Accumulated acid waste and inflammation are almost ALWAYS implicated as the cause or catalyst of the onset of disease, as well as the accelerator and the result of disease progression! That being said, excessive acid production in the body is a symptom of poor diet and lifestyle choices, in conjunction with environmental toxic exposure and the resultant retention of toxic waste in the body.
Excessive acid leads to the gaining and retaining of fat! Accumulating acids are responsible for creating or adding more FAT to fat cells attempting to store the excess waste to protect the blood and organ systems from acid damage. When these fat cells get too big they can explode and die, dispelling all that acidic toxic waste, initiating a chronic inflammatory immune response. When left unchecked, inflammation continues, and more acidity and fat are stored. The blood and lymph coagulate, less oxygen is available, cellular metabolism slows down, and therefore a lot less energy is produced. Toxic waste continues to accumulate, nutrient absorption is hampered, weight loss is a near impossible task, and the vicious cycle of degeneration continues.
Inflammation, often accompanied by pain, is one the symptoms of immune responses to foreign debris and pathogens and can manifest itself in many areas of the body. In the body’s attempt to protect itself from extreme pH fluctuations, accumulating acids also end up being stored in muscle tissue (like with fibromyalgia), joints and extremities (emerging as some form of arthritis), organs like the kidney and gallbladder (materializing as stones), in the brain as dementia, or the arteries (contributing to arteriosclerosis, especially in acid crystal form).
As the body stores this acid waste to save you from imminent death, other problems ensue as a result! For example, accumulating acids derived from too many acid-forming foods, drinks, inadequate hydration, and toxic thoughts can crystallize between joints and damage the synovial membrane. Joints that are weak, previously injured, overworked, and/or malnourished are primary targets. If these crystals tear the membrane, the synovial fluid that lubricates the joints can leak, resulting in degradation and painful inflammation, commonly associated with arthritis. These acid crystals are often formed when calcium combines with the accumulating damaging acids in its attempt to neutralize them or put out the inflammatory fire, thus creating further deposition (calcium deposits) in the joints and tissues.
So where does this calcium come from? The calcium most often comes from your own bones and/or from too much inorganic calcium supplementation without the support of co-factors like magnesium, vitamin D, K2, and other co-factors to escort the calcium to the bones. Even though they miss the obvious correlation between low pH tissue, inflammation, and calcium acid crystallization, Harvard Medical School still recognizes calcium loss from the bones as one of the main problems.
According to Harvard University researchers, “people prone to kidney stones excrete about one-third more of their calcium intake in urine than people who don’t have kidney stones.” They go on to say, “They may be losing calcium from their body, which raises their risk for low bone density as well as kidney stones.”
Even though it is not the purpose for this study, a little further investigating would uncover the cause (excessive acidity) as opposed to just the effect of calcium loss from the bones. The inflammation associated with arthritis and kidney stones can be very painfully obvious, but even worse, organs like the liver, pancreas, and kidney can be acidic, inflamed, and degenerating with little warning until the damage is severe and even life threatening!
Chronic Kidney Disease (CKD) is often referred to as the “silent” disease because many people do not begin to notice symptoms until their kidneys are about to fail. Testing urine pH levels regularly, while taking the appropriate dietary and lifestyle measures to prevent and correct imbalances, can deter severe, life altering surprises like CKD. Non-clinical LOW GRADE CHRONIC ACIDOSIS is the culprit and needs to be recognized!
Although referenced both directly and indirectly by very convincing studies and compiling data, the conventional medical establishment sadly does not yet consider non-clinical low grade chronic acidosis as a marker of disease initiation. There is plenty of research out there, but most doctors are still stuck in the conventional paradigm, severely LIMITING their access to highly valuable life-saving wisdom. The longer it takes to get this invaluable information out to the public, the more needless pain, suffering, and death there will be as a result!
LATENT ACIDOSIS LINK TO INSULIN RESISTANCE
With 50% of adults being diabetic or pre-diabetic you can only imagine how prevalent insulin resistance would be. Studies now show what we already suspected, that low pH tissues and fluids are highly suspect in the initiation of insulin resistance, a marker of metabolic dysfunction. Insulin resistance prevents energy producing glucose from entering the cell, decreases cellular energy and function, and increases your risk for many diseases. Not only do low pH fluids play a role in insulin resistance, but insulin resistance hinders the elimination of acid, creating further acidity issues.
In the recent 2014 study ‘Importance of pH Homeostasis in Metabolic Health and Diseases: Crucial Role of Membrane Proton Transport’, authors showed that before any diabetes symptoms were evident, the interstitial fluid and tissue in rats is lower than the normal pH of 7.4. While the buffering capacity of the blood is fairly high and somewhat high in the cytosol fluid of the cell, this is not true of the interstitial fluids between the cells. Interstitial fluid pH is much more unstable and can fluctuate, allowing for the potential development of insulin resistance. According to the researchers, “binding affinity to insulin of insulin receptors were significantly diminished in media with low pH. (along with a reduction in glucose uptake) These in vitro observations support the hypothesis that lower extracellular pH may cause insulin resistance in skeletal muscle cells.” (1)
Besides the research showing causation for insulin resistance due to hyperuricemia (excess uric acid in blood) and low pH tissue fluid, there is also an obvious resultant increase in other metabolic risk factors. Hypertension, low HDL cholesterol and high serum triglycerides, dangerous weight gain, high fasting blood sugar or insulin resistance, and hyperuricemia, are all associated with metabolic syndrome. Patients diagnosed with metabolic syndrome must have at least 3 of these risk factors present.
Insulin resistance is so closely tied to metabolic syndrome that it is often referred to as insulin resistance syndrome. When ignored, these factors greatly increase the likelihood of developing many dangerous conditions like obesity, diabetes type 2, heart disease, kidney disease, stroke, Alzheimer’s, dementia, cancer, and many others.
In a 2007 study ‘Low Urine pH: A Novel Feature of the Metabolic Syndrome’, researchers concluded that high acidic urine is an attribute of the metabolic syndrome and is associated with the degree of insulin resistance. They went on to say, “A significant inverse relationship was noted between 24-hour urine pH and the degree of insulin resistance.” Patients with metabolic syndrome reported a significantly lower 24-hour urine pH when compared to the normal subjects. The more negative metabolic risk factors present the greater the pH imbalance. (2)
In the 2007 study ‘Prevalence of the metabolic syndrome in Individuals with hyperuricemia’ authors made this powerful statement:
The link between hyperuricemia and insulin resistance has been noted. Our objective was to determine the prevalence of the metabolic syndrome according to serum uric acid levels in a nationally representative sample of US adults. By using data from 8669 participants aged 20 years and more in The Third National Health and Nutrition Examination Survey (1988-1994), we determined the prevalence of the metabolic syndrome at different serum uric acid levels. These findings from a nationally representative sample of US adults indicate that the prevalence of the metabolic syndrome increases substantially with increasing levels of serum uric acid. Physicians SHOULD recognize the metabolic syndrome as a frequent comorbidity of hyperuricemia and treat it to prevent serious complications. (3)
Other studies have demonstrated a close connection between excess acid production in the body and insulin sensitivity, not only in type 2 diabetes patients, but also in healthier subjects. In the cross-sectional study ‘Association of urine acidification with visceral obesity and the metabolic syndrome’, authors studied over 1,000 subjects. They showed that body weight and waist size are negatively associated with both insulin sensitivity and urine pH.