Acidity & Acidosis


Over acidity in the body is a dangerous condition that weakens all body systems. This condition is very common today. By keeping the body acidic gives rise to an internal environment conducive to disease, as opposed to a pH-balanced environment which allows your internal system to fight off and resist disease. Keeping the body healthy through proper hydration and adequate pH-balancing allows the body to maintain alkaline reserves. These reserves are necessary to meet emergency demands. However, when over acidity in the body is excessive alkaline reserves are depleted leaving the body in a weakened condition.

“Overacidification of the body is the single-underlying cause of all sickness and disease”

Acidosis is an increased acidity (i.e. hydrogen ion concentration) of blood plasma. Generally acidosis is said to occur when arterial pH falls below 7.35, while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes.Strictly speaking, the term acidemia would be more appropriate to describe the state of low blood pH, reserving acidosis to describe the processes leading to these states. Nevertheless, most physicians use the terms interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, where the relative severity of both determines whether the result is a high or a low pH. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g. healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage (Needham, 2004).

metabolic acidosis is a state in which the blood pH is low (under 7.35) due to increased production of H+ by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general types of acidosis. Symptoms are aspecific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite (either loss of or increased) and weight loss (longer term), muscle weakness and bone pains. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in a compensatory respiratory alkalosis. Extreme acidosis leads to neurological and cardiac complications:

Neurological: lethargy, stupor, coma, seizures.
Cardiac: arrhythmias (ventricular tachycardia), decreased response to epinephrine; both lead to hypotension (low blood pressure).

Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol (methyl alcohol) intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.

Type A: Decreased perfusion or oxygenation
Type B:
B1: Underlying diseases (sometimes causing type A)
B2: Medication or intoxication
B3: Inborn error of metabolism

Lactic acidosis is an underlying process of rigor mortis. Tissue in the muscles of the deceased resort to anaerobic metabolism in the absence of oxygen and significant amounts of lactic acid are released into the muscle tissue. This along with the loss of ATP causes the muscles to grow stiff.

Lactic acidosis: A life-threatening condition caused by too much lactate in the blood and low blood pH. Lactic acidosis is a condition caused by the buildup of lactic acid in the body. It leads to acidification of the blood (acidosis), and is considered a distinct form of metabolic acidosis. The cells produce lactic acid when they use glucose for energy in the absence of adequate oxygen. If too much lactic acid stays in the body, the balance tips and the person begins to feel ill. The signs of lactic acidosis are deep and rapid breathing, vomiting, and abdominal pain. Lactic acidosis may be caused by diabetic ketoacidosis or liver or kidney disease, as well as some forms of medication (most notably the anti-diabetic drug metformin). Some anti-HIV drugs (antiretrovirals) warn doctors in their prescribing information to regularly watch for symptoms of lactic acidosis caused by mitochondrial toxicity.

Respiratory acidosis: A condition in which a build-up of carbon dioxide in the blood produces a shift in the body’s pH balance and causes the body’s system to become more acidic

Ketoacidosis occurs in two very different situations — in type 1 diabetes (diabetic ketoacidosis) and in alcohol withdrawal (alcoholic ketoacidosis). The ultimate reason for ketoacidosis in both cases is the same: The cell does not have enough glucose (in the case of diabetes because lack of insulin prevents the cell from taking up glucose, in the case of starvation because there is less glucose around), so it begins metabolizing fat molecules instead of simple sugars. As a result of this metabolic change, acetyl-CoA is mainly produced from the breakdown of fatty acids and fed into the citric acid cycle. The intermediates of the citric acid cycle are used for other anabolic purposes as well and have to be replenished. Normally, this is done by converting pyruvate into oxaloacetate or L-malate (the so-called anaplerotic pathways). But pyruvate is the end product of glycolysis, the breakdown of glucose, and glucose levels are lower in the cases we consider. This means that the citric acid cycle intermediates cannot be replenished, the cycle slows down, acetyl-CoA accumulates and ketogenesis becomes more important.


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