Chronic Acidic Inflammation Reduced and/or Eliminated With Bicarbonates

The appended article below is another in a long string of recent articles illuminating how "chronic inflammation" in the human body results in a wide range of serious and often fatal complications. For example, inflammation has long been known to be the prime contributing factor to atherosclerosis, heart disease, diabetes, asthma, etc., etc.. In repeated lectures and writings I have noted the consequences of chronic acidic inflammation, and pointed out that stabilizing systemic bicarbonates results in better cellular oxygenation, and decreased acids that cause inflammation. It has been known for years, that bicarbonates will increase athletic performance in untrained athletes. Now we know that such increased athletic performance is the result of better tissue oxygenation mediated by the bicarbonates that reduces metabolic acids.

The appended article points out that the dramatic oxygen-deprived conditions in fatty tissue apparently contribute to (stimulate) an increase in angiopoietin-like protein 2 (Angptl2) resulting in the increased inflammation. There is a cascade into serious illness started by the accumulation of acidic stored, oxygen-deprived, fatty tissue resulting in wide-spread chronic inflammation.

I have encouraged the use of bicarbonate salts, such as pHour Salts, coupled with a life-style shift to the pH Miracle Alkaline Diet, drinking active, ionized / alkalized water, and engaging in age-appropriate exercise, to decrease fat accumulation, increase tissue oxygenation, reduce acid tissue inflammation and boast overall health. pHour Salts helps to properly alkalize body tissues and blood, increase oxygen transport, buffer excess metabolic acid which in turn will successfully decrease chronic inflammation.

We have not always known precisely all of the reasons "why" bicarbonate supplementation, with products such as pHour Salts, works so dramatically to improve health, but now every day we hear more from scientific communities around the world, as they discover and learn more about the "whys", and validate my teachings on "Alkalizing and Energizing" for health.

--------------------Referenced Article-------------------

From Fat to Chronic Inflammation

September 7, 2009

(Ivanhoe Newswire) -- Chronic inflammation within fat tissue is now recognized as a contributor to the many negative consequences that come with obesity -- from diabetes to cardiovascular disease, according to Yuichi Oike of Kumamoto University in Japan. Researchers hope a new discovery will point to a targeted therapy designed to limit the impact of the obesity epidemic.

The new culprit Oike's team identified is a fat-derived protein called angiopoietin-like protein 2 (Angptl2). In mice, Angptl2 levels are elevated in many organs, but especially in fat tissue. Those levels increase further under the oxygen-deprived conditions typically found within obese fat tissue. Researchers also found higher Angptl2 levels in the blood of humans with higher body mass index and insulin levels.

Obese mice lacking Angptl2 show less inflammation in their fat tissue and are less insulin resistant, researchers report. Likewise, otherwise healthy mice made to have higher than normal Angptl2 levels in their fat tissue develop inflammation and insulin resistance.

The researchers conclude that Angptl2 is a key adipocyte-derived inflammatory mediator linking obesity to systemic insulin resistance, and they have identified it as a new molecular target that could be used to improve the diagnosis and treatment of obesity and related metabolic diseases.

Oike is quoted as saying he thinks drugs that would act on Angptl2 not only have considerable promise, but are also likely to come with limited side effects.

"In healthy animals and people, the precise role of Angptl2 has not been clarified," he said. "However, mice in which Angptl2 was deleted genetically were born normally and showed normal growth compared to genetically normal mice. Therefore, we speculate that the possibility of the occurrence of a serious unfavorable side effect due to treatments that decrease Angptl2 expression in animals or people is low."

SOURCE: Cell Metabolism, September, 2009

Reference: http://ivanhoe.com/channels/p_channelstory.cfm?storyid=22364