Chapter 3 - Are Paida and Lajin suitable for those weak in Qi?

Are Paida and Lajin suitable for those weak in Qi?

Diseases and aging are caused by declined yang-qi (right qi) in the body. The way to replenish yang-qi is to clear our meridians, as “smooth flowing meridians are the best tonic”. However, many people, including experienced doctors of Chinese medicine, are not able to grasp this point. From a scientific perspective, Paida and Lajin can induce generation of “endogenous medicine” in the body. It has been proven in front-line scientific research (Please refer to Prof. Gerard Karsenty’s findings published in Cell Journal, August 2007 Issue) that joints, skin, muscles, tendons and bones are not only kinematic systems; they are the largest human endocrine system. As such, when Paida and Lajin work on them, meridians, tendons, blood vessels, lymphatic vessels, nerves and other systems will be gradually cleansed; organs, blood and even body cells will be re-optimized. This not only enhances the immune system, biochemical substances needed by the individual, or “endogenous medicines”, such as hormones, stem cells, insulin, adrenaline, enkephalin, etc. will also be automatically generated.

This is clearly explained in Chinese medicine: Paida and Lajin replenish yang-qi (right qi), which enhances the circulation. When aided with food therapy (e.g. ginger and date soup), the body will have sufficient yang-qi, and diseases are kept at bay. Smooth flowing meridians can enhance yang-qi, which acts as an anti-virus software in the body that automatically removes viruses, swellings, tumors and other diseases. Therefore, replenishing weak Qi should be done on the premise of smooth flowing Qi in meridians. Otherwise, nourishments entering the body may spur the growth of diseases instead of replenishing the body.

Hence, as long as one is alive, Paida and Lajin can be practiced; however, it should be noted that the intensity should be increased gradually from light to heavy; and the duration be lengthened gradually according to one’s condition and tolerance. 


COLUMBIA NEWS.

Research Shows Skeleton to be Endocrine Organ.

Crucial to controlling weight and metabolism; discovery opens door to therapy for type-2-diabetes. 

Bones are typically thought of as calcified,  inert structures, but researchers at Columbia  University Medical Center have now  identified a surprising and critically  important novel function of the skeleton.  They’ve shown for the first time that  the skeleton is an endocrine organ  that helps control our sugar metabolism  and weight, which makes it a major  determinant of the development of  type 2 diabetes. The research, published in the August 10  issue of Cell, demonstrates that bone cells  release a hormone called osteocalcin, which  controls the regulation of blood sugar  (glucose) and fat deposition through  synergistic mechanisms previously not  recognized. Usually, an increase in insulin  secretion is accompanied by a decrease in  insulin sensitivity. Osteocalcin, however,  increases both the secretion and sensitivity of  insulin, in addition to boosting the number of  insulin-producing cells and reducing stores of  fat.  In this published research, authors show that  an increase in osteocalcin activity prevents  the development of type 2 diabetes and  obesity in mice. This discovery potentially  opens the door for novel therapeutic avenues  for the prevention and treatment of type 2  diabetes.  “The discovery that our bones are responsible  for regulating blood sugar in ways that were  not known before completely changes our  understanding of the function of the skeleton  and uncovers a crucial aspect of energy  metabolism,” said Gerard Karsenty, M.D.,  Ph.D., chair of the department of Genetics and  Development at Columbia University Medical  Center, Paul Marks Professor in the Basic  Sciences, and senior author of the paper.  “These results uncover an important aspect of  endocrinology that was unappreciated until  now.”

Karsenty and his colleagues had previously shown that leptin, a hormone released by fat cells, acts upon and ultimately controls bone mass. They reasoned that bones must in turn communicate with fat, so they searched bone-forming cells for molecules that could potentially send signals back to fat cells.  

The researchers found that osteocalcin, a protein made only by bone-forming cells (osteoblasts), was not a mere structural protein, but rather a hormone with totally unanticipated and crucial functions. Osteocalcin directs the pancreas’ beta cells, which produce the body’s supply of insulin, to produce more insulin. At the same time, osteocalcin directs fat cells to release a hormone called adiponectin, which improves insulin sensitivity. This discovery showed for the first time that one hormone has a synergistic function in regulating insulin secretion and insulin sensitivity, and that this coordinating signal comes from the skeleton. Additionally, osteocalcin enhances the production of insulin-producing beta cells, which is considered one of the best, but currently unattainable, strategies to treat diabetes.

People with type-2-diabetes have been shown to have low osteocalcin levels, suggesting that altering the activity of this molecule could be an effective therapy. That hypothesis is supported by the Columbia research, which showed that mice with high levels of osteocalcin activity were prevented from gaining weight or becoming diabetic even when they ate a high fat diet. Analysis of mice lacking the osteocalcin protein showed that they had type 2 diabetes, increased fat mass, a decrease in insulin and adiponectin expression, and decreased beta-cell proliferation.

This research was supported by the National Institutes of Health, the American Diabetes Association, the Japan Society for the Promotion of Science and the Pennsylvania Department of Health.

The researchers are now examining the role of osteocalcin in the regulation of blood sugar in humans and are continuing investigations into the relationship between osteocalcin and the appearance of type 2 diabetes and obesity.

Published: August 09, 2007
Last modified: Aug 09, 2007