Part 1 of 2: Understanding metabolic acidosis
Do alkaline diets work?
The answer to the question is: Yes, quite likely. If you know what you’re doing, that is. Optimizing metabolic alkalinity likely plays a significant role in healing, but it’s not as straightforward as it might seem.
In part 1 of this 2-part post we’ll introduce the concept of metabolic acidosis and explore some of the conditions that may benefit from – and be even prevented by – an alkaline diet. In part 2 we’ll dig into the science behind how pH-balancing diets do (and don’t) work, and why acidic foods like apple cider vinegar and lemon juice are actually alkalinizing and good for our health.
Understanding metabolic acidosis
A chronic state of acidity (acidosis) within the fluids, cells, and tissues of the body has been linked to poor health and the development of a wide variety of diseases, including osteoporosis, kidney stones, arthritis, and even cancer. This suggests that pH (or the acid-alkaline state of the body) is a critical factor in health and well being.
But this is where controversy begins to arise, with two opposing schools of thought, which go something like this:
- The conservative view: The body is capable of maintaining pH balance whatever challenges it faces. pH changes thus only manifest as severe metabolic acidosis in discrete health conditions, such as renal disease. Focusing on acid-alkaline diets is therefore likely a waste of energy and time.
- The integrated view: Subclinical low-grade metabolic acidosis in the cells and tissues of the body is a real phenomenon underlying many chronic disease states. Addressing low-grade metabolic acidosis can therefore help restore and maintain optimal health.
Both schools of thought agree that the body must at all costs operate at a stable pH, so any increase in internal acid load, for whatever reason, must be neutralized by one of several homeostatic base-producing mechanisms.
How the body does acid-alkaline balance
It’s a well-researched and documented set of highly intelligent physiological and biochemical pathways that determine the exquisitely sensitive homeostatic mechanisms governing cell and tissue acid-alkaline levels in the body.
Firstly, we have bicarbonate, phosphate, and protein buffer systems that neutralize acids. One way in which they do this is by combining acids with alkaline minerals like magnesium, potassium, calcium, and sodium. This prevents strong acids from building up and causing damage in the blood, lymph, and tissue cells.,
The kidneys take center stage in neutralizing acids by combining them with bicarbonate and other alkalis before eliminating them through the urine. It is also well documented that when acidosis is triggered, the body responses elicited to correct the pH result in a measurable increase in renal net acid secretion. Breathing also helps us to alkalize, as we inhale oxygen and exhale acidic carbon dioxide. Finally, our skin eliminates acids through the action of sweating. All these systems, especially the kidneys, keep a tight rein on controlling pH, especially within the blood.
The pH challenges of modern-day living
Despite the body’s hard work, many factors in our lives – including diet, cigarette smoke, air pollution, and other environmental toxicants – challenge our homodynamic pH systems daily, leading to what many health practitioners recognize as a low-grade chronic metabolic acidosis.
This subtle sub-clinical rise in acidity within the body cells in turn negatively impacts and perturbs biochemical and physiological pathways, including important enzyme pathways and the production of cellular energy (ATP). This problem remains undiagnosed and even unrecognized by many in the medical profession. The established alternative view, however, argues that sub-clinical low-grade metabolic acidosis could contribute to chronic diseases if left unchecked.
Sub-clinical low-grade metabolic acidosis could contribute to chronic diseases if left unchecked.
So what links low grade metabolic acidosis to chronic disease, and what can we do about this sub-clinical condition? Let’s look at the science…
Since calcium is a strong alkaline mineral and bone contains the body’s largest calcium store, metabolic acidosis has been suggested to cause a release in calcium from bones. The thought here is that when the body is in a state of metabolic acidosis (whether low-grade or frank), the bones will release some calcium to neutralize that acidity. From there, the calcium doesn’t go back into the bones to keep them strong, but rather exits the body through the urine. Metabolic acidosis can also reduce renal tubular calcium resorption, the process by which the kidneys filter the calcium back into the body, sparring it from urinary elimination. [It’s been well established that raised acid levels in the body tissues can lead to hypercalciuria (high concentrations of calcium in the urine).]
Some studies have also shown that metabolic acidosis can increase 1,25-(OH)2 Vitamin D and decrease parathyroid hormone (PTH) levels in humans, as part of the early homeostatic mechanisms employed in response to calcium imbalances.,
The bones release calcium (and therefore get weaker) as the body attempts to neutralize the acidic environment.
This suggests that subtle, low-grade changes towards metabolic acidosis may alter calcium levels and bone response in the body. Some studies have even shown that the net result of these tissue acid changes is a reduction in bone density, as the bones release calcium (and therefore get weaker) as the body attempts to neutralize the acidic environment.
Arthritis & joint problems
According to classically trained practitioners, another type of calcium misplacement in the body can occur when acidic toxins (including those derived from cellular metabolic waste, gut bacterial endotoxins, or environmental toxins) accumulate in the joints of the fingers and toes, extremities far from vital soft tissue organs like the heart.
The body uses calcium to buffer the increasing acidity within the joints, leading to stiffness and arthritic changes.
The understanding is that the body uses calcium to buffer the increasing acidity within the joints, leading to stiffness and arthritic changes, beginning with the fingers and toes, and progressing onto the wrists, ankles, elbows, knees and other joints.
Studies have shown that high acid levels in the body contribute to negative nitrogen balance (high concentrations of nitrogen in urine). This contributes to skeletal muscle protein breakdown as the body ages, a phenomenon known as sarcopenia.
The amino acid glutamine found in skeletal muscle is responsible for binding hydrogen ions to form ammonium. Since hydrogen ions are acidic, glutamine may act much like calcium to neutralize the body’s accumulating acidosis. Skeletal muscle contains the body’s largest glutamine stores, therefore low-grade metabolic acidosis may contribute to muscle breakdown to liberate glutamine from the muscle. The amino acids from this muscle breakdown are then excreted, causing a net loss of muscle protein.
Clinical studies show that serum insulin growth factor-1 (IGF-1) concentrations are decreased in response to metabolic acidosis. The benefits of IGF-1 include building muscle mass and preventing muscle wasting, supporting bone mass, encouraging growth, managing blood sugar levels, and safeguarding against neurological disorders. A decrease in IGF-1 can therefore contribute to illness.
Thyroid hormone secretion (T3 and T4) is also reduced in metabolic acidosis, with the underlying potential to induce primary hypothyroidism.
Chronic metabolic acidosis has also been demonstrated to significantly increase cortisol levels, which may contribute further contribute to protein (muscle) breakdown and increase renal (kidney) acid load.
Kidney stones & renal disease
Clinical evidence demonstrates that many forms of kidney stones are made of calcium. This is but another example of calcium misplacement, and may suggest a maladaptive behavior the body uses to neutralize subclinical metabolic acidosis.
Organic citrates, such as those used as carriers in some high-quality food supplements to bind alkaline minerals like magnesium, may reduce the formation of kidney stones. Recent clinical studies have shown how eating a diet rich in fruit and vegetables and low in dietary acids can help successfully manage cases of chronic kidney disease.
Low-grade metabolic acidosis and chronic disease
Low-grade metabolic acidosis may very well worsen with age, potentially contributing to development of one of the conditions previously described. We could speculate that this is due to an age-related decline in kidney function and therefore the body’s ability to excrete acids. Some practitioners may also consider the increasing levels of acidic toxins (e.g. cellular metabolic waste and related dietary metabolites) that accumulate with advancing age, coupled with reduced detoxification capacity and increased dehydration, which may contribute to age-related body acid load.
The body is most likely to move through preliminary stages of low-grade metabolic acidosis before entering a deeper level of acidity and pH imbalance.
Many of the studies we’ve just discussed investigated cases of chronic acidosis or clinically induced acidosis. However, we can postulate that the body is most likely to move through preliminary stages of low-grade metabolic acidosis before entering a deeper level of acidity and pH imbalance.
Or, in other words: “We don’t catch chronic diseases, we create them by breaking down the natural defenses according to the way we eat, drink, think and live.” – Dr. Bernard Jensen (1908-2001)
Simply put, this means that by regularly employing a few simple acid-base strategies to help support optimal cellular function, we can help the health of our bones, muscles, and kidneys.
Check back tomorrow to read part 2 of this article, in which we answer to the question: “Do alkaline diets work?” and offer strategies for gently combating subclinical metabolic acidosis.
Click here to see References
 Wiederkehr M, et al. Metabolic and endocrine effects of metabolic acidosis in humans. Swiss Med Wkly. 2001;10:127-32.
 Baum M, et al. Glucocorticoids stimulate Na/H antiporter in OKP cells. Am J Physiol. 1993;264:F1027–31.
 Kinsella J, et al. Na/H exchange activity in renal brush border membrane vesicles in response to metabolic acidosis: the role of glucocorticoids. Proc Natl Acad Sci USA. 1984;81:630–4.
 Richards P, et al. Treatment of osteomalacia of renal tubular acidosis by sodium bicarbonate alone. Lancet. 1972;II:994-7.
 Wiederkehr, et al. Metabolic and endocrine effects of metabolic acidosis in humans. Swiss Med Wkly. 2001;10:127-32.
 Buclin, et al. Diet acids and alkalis influence calcium retention in bone. Osteoporos Int. 2001;12:493-9.
 Lee SW, et al. 25-hydroxycholecalciferol: conversion inhibited by systemic acidosis. Science. 1977;195:994–6
 New, S. Nutrition society medal lecture. The role of the skeleton in acid-base homeostasis. Proc Nutr Soc. 2002;61(2):151-64.
 May RC, et al. Metabolic acidosis stimulates protein breakdown from skeletal muscle. J Clin Invest. 1986;77:614–21.
 Welbourne TC, et al. Enteral glutamine spares endogenous glutamine in chronic acidosis. PEN. 1994;18(3):243-7
 Bru¨ngger M, et al. Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: New cause of growth hormone insensitivity in humans. Kidney Int. 1997;51:216–21.
 Trinchieri A, et al. Effect of potential renal acid load of foods on calcium metabolism of renal calcium stone formers. Eur Urol. 2001;39:33–6.
 Frassetto, et al. Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women. J Clin Endocrinol Metab. 1997;82:254-9.
 Scialla, J, et al (2013) Dietary acid load: A novel nutritional target in chronic kidney disease? Adv Chr Kid Dis 20:141-9.