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Milk is a bovine secretion that is intended to allow rapid growth to calves following immediate consumption from their mother. It is widely consumed by humans, generally after pasteurisation and chilled storage, but may also be sterilised or further processed by heat treatment.
Research shows that one of the growth-promoting actions of this substance may be caused by the action of leptin in the body.
Leptin is a hormone secreted by body fat cells that adjusts food intake relative to energy expenditure. Leptin also plays a general role in regulating many of the physiological responses that are observed with changes in nutritional state.
Discovered by Jeffrey Friedman in 1994, Leptin has been shown to travel to the brain and other body tissues, causing fat loss and decreased appetite. In the brain, leptin affects food intake by acting on distinct classes of neurons in the hypothalamus that express the leptin receptor.
Leptin decreases both the desire to eat, and the deposit of fat in the body by acting on two classes of neurons. Leptin suppresses the activity of neuropeptide Y (NPY) neurons and it enhances the activity of proopiomelanocortin (POMC) neurons. Conversely, the absence of leptin increases both the desire to eat and the deposit of fat by exciting NPY neurons and suppressing the activity of POMC neurons.
In humans, leptin concentration in the blood correlates with body fat content and is usually higher in obese subjects, suggesting that human obesity is generally associated with insensitivity to leptin. However, 5–10 percent of obese individuals have relatively low levels of leptin, indicating a reduced rate of leptin production. The fact that some obese individuals have low leptin levels suggests that decreased production can also lead to obesity. This suggests that in most cases the cause of leptin resistance and obesity is equivalent to insulin resistance in type II diabetes.
Diet-induced weight loss in humans results in a decrease in leptin concentration. This may explain the high failure rate of dieting, as low levels of leptin appears to be a strong stimulus to weight gain.
When fasting on water only, appetite is generally suppressed after the first one to two days, when liver stores of glucose are used up and the body moves into ketosis (fat-burning). After a prolonged fast when all body fat stores are used up, starvation occurs. Starvation is the breakdown of essential body organs.
Research in the journal Diabetes shows that fat-containing milk, and of which fats are 98% triglycerides, immediately inhibits leptin transport across the blood-brain barrier. Fat-free milk does not have this effect. In this study both starvation and diet-induced obesity elevated triglycerides in the blood and decreased the transport of leptin across the BBB, whereas short-term fasting decreased triglycerides and increased leptin transport.
Triglyceride-mediated leptin resistance may have evolved as a mechanism to restore this fasting loss of appetite at the onset of starvation. Decreasing triglycerides may potentiate the effect of leptin to reduce appetite by enhancing leptin transport across the blood-brain barrier (BB.
The Complete Blood Type Encyclopedia outlines natural approaches to reducing triglycerides. ------------ References:
W.A. Banks et al., “Triglycerides induce leptin resistance at the blood–brain barrier,” Diabetes, 53:1253-1260, 2004.
A.J. Kastin, V. Akerstrom, “Fasting, but not adrenalectomy, reduces transport of leptin into the brain,” Peptides, 21:679–682, May 2000.
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