which lowered ionized calcium concentrations and increased albumin-calcium binding. This factor was found in higher concentrations in serum from ill patients. Oleic acid and palmitic acid increased albumin-calcium binding from 2-28% in a dose-dependent manner when added in vitro to calcium-albumin solutions. Scatchard analysis demonstrated that 0.1 mM oleic acid increased the number of calcium-binding sites on the albumin molecule (from three to five sites per molecule) without altering binding affinity. A similar effect was found when we performed Scatchard analyses of ether extracts in serum from three critically ill patients (number of calcium-binding sites increased from three to six). We also found that lipid infusions (during parenteral nutrition) lowered mean serum ionized calcium values in six critically ill patients [4.6 +/- 0.2 (+/- SEM) to 4.1 +/- 0.2 mg/dL; P less than 0.05]. These data support the concept that FFAs increase calcium binding to the albumin molecule. Alterations in FFA concentrations during critical illness may contribute to the poor correlation between corrected total serum calcium and ionized calcium concentrations in critically ill patients. In addition, acute elevations in circulating FFA concentrations may contribute to hypocalcemia in patients with defects in bone calcium mobilization.
Btw, nice pics Pino.