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    Alternatives and Compliments for current
    Medical Protocols and Pharmaceuticals.
Grand Junction, Colorado

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Renee’ Calder, CNT, MNT
(970) 201-5723

Applying the Science of Nutrition to the
Art of Healing on the Western Slope of Colorado
Disclaimer:  Nutrition Therapy is not intended as a diagnosis, a treatment, a prescription, or a cure for any disease either mental or physical,
and is not intended as a substitute for regular medical care. Nutrition therapy does provide nutritional evaluation, balanced diet planning,
nutritional supplement suggestions and lifestyle recommendations for the purpose of enhancing health.
Biogenic Amines
***this page still under construction check back often***

Frustrated with your doctors’ failure to help make you feel well?

Tired of misdiagnoses and ineffective treatments?

Do you experience chronic ailments, or symptoms that have
your doctors’ scratching their head?

Unlike inflammation, which is recognized by conventional
doctors, acidosis is completely ignored.

Heart disease, diabetes, fatigue, digestive problems, kidney
stones, gout…and much, much, more, are generally a
combination of inflammation and acidosis that has spiraled out
of control.

- Food Allergies
- Food Allergy
- Lactic Acidosis
- Metabolic Syndrome
- Drug Induced
    Metabolic Acidosis
- Acidosis
    Natural Treatment
Biogenic Amines –
The Good, The Bad, and The Ugly

Some people who experience allergic types of reactions will test negative for allergies on standard LRA (lymphocyte response
assay).  Or, the test may result that they are allergic to things they don’t have any problems with, or vice versa.  Leaving many
doctors and patients without answers.  These people who are testing negative for allergies on standard LRA, yet, are continually
experiencing allergic type of reactions, are most definitely experiencing some sort of biogenic amine intolerance, or a failure of
the metabolic processes that utilize and dispose of them.  Or, they are experiencing a manipulation of metabolic process at the
cellular level by these enzymes and their byproducts.

High intake of biogenic amine foods can lead to biogenic amines entering the systemic circulation, causing the release of
adrenaline and noradrenaline, provoking gastric acid secretion, increased cardiac output, migraine, tachycardia, increased blood
sugar levels, and high blood pressure.
[2]    Most people experience the highest levels of sensitivity to the amines histamine and
tyramine, while the other amines don’t bother them at all.

Biogenic Amines have been causative agents behind several food poisoning episodes, notably; “Scombroid poisoning” caused by
histamine, and “Cheese reaction”  caused by tyramine, especially in combo with MAOIs as antidepressants.  Human sensitivity to
biogenic amines varies according to an individual’s detoxifying activities of the enzymes involved in the metabolism of said  
biogenic amines. Metabolic pathways include those for histamine, methyltransferase, MAO, DAO, and other less specific methods

The toxic level of biogenic amines is difficult to establish but some criteria have been established in the food and beverage
    100 mg histamine per kg of food.
    2mg of histamine per liter of alcoholic beverage.
    Alcohol toxic base is 8-20 ml/l for histamine 25, and 40mg/l for tyramine.
    As little as 3mg/l of phenylethylamine can cause negative physiological effects. [2]

Enzymes are produced in the body that render amines harmless.  But, sometimes these enzymes can become sluggish or blocked.  
Mutations of the MAO-A gene results in monoamine oxidase deficiency known as Brunner Syndrome.  Other disorders associated
with MAO-A deficiency include; autism, Alzheimer’s disease, aggression, panic disorder, bipolar affective disorder, major
depressive disorder, and ADHD.  Drugs like antibiotics and antidepressants can inhibit the actions of MAO enzymes causing
stomach problems, mental confusion, depression, migraine, vomiting, itching, fever, rash, and other symptoms.

MAO-A is a key regulator for normal brain function.  It is a flavoenzyme which degrades amine neurotransmitters, such as
dopamine, norepinephrine, and serotonin, via oxidative deamination.  It is highly expressed in neural and cardiac cells. Its
expression is regulated by transcription factors, via the CAMP pathway, in response to stress such as ischemia and inflammation.  
Besides the roles MAO’s have in maintaining serotonin, dopamine, and norepinephrine balance, the
MAO-A and MAO-B enzymes
also breakdown and deactivate phenethylamine, benzylamine, tyramine, and tryptamine.
 Phenethylamine is a central nervous
system stimulant. The inability to break down these compounds would have serious hyper-stimulatory effects in the brain and in
the heart.

A variant of the MAO-A gene has been popularly referred to as the “warrior gene”.  People with this MAO mutation have a unique
ability in that they can quickly produce an excess of adrenaline.  The body uses adrenalin to shift resources around during stress,
aka the fight or flight response.  Adrenalin helps sharpen focus, releases stored energy, increases blood pressure and muscle
strength.  People in this variant are some of the smartest, most-intelligent people you will ever meet because this mutation
increases dopamine, noradrenalin, and adrenalin in the frontal lobes of the brain, allowing better focus (like a laser at times), and
usually very detail oriented with a good memory—as long as their system is not overburdened.  Otherwise, such a person can look
like a “stress mess”.

The enzymes DAO and MAO are inhibited by several types of drugs (neuromuscular blocking drugs d-tubocurarine, pancuronium,
alcuronium, ethanol, and antidepressant drugs).  Use of these drugs along with consumption of fermented foods and drinks may
cause disorders including life-threatening serotonin syndrome.  Because of this, use of MAOIs has been limited.

MAOI’s (monoamine oxidase inhibitors), inhibit the breakdown of tyramine, causing a build-up in the body, leading to high blood
pressure, headaches, itchy skin rashes, heart palpitations and diarrhea.  Many patients died from strokes or heart attacks before
it was realized that dietary intakes of tyramine foods should be limited in persons taking MAOI’s.
[1]   The MAOI diet was created as
an accompaniment for doctors to offer patients when prescribing these medications.  The diet is designed to control tyramine
intake by omitting fermented products such as aged cheese, aged or cured meats, sauerkraut, soy sauce, and tap beer.
[2]  Click
here for an overview of such a diet on MayoClinic.

Low levels of enzyme DOA cannot break down all the histamine found in the body, creating histamine intolerance.  Other factors
that are of huge importance include alcohol consumption, and environmental exposure to things that may burden, or upset,
metabolic pathways.  These things can create inadequate detoxification of biogenic amines leading to persistent, progressively
worsening, complaints of “dis-ease”.  Without proper attention, and proper treatment, this
“dis-ease” will eventually turn to
DISEASE.  Biogenic amine levels are higher in patients with Parkinson’s disease, schizophrenia, and depression.[2]  Ask your doctor
about Diamine Oxidase (DAO) and Monoamine Oxidase (MAO).  If they seem perplexed, or say, “I don’t know”, then find another
doctor quickly.

Prokaryotic Cell vs Eukaryotic Cell
Biogenic amines carry both Physiological Roles
and can produce Toxicological Effects:

- In
eukaryotic cells, biogenic amine
biosynthesis is essential, as these compounds
function as precursors for the synthesis of
hormones, alkaloids, nucleic acids, and
    . Some biogenic amines have important
    roles as neurotransmitters (serotonin).
    . Some biogenic amines are needed for
    critical biological functions (putrescine
    and spermidine).

- In
prokaryotic cells, the physiological role of
biogenic amine synthesis is mainly related to
defense mechanisms used by bacteria to
withstand acidic environments.
Decarboxylation increases survival under
acidic stress conditions through the
consumption of protons and the excretion of
amines and CO2 helping to restore their
internal pH.

Relationships between the presence of the gene encoding the decarboxylase, and the capacity to synthesize biogenic amines
has been reported by several authors.
[2]  Recent reports of human infection with “myco”-insectides are emerging due to the
rising popularity of their use in farming.  Reinstating their ability to move and interact between hosts species.

Secondary amines, putrescine and cadaverine, can react with nitrite to form carcinogenic nitrosamines, that promote the
adherence to intestinal mucosa of some disease causing pathogens such as bacteria, fungi, protozoans, or viruses that can infect
and cause diseases.  The fungi can behave like parasites.  In wine high levels of putrescine and cadaverine are normally
associated with poor sanitary conditions of grapes.  Some starter strains for cheese have been enhanced with tyrosine and
histamine decarboxylase activity, designed to reduce tyramine and histamine levels in final product.  Biogenic amines may also
be oxidized by the action of amino oxidase, this amine degradation seems to be restricted to aerobic microorganisms.
Lactic acid bacteria (LAB) are generally considered to be
non-toxic and non-pathogenic.  Some LAB can produce
biogenic amines.  LAB can produce its own metabolic
energy and/or increase their acid resistance by using
catabolic pathways that convert amino acids into amine-
containing compounds.  

LAB strains also have the ability to simultaneously produce
different amines, suggesting that some strains might
possess more than one amino acid decarboxylase activity
under specific conditions.

Lactic Acid is an essential carbohydrate within cellular
metabolism.  Its levels rise with increased metabolism,
during exercise, and with catecholamine stimulation.

There are two forms of Lactate:
    L-lactate is the most common form. It is used to
    measure physical levels, because it is the only form
    produced in human metabolism.  Its excess
    represents increased anaerobic metabolism due to
    tissue hypoperfusion.[3]

    D-lactate is a byproduct of bacterial metabolism and
    may accumulate in patients with short-gut
    syndrome, or in those with a history of gastric
    bypass, or history of small-bowel resection.[3]
LAB Strains
Amine Produced
Lactic Acid Bacteria
Tyramine, Histamine
Pedi Coccus
Wine, Cheese
Leucon Stoc
Wine, Cheese
Tyramine, Histamine
Oeno Coccus
Lactobacillus Hilgardi
Lactobacillus Brevis
Lactobacillus Mali
Lactobacillus Mali
Raw Milk
Lactobacillus Mali
Processes Milk
Tyramine, Histamine,
Putrescine, Cadaverine,
phenylethylamine, tryptamine
Genera Enterococcus
LAB strains have the ability to simultaneously produce different amines
suggesting that some strains might possess more than one amino acid
decarboxylase activity under specific culture conditions.

Catecholamines are produced in the adrenal medulla
and post-ganglionic fibers of the sympathetic nervous
system during the fight or flight response.
    Epinephrine becomes Adrenaline,
    Norepinephrine becomes Noradrenaline,
    Dopamine bcomes Tyramine
    Epinephrine + Norepinephrine = Vanallyl Mandelic
    Acid (VMA), which is excreted in urine.  

Catecholamines increase heart rate, blood pressure,
blood glucose, and have general reactions with the
sympathetic nervous system.  High levels in the blood are
associated with stress, and light and sound sensitivity.

Lactic acid is byproduct of glycolysis, formed in
the cytosol and catalyzed by the enzyme lactate
dehydrogenase, this is a reversible reaction
which favors lactate synthesis (25:1).

The anaerobic metabolic pathway known as
glycolysis is the first step of glucose metabolism
and occurs in the cytoplasm of virtually all cells.  

The end product of this pathway is pyruvate,
which diffuses into the mitochondria and is
metabolized to carbon dioxide (CO2) by, another
more energy efficient metabolic pathway, the
Kreb’s cycle.

Lactate is the normal endpoint of the anaerobic
breakdown of glucose in the tissues, lactate
then exits the cells and is transported to the
liver, where it is oxidized back to pyruvate and
ultimately converted to glucose via the Cori
cycle.  Pyruvate is in equilibrium with lactate at
ratios of 25 lactate to 1 pyruvate.  
Courtesy of National Academy of Sciences

Raised Pyruvate levels can increase lactate synthesis, especially when rapid increase in metabolic rate occurs, or when oxygen
delivery to the mitochondria declines.
[3]  In the setting of decreased tissue oxygenation, pyruvate is not readily metabolized and
its intracellular levels rise, causing lactate levels to rise proportionally.  With persistent oxygen debt and an overwhelming of the
body’s buffering abilities, whether from long-term dysfunction or excessive production, hyperlacticaemia (excess amount of lactic
acid in blood stream), and metabolic acidosis ensue, commonly referred to as lactic acidosis.

The metabolism of glucose to pyruvate known as pyruvate dehydrogenase, results in a chemical reduction of the enzyme cofactor
oxidized from nicotinic acid dehydrogenase (NAD+) to nicotinic acid dehydrogenase (NADA) (reduced form).

Hepatic and renal tissues can use lactate to produce glucose via,
pathway gluconeogenesis, via the Cori cycle, where erythrocytes are
capable of carrying out glycolysis.  However, these cells do not have
mitochondria and cannot use oxygen to produce adenosine
triphosphate (ATP).

The pyruvate formed during glycolysis is metabolized by the enzyme
lactate dehydrogenase to lactate, this anaerobic pathway is
inefficient producing only 2 moles of ATP for each glucose that is
converted to lactate.

The lactate diffuses out of the cells, and is converted to pyruvate,
then this is aerobically metabolized to carbon dioxide and ATP, the
heart, liver, and kidneys use lactate in this manner.

Lactate uptake by liver is impaired by acidosis, hypoperfusion and
hypoxia, or inadequate profusion of tissue of O2 and nutrients.

Lactic acidosis leads to cardio pulmonary failure, sepsis, trauma,  
thiamine deficiency, side effects of drugs and toxins, oncologic
pathology, and various acquired and congenital diseases.

Lactate synthesis may also occur when the rate of glucose metabolism
exceeds the oxidative capacity of the mitochondria, as observed with
the administration of catecholamines, or from errors of metabolism.
graphic source here

Etiologies responsible for the presence of lactic acid include; circulatory failure, hypoxia, increased morbidity, and mortality for
patients with persistently elevated or increasing lactate levels.  

Lactic acidosis often persists because of altered oxidative phosphorylation and leukocyte production of lactate caused by
sustained increased inflammatory stimuli.

Critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones, or other measurable anions.  Irregular lactate
metabolism is frequent among the critically ill.  

Early diagnosis, vigilance, and routine measurements of the main anion gap are crucial for detection and proper treatment.
graphic source here

Metabolic acidosis is defined as a state of decreased
systemic pH resulting from either a primary increase in
hydrogen ion (H+), or a reduction in bicarbonate (HCO3-)
concentrations.  Respiratory compensation of acidosis occurs
by hyperventilation, resulting in a relative reduction in
PaCO2.  Chronically, renal compensation occurs by means of
reabsorption of HCO2.  

Metabolic acidosis arises from an increased production of
acids, a loss of alkali, or a decreased renal excretion of acids
causing an elevated anion gap.

Basically, the kidneys become unable to remove excess acid
allowing it to build up causing pH to increase (be more
acidic).  Fast proper treatment influences recovery (recovery
is possible).

Severe metabolic acidosis is an arterial pH of less than 7.2, it
is associated with impaired cardiac contractility and
suboptimal response to exogenous catecholamines.  
Elevation of serum lactate concentration may have inotropic
effects (weakened muscular contractions) independent of
serum pH.
The use of lactate as an index of tissue
perfusion has several limitations.

Liver disease causes a decreased ability to
clear lactate during periods of increased

Various causes of Type B lactate acidosis
may produce hyperlactemia and lactate
acidosis in the absence of inadequate tissue

Intracellular accumulation of lactate creates
a concentration gradient favoring its release
from the cell.

Lactates leave the cell in exchange for a
hydroxyl anion (OH-), which is a
membrane-associated, pH dependent,
antiport system.  

Extracellular H+ combines with lactate
leaving the cell forming lactic acid while
intracellular OH- binds to H+ resulting from
hydrolysis of anaerobically generated ATP.  

During declines of the cardiac output, the
cell must employ anaerobic sources of
energy to produce ATP, resulting in the
generation of H+.

In cellular hypoxia, anaerobic glycolysis is a
second cellular source of anaerobic ATP
(adenylate kinase reaction), another is
myokinase reaction, where 2 molecules of
ADP join to form ATP and adenosine
monophosphate (AMP).  This reaction leads
to increased intracellular levels of AMP, Pi,
and H+, thus H+ is able to increase during
hypoxemia (low blood O2), without the
notable increase in cellular lactate

During cellular hypoxia, the hydrolysis of ATP
leads to accumulation of H and Pi (inorganic
phosphate) in the cytosol.  

ATP hydrolysis is the source of cellular
acidosis during hypoxia, and not the
formation of lactate from glucose, which
neither consumes nor generates H+.  

With adequate O2 supply the metabolites of
ATP are recycled in the mitochondria and
the cytosolic lactate concentration rises
without acidosis.
Type A
. Occurs in association with clinical evidence of poor tissue perfusion or
oxygenation of blood (hypotension, cyanosis, cool and mottled extremities).
. Can be caused by the overproduction of lactate or the underutilization of
    .overproduction lactate = circulatory, pulmonary, and hemoglobin
    transfer disorders are commonly responsible.
    .underutilized lactate = liver disease, gluconeogenesis inhibition, thiamine
    deficiency, and uncoupled oxidative phosphorylation can be responsible.
. Respiratory starts in lungs when too much CO2 builds up as in peeps with
asthma, injury to chest, obesity, muscle weakness in chest, deformed chest
structure (or anything that makes breathing difficult), sedative misuse, overuse
of alcohol, nervous system problems.
. Symptoms of Respiratory Metabolic Acidosis:  fatigue & drowsiness, becoming
tired easily, confusion, shortness of breath, and headache.
Type B
. Occurs when no clinical evidence of poor tissue perfusion or oxygenation
    ** Occult tissue hypoperfusion is now recognized to accompany the
    primary etiology. [3]
Metabolic starts in kidneys and has a couple of subtypes.
    . Diabetic – lack of insulin allows ketones to build up in body and acidify
    . Hyperchloremic – loss of sodium bicarbonate which is a base that helps
    keep blood neutral (diarrhea and vomiting can cause this).
    . Lactic acidosis – too much lactic acid from chronic alcohol use, heart
    failure, cancer, seizures, liver failure, prolonged lack of oxygen, low
    blood sugar, and prolonged exercise
    . Renal tubular – kidneys unable to excrete acids into urine. [5]
. Symptoms of Metabolic Acidosis: rapid & shallow breathing, confusion, fatigue,
headache, sleepiness, lack of appetite, jaundice, increased heart rate, fruity
breath (ketoacidosis).
subType B1
. Type B1 Lactic Acidosis is associated or can occur with, diabetes mellitus,
bowel ischemia, severe iron-deficiency anemia, liver disease, alcoholic
ketoacidosis, pancreatitis, malignancy (leukemia, lymphoma, lung cancer),
infection, renal failure, seizures, heat stroke, pheochromocytoma, thiamin
deficiency, short gut syndrome, and other carbohydrate malabsorption
subType B2
. Type B2 is caused by several classes of drugs and toxins, including:  
iron, isoniazid, zidovudine, acetaminophen, alcohols and glycols (ethanol,
ethylene glycol, methanol, propylene glycol), antiretroviral nucleoside analogs
(zidovudine, didanosine, lamivudine), beta-andrenergic agents (epinephrine,
ritodrine, terbutaline), biguanides (phenformin, metformin ((antihyperglycemic
treatments))), cocaine, cyanogenic compounds (cyanide, nitroprusside,
amygdalin), diethyl ether, 5-fluorouracil, halothane, isoniazid, propofol, sugars
and sugar alcohols (fructose, sorbitol, xylitol), salicylates, strychnine,
sulfasalazine, valproic acid.
subType B3
Type B3 lactic acidosis results from inborn errors of metabolism
(glucose-6-phosphatase deficiency (von Gierke disease)),
fructose-1,6-diphosphatase deficiency, pyruvate carboxylase deficiency,
pyruvate dehydrogenase deficiency, oxidative phosphorylation deficiency, and
methylmalonic aciduria.
  Lactic acidosis may present in the MELAS Syndrome (mitochondrial
encephalopathy, lactic acidosis, and stroke-like episodes) due to point mutation
in mitochondrial DNA tRnaleu (UUR) gene. Characterized by migraine like
headaches, dementia, hearing loss, ataxia, and episodic vomiting.
***Within all of the above categories, septic shock may move from Type A to Type B as the initial
presentation, and is associated with hypoperfusion, and with aggressive fluid resuscitation.
***Lactic acidosis is an elevated plasma lactate concentration, while metabolic acidosis may
result from numerous conditions.

Risk factors for Acidosis:
    High fat diet with low carbs, kidney failure, obesity, dehydration,
    aspirin or methanol poisoning, diabetes.
Most common causes:
    Cardiogenic shock, hypovolemic shock, severe heart failure, sepsis,
    and severe trauma.
Other causes:
    Kidney conditions, liver disease, diabetes mellitus, HIV treatments,
    extreme physical exercise, alcoholism, supplements, OTC drugs,
    and prescription medications.
Tests for Acidosis:
    . Arterial blood gas (check O2 and CO2 levels) it also reveals pH.
    . Basic metabolic panel (check kidney function and pH; also
    measures calcium protein, blood sugar, and electrolyte levels).
    . Respiratory - chest x-ray and pulmonary function test.
    . Urine sample.
    . Sodium bicarbonate to raise pH of blood by mouth or
    intravenously, this is useful for hyperchloremic acidosis also.
    . Respiratory: Drugs to dilate airway, oxygen or Cpap.
    . Kidney: Sodium citrate for diabetics.
    . Diabetes: IV fluids and insulin to balance pH and antibiotics.
Complications can lead to:
    Kidney stones, chronic kidney problems, kidney failure, bone
    disease, and delayed growth.
Reduce risks:
    . Maintain a healthy weight.
    . Raise Oxygen Levels.
    . Stop smoking.
    . Never mix prescription medications with alcohol.
    . Stay hydrated.
    . Maintain healthy blood sugar levels or properly manage
    . Stop alcohol because it increases lactic build up.
    Organ mis-function, respiratory failure, kidney failure, shock,
Severe anemia
Cardiac arrest
Global hypoxia
Carbon monoxide
Respiratory failure
Severe asthma
Regional hypo fusion
Limb or mesenteric
Delayed clearance
Renal or hepatic dysfunction
Pyruvate dehydrogenase
Thiamine deficiency
Catecholamine excess
Alcoholic and diabetic
Uncoupling of oxidative
Methanol & ethylene glycol
Retroviral drugs
Valproic acid
Accelerated aerobic glycolysis
Increased effort
Large fructose loads
Hyperlactatemia  vs  Lactic Acidosis [3]
Lactic Acidosis
Hyperlactatemia is defined as a
persistent, mild to moderate (2-4
mmol/l) increase in blood lactate
concentration without the
metabolic acidosis

Hyperlactatemia and lactic acidosis
may be associated with acidemia, a
normal pH, or alkalemia.

Hyperlactatemia can occur in the
setting of adequate tissue
perfusion, intact buffering systems,
and adequate tissue O2

Increased lactate production
during anaerobic and aerobic
metabolism and decreased lactate
Normal blood lactate concentration in
unstressed patients is .5-1 mmol/l
(normal at 2mmol/l)

Lactic acidosis is characterized by
persistently increased blood lactate
levels (usually >5 mmol/l) in association
with acidosis

Patients with critical illness can be
considered to have normal lactate
concentrations of less than 2 mmol/l.

Lactic acidosis is associated with major
metabolic dysregulation, tissue
hypoperfusion, the effects of certain
drugs or toxins, and congenital
Lactic acidosis also occurs on markedly
increased transient metabolic demand
(eg, post-seizure lactic acidosis)

Lactic acidosis may not necessarily
produce acidemia in a patient

Lactate synthesis may also occur when
the rate of glucose metabolism exceeds
the oxidative capacity of the

Development of lactic acidosis depends
on magnitude of hyperlactatemia, the
buffering capability of body and the
coexistence of other conditions that
produce tachypnea and alkalosis (liver
disease and sepsis).
    Pathophysiological Mechanism of Metabolic Acidosis
    Along with Individual Drug Characteristics: [4]
Overproduction acidosis from pharmaceutical agents.
    . The excess use of amino acids with a net positive charge (lysine and arginine)
    would result in liberation of H+, in intravenous feeding with inadequate concomitant
    administration of alkali.
    . Propylene glycol is metabolized to lactate (GRAS rec daily intake of PG less than 25
    mg/kg/day (equivalent to 21 mmol/day for 70 g person)). Beware renal impairment
    . Propylene glycol intoxication from intravenous vitamin therapy was reported as
    developing stupor.
    . Intoxication with lactic acidosis and hyperosmolality were found during treatment
    for schizophrenia, with use of intravenous benzodiazepines, etomidate,
    nitroglycerine, and barbiturates, all with Prp[ylene glycol as a vehicle.
    . Propylene glycol oxidizes to propionaldehyde and pyruvate, and to acetic and lactic
    acid, the remainder (50%) is excreted unchanged in urine.
    . Patients with hepatic dysfunction, renal insufficiency, and diabetic ketoacidosis
    are more susceptible to Propylene glycol toxicity and development of lactic acidosis.
Drugs causing external base loss:
    Renal loss of bicarbonate:
    . Carbonic anhydrases (CAs) are critical enzymes for bicarbonate
    . Acetazolamide is a commonly used Carbonic anhydrase inhibitor in the
    treatment of ocular and convulsive disorders causing bicarbonaturia and a
    mild degree of hyperchloremic metabolic acidosis, along with reports of
    symptomatic anion gap.
    . Topiramate generates a mild hyperchloremic metabolic acidosis but
    increases urinary pH and drastically lowers urinary citrate excretions, thus
    increasing the risk of calcium phosphate urolithiasis
    . Sulfonamide drugs also have inhibitory activity causing extremely high
    blood levels and systemic Carbonic anhydrase inhibition resulting in more
    than mere renal bicarbonate loss but a systemic disequilibrium syndrome.
    Gastrointestinal loss of bicarbonate:
    . Cholestyramine used for hypertriglyceridemia and cholestasis binds and
    sequesters bile acids from the entero-hepatic circulation, but in GI tract
    cholestyramine also binds phosphate, sulfate, and bicarbonate leading to
    potential loss of bicarbonate from the body  
    . Sevelamer Carbonate over Sevelamer Hydrochloride and that over Calcium
    Acetate.   Sevelamer carbonate binds to phosphate and releases carbonate
    instead (bixalomer), which contains no chloride and binds with phosphate.
    . Laxative abuse, calcium chloride, and magnesium sulfate could cause
    hyperchloremic acidosis, because the secreted bicarbonate from the pancreas
    is trapped by calcium and magnesium and then excreted in the stools
Drugs causing increased endogenous acid:  
    . Lactic acidosis is produced under metabolic conditions and H+ ions are released.
    . Metaformin is associated with lactic acidosis (MALA).  Blood Ph and lactate
    levels are not prognostic in MALA. Although incidence of MALA is low, once
    developed the mortality can be high.
    . HAART, Highly Active Antiretroviral therapy, drugs have high incindences
    of lactic acidosis, with nucleoside and nucleotide reverse transcriptate
    inhibitor (NRTI)-based regimens (didanosine, stavudine, lamivudine,
    zidovudine, and abacavir), combining these drugs increased risk.
    Didanosine, cidofovir, lamivudine and stavudine could cause Fanconi
    syndrome with pan-proximal tubular dysfunction leading to exacerbation of
    acidosis and reduction of plasma anion gap (mortality rate is 50%).
    . Linezolid (long term antibiotic for resistant gram-positive organisms) has
    adverse effects of bone marrow toxicity, optic/peripheral neuropathy, and
    lactic acidosis.
    . SSRi’s, Selective Serotonin Uptake Inhibitors (citalopram and sertraline)
    predispose peeps to lactic acidosis.
    . Isoniazid used for tuberculosis (more than 300 mg/day) leads to refractory
    grand mal or localized seizure, coma, and lactic acidosis (possibly by
    inhibition of conversion of lactate to pyruvate).
    . Propofol used for induction and maintenance of anesthesia, sedation, and
    interventional procedures has been reported to cause severe metabolic
    . Ketosis develops when metabolism of fatty acid exceeds the removal of
    ketoacids (acetoacetic and b-hyroxybutyric), typically with insulin deficiency
    and/or resistance coupled with elevated glucagon and catecholamine.  
    Glucose utilization is increased, augmenting the delivery of glycerol, alanine,
    and fatty acids for ketoacid generation.
    Metabolic acidosis:
    Occurs during salicylate toxicity due to uncoupling of oxidative
    phosphorylation and interfering with the Krebs cycle resulting in accumulation
    of lactic acid and ketoacids (anion gap mainly composed of ketoanions and
    lactate, while salicylate anion seldom exceeds 3meq/l).
    Alcoholic ketoacidosis:
    Depletes bicarbonate due to the metabolism of ketoacid anions.
    Pyroglutamic acidosis:
    . Glutathione is involved in the inactivation of free radical, detoxification of
    many compounds and amino acid transport.
    . Acetaminophen can deplete glutathione, leading to increased formation of y-
    glutamyl cysteine, which is converted and accumulated and pyroglutamic acid
    (5-oxoproline).  Increased risk for peeps with malnutrition, sepsis, alcohol
    abuse, underlying liver disease and or renal insufficiency.  Acetaminophen
    combined with (concomitant use) of other drugs aminoglycoside and b-lactum
    penicillin increased risk.
Drugs causing decreased renal acid excretions:
    . Syndromes of hyper-hypkalemia and reduced distal hydrogen secretion:
    . Angiotensin II and alsosterone are stimulators of H+-ATPase, A-intercalated
    cells in the cortical collecting tubule adding H+ into urinary luminal. Inhibition
    of the renin-angiotensin-aldersterone system (RAAS), which leads to
    secondary inhibition of H+-ATPase, which can lead to decreased H+ secretion
    and metabolic acidosis.  Same mechanism can cause hyperkalemia.
    Hyperkalemia suppresses ammoniagenesis in the proximal tubule, impairs
    NH4+ transport in the mudullary thick ascending limb, and reduced medullary
    interstational ammonium concentration, all of which can lower urine acid
    Cyclooxygenase (COX) inhibitiors; b-adrenergic receptor blockers;
    angiotension-converting enzyme inhibitors (ACEIs); angiotension II receptor
    blockers (ARBs); and direct renin inhibitors (herparing and ketoconazole,
    spironolactone and eplerenone); potassium-sparing diuretics (amiloride and
    triamterene); pentamidine and trimethoprim; calcineurin inhibitors
    (cyclosporine and tacrolimus).]]  Riskes increased if these drugs are
    . Some medication can mimic these deficits by altering membrane
    permeability, causing leaky pathways (amphotericin B, lithium, and
    . Drugs causing Fanconi syndrome and proximal renal tubular acidosis: CA inhibitors
    (acetazolamide); anti-viral/HIV drugs (lamivudine, stavudine and tenofovir);
    platinum containing agents (cisplatin); and DNA alkylating agents (ifosfamide);
    valproic acids (VPAs); outdated tetracycline, aminoglycoside, and deferasirox.

Assessing your acid status is quick and easy.  A simple test, done
with litmus paper, can be performed in your own home.  Using
litmus paper to measure the pH levels of saliva, or urine, provides
a useful indication of net acid status.

. A healthy after-rest urine pH range is in the range of 6.5 - 7.5.
The body routinely uses the overnight rest time to concentrate
excess acids in the urine. This capacity varies based on toxin
loads, and an individual's ability to make energy, detoxify toxins,
and actively excrete them.

. Too much acid in the urine after rest indicates mineral deficits
in the cells.

. Daily pH should be slightly alkaline, in the range of 7.2 to 7.4
(just a bit more alkaline than water)

. If your pH is lower than 7.2, you’re in a state of acidosis.

. pH above 7.43 signals excessive alkalinity, or alkalosis, which is
very rare.

. If litmus paper shows you’re acidic, simply increase your intake
of fruits and vegetables.  Almost all fruits and vegetables – even
citrus – are alkalizing (it may sound odd that acidic citrus fruits
are alkalizing but that is really the effect in your body).  Only
tomatoes, cranberries, and blueberries are non-alkalizing, while
balancing you should go light on these.

. To quickly alkalinize your system, add 1/2 teaspoon of baking
soda to 8 ounces of pure room temperature water and drink.

. For daily pH balance make alkaline water utilizing citrus fruit
juices.  Squeeze the juice of 1/2 to 1 of a lemon or lime into
room temperature water and drink within an hour after you wake

Dietary sugars and refined flours lacking the naturally occurring
potassium and magnesium are arguably the single biggest triggers
of repair-deficit inflammation.  

Diets high in dietary sugars, low in fiber, high in pro-
inflammatory edible oils (soybean, safflower, canola,
hydrogenated, partially hydrogenated, and corn oil), and lacking
in anti-inflammatory omega-3s oils, result in net acid excesses
that impair immune defense and repair functions.  

Amino Acids and B vitamins also play a big role for better, or for
Here is the most important thing you need to know about acidosis:
Every illness exists in an acidic state!!
graphic source here

Balancing acidosis, on any level, will require at least a short-term
diet change.  Some changes you may find will need to be lifelong
changes to remain in balance, depending on your biochemical

Foods to Avoid–  
    - Remove artificial sweeteners, high fructose sweeteners,
    refined sugars, corn syrup, and glucose from you diet.

    - Avoid biogenic amines by avoiding commercially fermented

    - Eliminate soft drinks and beer because they generate large
    amounts of acid inside the body.

    - Canned, processed, and preserved goods are high in
    biogenic amines.    

    - Wheat, some dairy products, chocolates, prunes, peanuts,
    beans, eggs, beef and pork produce high amounts of acids,
    be vigilant about excesses.

    - Coffee (w/sugar and creamer), sodas, alcohol, and
    anything with added sugar can create acid.  

    - Avoid Energy Drinks.  Energy drinks contain high levels of
    biogenic enzymes which greatly contributes to the acid
    load.  Discontinue use while clearing metabolic pathways.  
    When pathways are clear you will no longer lack energy.

    - Avoid anything you are sensitive to or have shown
    reactive by LRA tests.

    - If you are suffering from a histamine intolerance or any
    type of allergic reactions, then keep in mind the chart to
    the right.  While some foods are often considered high in
    histamine levels, some foods are not considered high in
    histamine but have the ability to promote the release of

Foods with High Histamine Levels
Foods that Stimulate
Release of Histamine
Dried fruits (peaches, dates, prunes,
figs, raisins)

Vinegar or vinegar containing foods
like mayonnaise, salad dressing,
ketchup, chili sauce, pickles, pickled
beets, relishes, olives

Soured bread, pumpernickel, coffee

Foods made with large amounts of

Fermented foods, pickled or smoked
meats commercially produced

Aged or fermented cheese,
parmesan, blue and Roquefort other
sour cream, sour milk, buttermilk

Yogurt (especially if not fresh)

Processed meats (sausage, hot dogs,
salami more)

Smoked fish (herring, sardines, and

Alcoholic beverages

Cider and homemade root beer



Avocados (avoid while figuring out
which biogenic amine you are having
difficulty metabolizing)














Lactate producers = skeletal muscle, the brain, the gut, and

Lactate metabolizers = liver, kidneys, heart
(above .4mmol/l skeletal muscle become net consumer).

Foods to Add:  
- Organic raw pumpkin seeds are high in minerals especially
magnesium and potassium.  They are a good source of
essential fats.  They also possess the ability to kill many bad
bacteria found in the digestive tract.  ¼ cup daily for three
days can kill most bad parasites found in the digestive track.
Sprinkle these seeds on dishes like salads and in soups for
daily added protection and better detoxification.

- Add foods to your diet that are known to be alkaline rich
such as grapefruits, asparagus, garlic, limes, almonds, olive
oil, pears, onion, apple, bananas, cantaloupe, cherries,
cranberries, dates, figs, squash, celery, green tea, fresh
fruits, string beans, dandelion greens, raisins, and foods that
are rich in fiber.   Include roasted or baked alkaline-rich
foods like sweet potatoes, yams, lentils, beans, chickpeas,
and other root vegetables like parsnips, rutabaga, turnips,
and kohlrabi.

- Food that is rich in alkaline minerals like magnesium can
balance acidity inside the body, these minerals are required
for the break down of acid (seaveggies).

- Honey is known to be very efficient home remedy for
acidosis.  Eat a teaspoon of honey several times throughout
the course of the day– this can be extremely helpful.

- Increase garlic in your diet. It has the ability to kill  
pathogenic organisms and optimize bowel flora.

- Drinking alkaline water is an easy and efficient way to help
neutralize an acidic human body. Make sure you drink at
least 8 glasses of pure water per day, which helps to detox
the body naturally.
Some foods contain salicylates and glutamates
which can cause histamine reactions.  
Individual reactions will vary.  Nuts (almonds,
walnuts, flaxseeds, pumpkin seeds, and
cashews), dried fruit (raisins, currants, or
dates), sprouts, and seeds provide a variety of
healthier choices.  

Dried fruits and processed nuts can contain
high amounts of sulfites which can cause
allergic reactions.  Find the ones that you
prefer and choose the highest quality, least
processed (organic certified or biodynamic)
that is available.  Be sure to test for sensitivity
and limit overall amounts.
In Conclusion:
You are what you eat.  Sometimes it is difficult to realize
that the food choices made daily can have dire
consequences.  Often, the foods we crave the most are
the ones that cause the most harm.  The inflammation
process releases neurotransmitters that make us feel good,
for a little while.  Biogenic amines in your body utilize this
mechanism so they can live better.  (If you could control
the weather and your overall environment, you would,
Biogenic amines in abundance or those which we are
unable to properly metabolize, create imbalance.  Often
doctors will prescribe medications without checking for
lactate capabilities, often contributing to, and even
acerbating, weakened immune conditions.  Most
medications contribute to lactate load via their inactive
ingredients and via their mechanisms of action.  
If you would like more information or assistance getting
well give me a shout.  Have an awesome day.
[1] Fermented Food Allergy – Reveal Hidden Causes; Ken Silvers; 05/19/2018
[2] Biogenic amines in fermented food; European Journal of Clinical Nutrition volume 64, pages S95-S100; 11/03/2010); https://www.nature.
com/articles/ejcn2010218G Spano
[3] Lactic Acidosis: Background, Etiology, Epidemiology; Kyle J Gunnerson, MD and more.; 04/27/2018;
oberview#showall ;
[4] Drug Induced Metabolic Acidosis; version 1; Amy Quynh Trang Pham, Li Hao Richie Xu, Orson W. Moe; 12/16/2015, revised 02/15/2016; https:
[5] Healthline- Acidosis; 06/06/2017:
[6] The Alkaline Way: Ten Tips for Reversing; Russell Jaffee, MD, PhD; Summer 2015;
[7] Cure Acidosis & Inflammation – Root Causes of Disease; Leigh Erin Connealy, MD; 02/28/14;
[8] 5 ways to control acidosis & to alkalize your body; Marla; 01/27/2012;
[9] Wikipedia:; and other topics found at this site have been utilized in the preparation of this paper.
[10] Turmeric, MAO Mutations, and Hypertension: A Ticking Time Bomb; by Chandler Marrs, PhD; 10/25/2017;
[11] A Genetic Cause of Pain and Anxiety: COMT, MAO, and MTHFR; by Dr Andrew, c/o Dr. Rostenberg; 11/18/2014;
[12] Renal Regulation of Acid-Base Balance; 03/30/2011;
Histamine is the root of inflammation.
To treat inflammation:  Visit my Inflammation page to learn about
foods that cause inflammation and then avoid them.
    Histaminum Hydrochloricum
    is a natural anti-inflammatory that works very
    quickly.  Histaminum hydrochloricum is a kind of
    histamine used as a homeopathic remedy. It is
    primarily used to treat various allergies, including
    those caused by food, insect bites and pollen, and
    allergy symptoms such as skin irritations, nasal
    congestion and breathing difficulties.  Histaminum
    hydrochloricum is also used as a remedy for non-
    allergic conditions like bronchitis, gastric pain,
    muscular pain and joint pain.  Homeopathic
    practitioners often recommend it as a treatment for
    problems like asthma, eczema, hay fever, runny nose,
    hives and itchy eyes. It is used both to alleviate
    immediate allergy symptoms and to reduce future
    allergic reactions.
    . Turmeric is often used as a spice in cooking, it adds
    a garlicy flavor to dishes with a body warming
    undertone.  Sprinkling a little bit on to your dishes is
    a simple way to introduce this spice into your diet.  
    Peperine found in black pepper enhances the
    properties of turmeric.
    . Curcumin is found in the root of the turmeric plant.  
    Fresh ground turmeric contains 200 mg of curcumin
    per teaspoon, use with black pepper to increase
    effectiveness.  500-1000 mg daily for reduced
    - Supplementation with Turmeric is often suggested
    for inflammation, but people experiencing MAO-A
    deficiencies, or those who are taking MAOI
    medications should use caution because turmeric is a
    natural MAOI.  Consult your physician that prescribes
    your medications before using turmeric.
    . If you experience any form of anxiety attack,
    tachycardia, or other stimulatory symptoms
    discontinue use.  If they are extreme,
    immediate supplementation with liquid
    magnesium should reduce symptoms within 30
    minutes.  A glass of alkalized water will assist in
    reducing stimulatory symptoms.
    . Inhibition of the actions of MAO enzymes can
    present stomach problems, mental confusion,
    depression, migraine, vomiting, itching, fever,
    rash, and other symptoms.[1]

Inflammation can be easily measured with a
blood test for CRP (C-reactive protein).  A
score higher than 1 means there is active
inflammation in your body. But this is not a
standard test and you will have to ask your
doctor to write you a prescription for this test.

Metabolic acidosis is a biochemical condition
in the body that paralyzes every cell,
preventing the absorption of oxygen and
essential nutrients.  Excess acid can be due to
stress, environmental toxins, insufficient
oxygen, and a poor diet based on processed
and fast foods.

Metabolic acidosis causes internal symptoms
that are easy to miss.  Excess levels of acid
damage tissues and organs so badly, for
example, that they can harden or develop
lesions to prevent acid from penetrating

Acidosis can also wreak havoc on the body’s
mineral supply, elevating the risk of
osteoporosis, diabetes, heart disease, and
other disorders.  

Acidosis can cause: cardiovascular damage,
weight gain, obesity, diabetes, bladder and
kidney conditions, immune deficiency,
acceleration of free radical damage (cancer),
premature aging, osteoporosis, joint pain,
aching muscles, headaches, stress, chronic
constipation, and chronic fatigue.

It is important to understand that blood  
(plasma) pH is highly conservative: it is one of
the most tightly controlled of physiological
parameters.  The body has numerous
mechanisms for keeping the blood plasma pH
within a very tight range.
Useful Herbs:
. Turmeric as an antioxidant that also relieves
inflammation. (CAUTION: May behave like MAOI)

. Ginger root soothes inflammation of all cells and more.

. Consider digestive bitters like Campari or Unterbrg to
strengthen digestion.

. Supplements that alkalize the body may help your body
regain its balance. These include spirulina, barley,
blue-green algae, and chlorella.

. Blood cleansers and digestive aids such as hyssop tea,
cinnamon tea, coffee berries, coffee leaves, and
peppermint tea reduce acidity caused by biogenic amine
byproduct buildup.

. Dandelion tea for spleen health.  The spleen is an
important, yet often overlooked, part of the lymphatic
system which is imperative to the detoxification
processes of the human body.

.Herbs, seasonings, and spices are also nutrient rich.

. Coffee acts like a diuretic; 1 cup mid-morning is useful in
promoting elimination of toxins from your system.
Some tips to prevent biogenic amine induced acidosis, to
reverse excess cellular acid buildup, and to improve energy
production, while also enhancing detoxification pathways and
interstitial repair include:

- Water / Hydration:  adequate water supply is crucial for
interstitial fluid health.  The molecules in water assist in the
metabolism of biogenic amines and in their byproduct
detoxifying mechanisms.
. Overall daily consumption of pure water should equal to ½ your
current body weight in ounces of water. (140 pounds / 2 = 70
ounces / day)
. Include at least 20 oz of pure mineralized water into your daily
water intake.  Mineralized is not the same as tap water, nor is it
the same as hard water.
. Replace all other commercial beverages with water and
homemade teas.  
. Reducing commercial beverages, especially sodas and energy
drinks, will help with weight management, help reduce toxic
burden, will bring restorative sleep, and promote healing on the
cellular level.
. Warm or room temperature beverages are better than cold
ones.  Iced beverages slow down and impair digestion.  
. For proper digestion and assimilation of nutrients drink 8oz of
water 30 minutes before meals, try not to drink during the meal,
and then wait 30 minutes until after your meal to drink again.
. If the need to urinate during the night is a problem than
reduce water intake a few hours before going to bed.
- Essential Fatty Acids (EFAs) are necessary for the formation of
healthy cell membranes, the proper development and
functioning of the brain and nervous system, and for the
production of hormone-like substances called eicosanoids
(thromboxanes, leukotrienes, prostaglandins). These chemicals
regulate numerous body functions including blood pressure,
blood viscosity, vasoconstriction, immune and inflammatory
responses.  They are necessary for the natural enzymic activity
within all cells that is required for successful breakdown of
biogenic amines.
60% of brain is composed of fatty acids.
. The primary sources of essential fatty acids are plants on land
and in the sea. Linoleic acid is found primarily in seeds, nuts,
grains and legumes. Alpha-linolenic acid is found in the green
leaves of plants, including phytoplankton and algae, and in
selected seeds, nuts and legumes (flax, canola, walnuts and
soy). Arachidonic acid (AA) and docosahexaenoic (DHA) acid are
obtained directly from animal foods - AA from meat and poultry
and DHA and EPA from fish.
. Shoot for at least 1,000 mg of essential fatty acids daily.
. Easy way to increase intake is to take 2-4 Tablespoons of Flax
Seed Oil or Hemp Seed Oil daily.  Look for it in the refrigerated
section of your favorite health food store, pill forms will most
probably add to lactate load, while packaged pre-ground
powders, are a processed food, and can become rancid quickly.  
Grinding your own fresh flax seed is a great option and can be
added to smoothies and other dishes with ease.  Be sure to
grind it as you need it so it is guaranteed fresh.  
. Adding an oceanic based EFA supplement is helpful in getting a
nice blend going on.  Krill oil is a great option for this and can
often be used in place of the more recognized fish oil
supplements, which can be high in mercury and other
contaminants.  Fish based oil supplements have been reported
as source of food based allergic reactions.
. Foods high in essential fatty acids include:  Whole fish from
deep cold water or wild, line caught fish; nuts, seeds, grains,
. Extra virgin olive oil, organic coconut oil, ghee (clarified
butter), and almond oil, are recommended dietary and cooking

Biogenic amines are everywhere and cause many serious
health conditions, if they are not addressed properly.  Often,
when these conditions arise they are overlooked,
under-treated, and even mis-treated, which leads to further
complications.  There are several ways to protect your health
from the destructive processes that can happen when these
biogenic amines begin to overwhelm bodily systems.

Biogenic amines are organic, basic, nitrogenous compounds,
mainly formed through decarboxylation of amino acids.  They
are created by certain bacteria that break down amino acids
in food.  They are lactic acid byproducts which are present in
some, but not all, foods.  Foods that are over-cooked,
processed, ripened, fermented, or decomposed tend to have
higher levels of biogenic amines.  Poor quality food also tends
to contain higher amounts of amines, as does food not
properly stored, cleaned, or prepared.
[1]   Biogenic amines
cannot be removed by boiling or any other method.  
Consumption of foods with high amines can have toxicological

Biogenic amines can affect a person mentally, by causing blood
pressure changes affecting body temperature, and other body
processes.  Different degrees of intolerance exist.  Some
people are just a little sensitive, while others experience
severe reactions even from small amounts of amines.  Migraine
attacks from the consumption of tap water containing as little
as 1 mg of the amine tyramine chloride have been
[1]   Many people are aware of the PKU
(phenylketonuria) allergy, which is a disorder that causes an
amino acid called phenylalanine to build up in the body.  
Similar amine sensitivities include, gluten intolerance and
lactose intolerance.

Drug Induced Metabolic Acidosis could emerge
from drugs that disrupt the acid-base
equilibrium, or through ingestion of toxic
chemicals with the same mechanism.  

Drug Induced Metabolic Acidosis has four
    1. Drugs as exogenous acid loads
    2. Drugs leading to loss of bicarbonate in
    the gastrointestinal tract or in the
    3. Drugs causing increased endogenous
    acid production
    4. Drugs that decrease renal acid
    *Many medications fall in more than one
    category. [4]

It is important to identify drugs that are
culprits in either the generation or the
exacerbation of the disorder.  Early diagnosis,
vigilance, and routine measurements of the
anion gap, are crucial for detection and for
proper treatment.

Instead of memorizing the catalogue of drugs,
clinicians should classify these agents based on
their pathophysiologic mechanisms to
facilitate the recognition of potential casual

All metabolic, neurohormonal, and immune
system processes produce a net excess of
acids.  When foods induce immune reactions,
it is important to identify the causes of
immune reactions by avoidance provocation,
or ex-vivo lymphocyte response assays (LRA).

Untreated, acidosis sets the stage for
inflammation.  Signs of inflammation might
present as painful, arthritic joints; or digestive
issues (gastritis); as repeated urinary tract
infections; as skin problems such as eczema,
hives and acne; or as immune disorders leading
to one cold after another.  

When tissue hypoxia is present, pyruvate oxidation
decreases, lactate production increases, and ATP formation
continues via glycolysis.  The amount of lactate produced is
believed to correlate with the total oxygen debt, the
magnitude of hypoperfusion, and the severity of shock.

During cellular hypoxia, the hydrolysis of ATP leads to accumulation of H and Pi (inorganic phosphate) in the cytosol.  ATP hydrolysis
is the source of cellular acidosis during hypoxia and not the formation of lactate from glucose which neither consumes nor generates
H+.  With adequate O2 supply the metabolites of ATP are recycled in the mitochondria and the cytosolic lactate concentration rises
without acidosis.

People presenting with septic shock have lactate levels of more than 5mmol/l, a lactate to pyruvate ration greater than 10-16:1, and
an arterial pH of less than 7.35.

Every illness exists in an acidic state.  When cells are more
alkaline, they are more tolerant, better able to detoxify, and
more able to maintain a high energy potential (as indicated by an
ATP:ADP ratio of 100:1).  
It is minerals such as potassium and
magnesium, along with short/medium
chain fats, that counter this acidity
and alkalinize the body.

Latent magnesium deficiency inside
the cells can be difficult to detect.  
There can be significant mineral
starvation and substantial net acid
excess long before it would ever show
up as a critical illness or reflect
significant changes in blood pH.
A metabolically alkaline diet includes foods that have a buffering,
alkalinizing effect on cell chemistry.  This is often different than
a food's ash residue or physical chemistry.  Failure to recognize
this distinction has led to a lot of confusion both among
clinicians and among people eager to follow an "alkaline" diet.

For example, citrus fruits are alkalinizing because the metabolism
of citrate, malate, succinate, and fumarate generates more than
twice as much bicarbonate buffer as there is acid in the food
itself. This means that citrus fruit and similar foods are acidc in
their food state, yet “alkaline-forming” in the body.