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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
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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.
Metabolic Acidosis
***this page still under construction check back often***

Frustrated with the medical communitys inability to help
make you feel well?

Tired of misdiagnoses and ineffective treatments?

Do you experience chronic ailments, or symptoms that
have your care givers scratching their heads?

Unlike inflammation, which is recognized by conventional
medicine, 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.  

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]

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).
[3]

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.
[3]

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 http://www.pnas.org/content/98/2/395/tab-article-info
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.
[3]

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).
[3]

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).
[3]  

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
(energy) for each glucose that is converted to lactate.
[3]

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.
[3]

Lactate uptake by liver is impaired by acidosis,
hypoperfusion and hypoxia, or inadequate profusion of
tissue of O2 and nutrients.
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.
[3]  

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.
[3]
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.  

Severe metabolic acidosis is an arterial pH of less
than 7.2, it is associated with impaired cardiac
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
production.

Various causes of Type B lactate acidosis may
produce hyperlactemia and lactate acidosis in
the absence of inadequate tissue perfusion.
[3]

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+.
[3]

In cellular hypoxia, anaerobic glycolysis is a
second cellular source of anaerobic ATP
(adenylate kinase reaction), another is
myokinase reaction, where 2 molecules of
TYPES OF LACTIC ACIDOSIS
Type A
(Respiratory)
. Occurs in association with clinical evidence of poor tissue perfusion or
oxygenation of blood (hypotension, cyanosis, cool and mottled extremities).
[3]
. Can be caused by the overproduction of lactate or the underutilization of
lactate.
    .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. [3]
. 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.
[5]
. Symptoms of Respiratory Metabolic Acidosis:  fatigue & drowsiness,
becoming tired easily, confusion, shortness of breath, and headache.
[5]
Type B
(Metabolic)
. Occurs when no clinical evidence of poor tissue perfusion or oxygenation
exists.
    ** 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
    blood.
    . 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).
[5]
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
syndromes.
[3]
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.
[3]
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.
[3]
  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.
[3]
***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.
[3]

***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.
Treatment:
    . 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:
    Respiratory:
    . Maintain a healthy weight.
    . Raise Oxygen Levels.
    . Stop smoking.
    . Never mix prescription medications with alcohol.
    Metabolic:
    . Stay hydrated.
    . Maintain healthy blood sugar levels or properly manage
    diabetes.
    . Stop alcohol because it increases lactic build up.
Outlook:
    Organ mis-function, respiratory failure, kidney failure, shock,
    death.
    [5]
Hyperlactatemia  vs  Lactic Acidosis [3]
Hyperlactatemia
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 clearance
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 mitochondria

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).
Here is the most important thing you need to know about acidosis:
Every illness exists in an acidic state!
graphic source here

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
    foods.

    - 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
    histamine.
HISTAMINE  FOOD SOURCES

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
cakes,

Foods made with large amounts of
yeast

Fermented foods, pickled or smoked
meats commercially produced
sauerkraut;

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
more)

Alcoholic beverages

Cider and homemade root beer

Mushrooms

Anchovies

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

Spinach

Tomatoes

Eggplant

Mackerel
Eggs

Fish

Milk

Alcohol

Papayas

Bananas

Shellfish

Chocolate

Pineapple

Tomatoes

Strawberries

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

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

[1]

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.

- 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 with the least processing
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,
right?)
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.
=====================================
References:
[1] Fermented Food Allergy – Reveal Hidden Causes; Ken Silvers; 05/19/2018 https://www.probioticscenter.org/fermented-food-allergy/
[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; https://emedicine.medscape.com/article/167027-
oberview#showall ; http://emdidactic.blogspot.com/2016/10/hyperlactatemia-and-lactic-acidosis.html
[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:
//f1000research.com/articles/4-1460/v1
[5] Healthline- Acidosis; 06/06/2017:  https://www.healthline.com/health/acidosis
[6] The Alkaline Way: Ten Tips for Reversing; Russell Jaffee, MD, PhD; Summer 2015; https://www.holisticprimarycare.net/topics-o-z/prevention-practice-
perarls/1709-the-alkaline-way-ten-tips-for-reversing.html
[7] Cure Acidosis & Inflammation – Root Causes of Disease; Leigh Erin Connealy, MD; 02/28/14; https://www.newportnaturalhealth.com/2014/08/cure-acidosis-
and-inflammation-root-causes-of-disease/
[8] 5 ways to control acidosis & to alkalize your body; Marla; 01/27/2012; http://organic4greenlivings.com/5-ways-to-control-acidosis-to-alkalize-your-body/
[9] Wikipedia: https://en.wikipedia.org/wiki/Monoamine_oxidase_A; 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; https://www.hormonesmatter.com/turmeric-
mao-mutations-hypertension-ticking-time-bomb/
[11] A Genetic Cause of Pain and Anxiety: COMT, MAO, and MTHFR; by Dr Andrew, c/o Dr. Rostenberg; 11/18/2014; http://redmountainclinic.com/a-genetic-
cause-of-pain-and-anxiety-comt-mao-and-mthfr/
[12] Renal Regulation of Acid-Base Balance; 03/30/2011; http://editthis.info/iusmphysiology/Renal_regulation_of_acid-base_balance/

To treat inflammation:  Visit my Inflammation page to learn about
foods that cause inflammation and then avoid them.

Histaminum Hydrochloricum
    This 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/Curcumin:
    Supplementation with Turmeric is often suggested for
    inflammation
    . Turmeric is a bright yellow spice used in cooking.  It adds a
    garlicy flavor to dishes with a body warming undertone.  
    Sprinkling a little into your dishes is a simple way to
    introduce this spice into your diet.  
    . Curcumin is found in the root of the turmeric plant.  Fresh
    ground turmeric contains 200 mg of curcumin per teaspoon.  
    An intake of 500-1000 mg daily is recommended for reducing
    inflammation.
    . Peperine found in black pepper enhances the properties of
    turmeric.
    . Turmeric is a natural MAO Inhibitor.  It is suggested to use
    this natural remedy before utilizing prescription medications
    which will contribute to the acidic load and future reliance
    on the medical system.
    .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 also
    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]

    . Turmeric is a natural blood thinner. ?true?

Histamine is the root of inflammation.

Tyramine occurs widely in plants and animals.  An abundance of
tyramine in the body will cause symptoms similar to those caused
by histamine.  In foods, it often is produced by the decarboxylation
of tyrosine during fermentation or decay.  

Foods containing considerable amounts of tyramine include meats
that are potentially spoiled or pickled, aged, smoked, fermented, or
marinated (some fish, poultry, and beef); most pork (except cured
ham).

Other foods containing considerable amounts of tyramine are
chocolate; alcoholic beverages; most cheeses (except ricotta,
cottage, cream and Neufchâtel cheeses), sour cream, yogurt,
shrimp paste, soy sauce, soybean condiments, teriyaki sauce,
tempeh, miso soup, sauerkraut, kimchi, broad (fava) beans, green
bean pods, Italian flat (Romano) beans, snow peas, edamame,
avocados, bananas, pineapple, eggplants, figs, red plums,
raspberries, peanuts, Brazil nuts, coconuts, processed meat, yeast,
an array of cacti and the holiday plant mistletoe.
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
oils.

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
categories:
    1. Drugs as exogenous acid loads
    2. Drugs leading to loss of bicarbonate in
    the gastrointestinal tract or in the kidney
    3. Drugs causing increased endogenous
    acid production
    4. Drugs that decrease renal acid excretion
    *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.  
See "Pathophysiological
Mechanism of Metabolic Acidosis" table below.  
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 relationships
.
[4]

This is the reasoning behind all the side effects
medications can produce and if consuming more
than one medication than risk factors are greatly
increased.

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.
[3]

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.
[3]

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).
 
Minerals such as potassium and magnesium, along with
short/medium chain fats, that counter this acidity and
alkalinize the body.
[6]

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.
[6]

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.
[8]
The toxic level of biogenic amines is difficult to
establish but some criteria have been established
in the food and beverage industry:
    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]
Depression
Inflammation
Rash / Hives
Migraines
Anxiety
Pre-Diabetes
Allergies
Gastrointestinal
Arthritis
Addiction
Osteoporosis
Heart Disease
Obesity
Stress
Weight Gain
Immune Conditions
Headaches
Cancer
Fatigue
Joint Pain
Muscle Ache
Accelerated Aging
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
and for worse.

Metabolic acidosis is a biochemical condition in the body that
paralyzes every cell, preventing the absorption of oxygen and
essential nutrients.  
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).

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.
[6]
LACTATE
Metabolic Syndrome
It is important to understand that blood pH is highly
conservative, it is one of the most tightly controlled of all
physiological parameters.  The body has numerous mechanisms
for keeping the blood plasma pH within a very tight range.
[6]  
However, blood pH does not reflect what is happening within
the cells.

Metabolic acidosis causes internal symptoms that are easy to
overlook.

Metabolic acidosis arises from an increased production of acids,
a loss of alkali, or a decreased renal excretion of acids.
[3]   The
kidneys become unable to remove excess acid allowing it to
build up causing pH to increase creating an overly acidic cellular
environment.

All metabolic, neurohormonal, and immune system processes
produce a net excess of acids inside the body.

Excess acid can also be due to stress, environmental toxins,
insufficient oxygen, and diets based on processed and fast
foods.

Excess levels of acid can damage tissues and organs so badly
that they can become harden or develop lesions in an effort to
prevent acid from penetrating tissues.

Metabolic acidosis can wreak havoc on the body’s mineral
supply, elevating the risk of osteoporosis, diabetes, heart
disease, cardiovascular damage, weight gain, obesity, diabetes,
bladder and kidney conditions, immune deficiency, acceleration
of free radical damage (cancer), premature aging, joint pain,
aching muscles, headaches, stress, chronic constipation, and
chronic fatigue.
[6]

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.
Biogenic Amines are the leading cause of metabolic
acidosis which is the starting point for all the conditions of
disease.
Click here to learn more.

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

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

[1]

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

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

[1]

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

Lactate metabolizers = liver, kidneys, and heart.

Lactate above .4 mmol/l = skeletal muscle becomes net
consumer
[1]

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
.[2]
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
contractility and suboptimal response to exogenous
catecholamines.

Elevation of serum lactate concentration may have
inotropic effects (weakened muscular contractions)
independent of serum pH.
[3]

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 concentration.
[3

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.
[3]
PATHOPHYSIOLOGICAL CLASSIFICATION
OF LACTIC ACIDOSIS
HYPOXIC
NON-HYPOXIC
Ischemia
Shock
Severe anemia
Cardiac arrest
Global hypoxia
Carbon monoxide poisoning
Respiratory failure
Severe asthma
COPD
Asphyxia
Regional hypo fusion
Limb or mesenteric ischemia
Delayed clearance
Renal or hepatic dysfunction
Pyruvate dehydrogenase dysfunction
Sepsis
Thiamine deficiency
Catecholamine excess
Alcoholic and diabetic ketoacidosis
Uncoupling of oxidative phosphorylation
Cyanide
Silicates
Methanol & ethylene glycol metabolites
Retroviral drugs
Valproic acid
Biguanides
INH
Accelerated aerobic glycolysis
Increased effort
Seizures
Large fructose loads
Malignancies
Lactic acidosis leads to cardio pulmonary failure, sepsis, trauma, thiamine deficiency, increased side effects to drugs and toxins,
additional oncologic pathologies, 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.
[3]  

    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 propylene 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 reabsorption.
    . 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 acidosis.
    Ketoacidosis:
    . 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 excretion.
    .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 combined.
    . Some medication can mimic these deficits by altering membrane permeability, causing leaky
    pathways (amphotericin B, lithium, and foscarnet).
    . 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.
    [4]

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, to detoxify
toxins, and to 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 are in a state of acidosis.

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

. If litmus paper shows you are 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 lemon or lime into room
temperature water and drink within an hour after you wake up.  

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 makeup.