Mitochondrial Diseases and Adrenal Fatigue Syndrome – Full Version

By: Michael Lam, MD, MPH; Dorine Lam, RDN, MS, MPH


Mitochondria help with energy and prevent adrenal gland diseasesThe mitochondria in all our cells are the energy power plants or the engine block for our bodies. They produce a chemical called ATP, the body’s currency for energy. Mitochondria provide over 90 percent of the body’s energy. When someone is diagnosed with mitochondrial disease, it means that they are not functioning properly in the area of energy production.

Medically, mitochondrial disease is a category of different diseases grouped together. These different diseases present in different forms and vary widely with no two patients presenting with the same symptoms.

The symptoms appear similar to quite a few diseases, including Alzheimer’s disease, autism, chronic fatigue, Lou Gehrig’s disease, muscular dystrophy, and Parkinson’s disease. Mitochondrial weakness at the sub-clinical state also mimics conditions such as liver sluggishness, extracellular matrix congestion, and Adrenal Fatigue Syndrome (AFS).

When the mitochondrial system is malfunctioning then it can be fatal, such as Leigh’s disease. This affects one in 25,000. Most mitochondrial dysfunction is not fatal, but living a normal and vibrant lifestyle can be severely compromised. One in 2,500-3,000 people are affected in some way by mitochondrial disease.

Symptoms of Mitochondrial Disease

Each mitochondrion is an energy factory within the cell. Sugars and fats are imported, broken down, converted and exported as ATP. This highly complex process requires various special protein complexes at different stages for fruition. Mitochondrial diseases are caused by genetic mutations, resulting in deficiencies in one or more of the protein complexes required to make ATP. When a cell is filled with defective mitochondria, not only does it become deprived of ATP, it also can accumulate a backlog of unused fuel molecules and oxygen. Potentially harmful byproducts such as lactic acid can accumulate. A state of lactic acidosis can result, and symptoms can be mild to severe. They include muscle fatigue, aches, and cramps. Meanwhile, unused oxygen in the cells can be converted into highly destructive compounds called reactive oxygen species, including free radicals that cause oxidative stress.

ATP made from mitochondria provides the predominant source of power for muscle cells to contract and supports proper nerve cell firing. The combination of reduced energy availability with mitochondria disease and resulting free radical accumulation in these cells can also give rise to subtle signs and symptoms such as brain fog, joint pain of unknown origin, psoriasis, and fatigue.

When the mitochondrion fails, energy production slows down inside the cell, which is injurious and can even cause the cell to die off. Symptoms all depend on which cells in the body have the malfunctioning mitochondria. Diseases of the mitochondria appear to cause the most damage to cells of the brain, heart, liver, skeletal muscles, kidney and the endocrine and respiratory systems.

Low energy is common with adrenal gland diseasesSymptoms include:

  • Low energy state and fatigue, with low exercise tolerance level and fatigue on exertion.
  • Low cardiac output, leading to congestive heart failure.
  • Developmental delays below the normal growth curve
  • Gastrointestinal disorders, such as leaky gut, irritable bowl, and constipation
  • Lactic acidosis, with symptoms such as muscle soreness, pain and cramps.
  • Liver disease and congestion, with symptoms such as brain fog, and an inability to tolerate medications or supplements
  • Loss of motor control, coordination
  • Neurological problems
  • Seizures
  • Susceptibility to infection
  • Swallowing difficulties
  • Thyroid dysfunction

Mitochondrial disease can make its appearance at any age, though childhood onset is most common. In many people, this disease is not even diagnosed, as there is a lack of awareness in the medical community and in the public at large.

Mitochondria—Much More Than Energy Factories

There are as many as 3,000 genes that make up one single mitochondrion. In addition to energy production, mitochondria are what contain the rate-controlling enzymes for the biosynthesis of pyrimidine (dihydroorotate dehydrogenase) and the synthesis of heme (D-aminolevulinic acid synthase). In the liver, mitochondria work in a specialized manner to detoxify ammonia, which forms in the urea cycle. Mitochondria are also needed to metabolize cholesterol, for the synthesis of testosterone and estrogen, to metabolize neurotransmitters and for the production and detoxification of free radicals. They perform all of these functions as well as metabolizing or oxidizing the fat, carbohydrates and protein we consume.

Genocopies and Phenocopies

Since mitochondria are responsible for performing so many varied and different functions in all the different bodily tissues, there are hundreds of different kinds of mitochondrial diseases and disorders. Every single one has its own spectrum of abnormalities. This is very confusing to patients and physicians alike, especially when trying to diagnose the problem.

Because of the complexity of the interactions between the hundreds of cells and genes that all must work together to keep our metabolic systems running well, it is a feature of mitochondrial disease that the identical mtDNA mutations may not necessarily result in the same diseases. Genocopies are diseases caused by the identical mutation, but that may not look identical clinically.

The opposite is also true: different DNA mutations can progress to the exact same diseases. These diseases are known in genetics as phenocopies. A solid example of this phenomenon is Leigh syndrome, a fatal disease that can actually be caused by perhaps a dozen very different genes.

Diagnosing Mitochondrial Disease

Identifying mitochondrial disease and adrenal gland diseasesWhen considering a diagnosis of mitochondrial disease, patients must be evaluated very carefully for other diseases as well. Anytime anyone presents with fatigue and low energy state, a complete cardiac, hormonal, hematological, oncological and metabolic workup is needed. When the investigation result is normal, an out of the box differential diagnosis needs to be considered. They include Adrenal Fatigue Syndrome and mitochondrial disease.

Unfortunately, there isn’t a single test developed yet to diagnose mitochondrial disease in the majority of patients. In today’s medical environment oxidative phosphorylation (OXPHOS) enzymology alone is not sufficient for an accurate diagnosis.

Mitochondrial disease is diagnosed by using an integrated approach with multiple means and a detailed history, which would include:

  • Brain imaging
  • Clinical observations
  • Evaluating laboratory results
  • Muscle biopsies

An alert physician with experience in orthomolecular medicine is usually required for a proper diagnosis as it is rare that genetic testing would be adequate for an accurate diagnosis of the disease.

Tests Used for Diagnostic Purposes

There are three different categories of diagnostic criteria:

  • Genetic testing of mitochondrial DNA (mtDNA) and nuclear DNA
  • Metabolic markers of blood, urine and cerebral spinal fluid
  • Muscle testing assessing liver respirometry, CoQ levels, and muscle pathology

Diagnosis is considered positive if two or more tests from two categories show abnormal results.

Defective mitochondria produce large quantities of oxygen free radicals. Comparing patients who have a mitochondrial disorder with healthy people, researchers have found that their blood glutathione level was significantly reduced in white blood cells from mitochondrial diseased patients. This indicates a low level of antioxidant defenses. Measuring blood glutathione levels can be used as a biomarker to monitor the mitochondrial disorders.

Thyroid Hormones and Mitochondria

Thyroid hormones are vital to the proper functioning of the mitochondria. These hormones affect mitochondria in two ways. First, thyroid hormone quickly stimulates cellular respiration. The second effect is an increase in the biogenesis of mitochondria and changes in the mitochondrial mass, which can occur from one to a few days after having hormone administration.

Thyroid hormones trigger the uncoupling of the process of oxidative phosphorylation using various mechanisms involving the proteins and lipids of the inner membrane of mitochondria. This enhanced uncoupling activity can increase the metabolic effects of taking thyroid hormones.

Additionally, 3,3’,5-triiodo-L-thyronine (T3) is actively involved in regulating mitochondrial function in a number of metabolically active tissues, which include the heart, liver, kidneys and skeletal muscles.

Mitochondrial Disorders and Adrenal Fatigue Syndrome

Adrenal Fatigue Syndrome is a stress induced neuro-endocrine dysfunction of the body. The hallmark symptom is fatigue of unknown origin despite normal medical investigation. There are four clinical stages of clinical progression, from mild to severe. In advanced stages, one can be incapacitated and housebound, unable to work or lead a normal social life.

Most people with AFS carry on normal lives and are thus unaware of the potential negative natural progression of this condition until quite late. Allopathic physicians are ignorant of this condition and thus reject its notion. Do not be surprised if your doctor tells you AFS does not exist.

Many symptoms of mitochondria disease and AFS are similar. Fatigue caused by a purposeful down regulation of bodily function to conserve energy in the case of AFS ultimately results in reduced formation of ATP from the mitochondria to achieve its effect. Diseases of mitochondrial dysfunction will result in a body that is unable to produce the necessary amount of ATP. The common clinical pathway for both AFS and mitochondrial disease is fatigue.

Mitochondrial Disorders and Adrenal Fatigue Syndrome

Adrenal Fatigue Syndrome is a stress induced neuro-endocrine dysfunction of the body. The hallmark symptom is fatigue of unknown origin despite normal medical investigation. There are four clinical stages of clinical progression, from mild to severe. In advanced stages, one can be incapacitated and housebound, unable to work or lead a normal social life.

Most people with AFS carry on normal lives and are thus unaware of the potential negative natural progression of this condition until quite late. Allopathic physicians are ignorant of this condition and thus reject its notion. Do not be surprised if your doctor tells you AFS does not exist.

Many symptoms of mitochondria disease and AFS are similar. Fatigue caused by a purposeful down regulation of bodily function to conserve energy in the case of AFS ultimately results in reduced formation of ATP from the mitochondria to achieve its effect. Diseases of mitochondrial dysfunction will result in a body that is unable to produce the necessary amount of ATP. The common clinical pathway for both AFS and mitochondrial disease is fatigue.

Mitochondria Cocktail

Now there are no effective treatments for mitochondrial disease from a prescription medication perspective.

We know that many vitamins are required for synthesis of mitochondrial respiratory chain components. Biosynthesis of the key components of mitochondrial respiratory chain, coenzyme Q, for example, is dependent on vitamins B2, B6, B12, folic acid, pantethine, pantothenic acid, niacinamide and vitamin C.

As well, vitamins B1, B2, B6, niacin, biotin, folic acid, pantethine, and pantothenic acid are important for metabolic pathways in mitochondrial respiration and energy production. Vitamins C, E, niacin and folic acid are excellent scavengers of free radicals once formed. They help prevent mitochondrial oxidative damage and mitochondrial aging.

Many mitochondrial diseases are linked to vitamin deficiencies and can be improved by vitamin supplementation. Proper nutritional supplements targeted to enhance the mitochondria require a nutritional cocktail for best results.

Substrates to be considered for the mito-cocktail include coenzyme Q10, L-carnitine, vitamin C, glutathione, B complex, trace minerals, marine phytoplanktons, pantethine and pantothenic acid, vitamin D, and magnesium.

Delivery System and Bioavailability

Because the mitochondrial is located inside the cell, fat-soluble nutrients such as vitamins A and E can reach it easily. They therefore tend to be more effective as mitochondrial anti-oxidants when compared to water-soluble nutrients like vitamins C and B, which are less able to cross the phospholipid bilayer cell wall comparatively speaking.

The advancement of nanotechnology and liposomal encapsulation technology offers a significantly enhanced oral liquid delivery system that overcomes this problem. Absorption is primarily in the small intestine rather than from the stomach. This dramatically improves assimilation and bioavailability. Always consider liposomal delivery systems for nutrients if available. Fortunately, this delivery system is available for glutathione, vitamin C, magnesium, vitamin D, and coenzyme Q10.

Phospholipids from lecithin remain the time tested and proven carrier of choice. Liposomal spheres so created are strong. Premature separation of the substrate from the carrier sphere is avoided. This is a common technical problem encounter when other forms are used. Care should be taken to avoid any formula that contains alcohol as a preservative. Always buy high quality brands because only advanced technology can prevent separation between the carrier lipid and the substrate, resulting in a liquid that is grainy instead of smooth if the liposomal is intact.

Liposomal Coenzyme Q10 (Ubiquinol)

Coenzyme Q10, also known as CoQ10, is an enzyme that is made by the body and is found in seafood. After about age twenty, and continuing as we age, the body’s production of CoQ10 slows down, declining by 50 percent. By age seventy, only 50 percent of the CoQ10 is produced by the body.

CoQ10 can be found in many different products including fatty fish (such as sardines) and organ meats such as heart, liver, and kidney. It can also be found in beef, soy, and peanuts. Diet alone does not provide sufficient CoQ10. For example, one pound of sardines or two-and-a-half pounds of peanuts are needed to provide 30 mg of CoQ10. Vitamin E, selenium, and the B vitamins all enhance and boost the biosynthesis of CoQ10 internally.

CoQ10 is a powerful antioxidant and stabilizes cell membranes. It also energizes and facilitates the efficiency of the mitochondria. The range of heart conditions for which research has found CoQ10 to be beneficial includes congestive heart failure, cardiomyopathy, arrhythmia, and angina when there is a lack of oxygen and muscular dystrophy. In some countries, cardiologists prescribe CoQ10 to patients with congestive heart failure routinely. In Japan, millions take CoQ10 as a prescription drug for cardiac problems.

The therapeutic effect of CoQ10 is highly dependent upon the delivery system.

Dosage Consideration: 100-300 mg per day in liposomal form for better bioavailabity. Much more is needed in case of cardiac failure.

L-Carnitine

L-carnitine is a semi-essential nutrient that acts as a transport carrier of fatty acid into the mitochondria where energy is produced. It is made from two essential amino acids (lysine and methionine). In addition to the transport function, L-carnitine helps in the metabolism of the fat within the mitochondria to generate energy. Studies have shown that dietary supplementation of L-carnitine markedly improves the overall mitochondrial function. The amount found in whole foods such as meat is unfortunately small.

Dosage Consideration: 300-2000 mg per day

Note: Taking L-carnitine with thyroid hormone might decrease the effectiveness of the thyroid hormone and make symptoms of hypothyroidism worse. Those with primary low thyroid function or secondary hypothyroidism from Adrenal Fatigue Syndrome should proceed with care. As well, L-carnitine might increase the effects of warfarin (Coumadin) and increase the chances of bruising and bleeding. Be sure to have your blood checked regularly. The dose of your warfarin (Coumadin) might need to be changed.

Arginine

Arginine is also a semi-essential amino acid. It is a precursor to nitric oxide (NO) in the body. NO is an essential compound that helps blood circulation by relaxing blood vessels. It enhances blood flow so mitochondria in the heart muscle do not have to work as hard.

Even thought the body normally makes enough, supplementation can be very beneficial when more protein is needed in the body. Those in advanced AFS where the body is in a catabolic state will find this nutrient very helpful. In addition, people with protein malnutrition, excessive ammonia production and infections may not have enough arginine due to depletion.

Symptoms of arginine deficiency include poor wound healing, hair loss, skin rash, constipation, and fatty liver. Early studies have shown that arginine supplements may help treat erectile dysfunction (ED) in men with low nitrate levels in their blood or urine.

Dosage Recommendation: 500-6000 mg per day in powdered form. Higher doses of L-arginine can increase stomach acid and may aggravate symptoms in people with herpes. Those with low blood pressure need to be careful not to take too high a dose without supervision.

Reduced Liposomal Glutathione

Glutathione (GSH) is a key intracellular antioxidant and detoxifying enzyme. While synthesized exclusively in the cytosol from its constituent amino acids, GSH is distributed in different compartments, including the mitochondria where its concentration in the matrix equals that of the cytosol. Almost 80 percent of people with chronic ailments are found to be deficient in glutathione. In fact, low levels of glutathione are involved in all disease states. Glutathione promotes the healthy flow of electrons and maintains their steady supply in the body’s cells. This is the source of its effectiveness. Cells heal and live longer when electron flow is abundant and smooth. Poor flow of electrons corresponds to low energy, higher disease rates, low cell integrity, and cell death. Glutathione donates electrons to the body’s antioxidant pool, including antioxidants such as vitamin C, vitamin E, alpha-lipoic acid, and superoxide dismutase (SOD). In addition, glutathione neutralizes disease-causing oxidants and is capable of eliminating heavy metals. By protecting the body from free radicals and pathogenic attacks, it is keeping the cellular structure intact.

Dosage Recommendation: 50-400 mg per day of reduced glutathione in liposomal form for better bioavailability.

B Vitamins

Some B vitamins are cofactors, which participate in important mitochondrial reactions. Only a small amount is needed. Most of the B vitamins have a bitter taste and are more palatable if flavored. B vitamins are water-soluble; that is, they are excreted if not used, and the benefit from taking these vitamins should be felt immediately. Thiamin is a cofactor for the pyruvate dehydrogenase complex, and in some patients has improved lactate and pyruvate levels. Thiamin has also helped some patients by improving their clinical symptoms.

Riboflavin (B2) is helpful for some patients with headaches and migraines, and is another important cofactor that participates in important mitochondrial reactions. Pantethine and pantothenic acid should also be considered.

Liposomal Magnesium

Magnesium helps regulate neuromuscular activities of the cell and the mitochondria. The mitochondria cannot produce energy without this necessary component. Advanced age and a low plasma magnesium concentration are two key risk factors for poor mitochondrial function.

Unfortunately, the common American diet is high in calories and low in nutrition, resulting in a malnutrition epidemic of massive proportions. The modern day diet supplies limited magnesium per day, and most Americans are deficient in magnesium even by RDA standards of 300 mg a day and are not even aware of it. Common prophylactic intake of 400 mg to 1000 mg a day as a nutritional supplement is recommended. Excessive magnesium can cause diarrhea. Most can tolerate taking up to a 1000 mg supplement without problems. If you are getting loose stools, cut back and take just enough to avoid the runs. Do not take high levels of magnesium if you have kidney problems.

The best forms of magnesium for absorption are liposomalized magnesium gluconate and magnesium bisglycinate (magnesium bound to the amino acid glycine). With liposomal delivery, unabsorbed magnesium reaching bowl tolerance level and subsequent diarrhea and loose stools is avoided.

Dosage Recommendation: 100-500 mg as tolerated in liposomal form. Much more is needed for regular forms.

Liposomal Vitamin D

This hormone is normally produced in the skin using energy from sunlight. Vitamin D can also be found in a few foods—including fish, fish liver oils, egg yolks and fortified cereals but it can be effectively boosted with vitamin D supplements.

Vitamin D is vital for making our muscles work efficiently and boosting energy levels by enhancing mitochondria function. Muscle fatigue is a common symptom in vitamin D deficient patients, and this can be reversed with vitamin D supplementation.

Mitochondria use glucose and oxygen to make energy in a form that can be used to run the cell—an energy-rich molecule called ATP. Muscle cells need large amounts of ATP for movement and they use phosphocreatine as a ready and available energy source to make ATP. The mitochondria also replenish this phosphocreatine store after muscle contraction and measuring the time taken to replenish these stores is a measure of mitochondrial efficiency: better mitochondrial function is associated with shorter phosphocreatine recovery times. Low vitamin D levels were associated with reduced mitochondrial function.

Dosage Recommendation: 1000-10,000 IU. Much more may be needed for therapeutic effect or reversal of vitamin D deficiency. A liposomal delivery system is preferred. Oral sublingual intake in the morning is best for normal people. Nighttime administration is best for those with insomnia associated with AFS.

Liposomal Vitamin C

Despite the clinical importance of preventing mitochondrial oxidative damage, antioxidants such as vitamin C has limited effect primarily due to its limited ability to cross the cell wall from extracellular space to intracellular space where mitochondria is located.

Liposomal forms of vitamin C solves this problem as it is able to move through phospholipid bilayers and enables their accumulation on the mitochondrial matrix in response to the large, negative-inside mitochondrial membrane potential that does not require any specific import mechanism.

Within the mitochondria, ascorbic acid is released from the liposome. It goes to work and reduces mitochondrial oxidative stress.

Dosage Recommendation: 100-1200 mg per day in liquid liposomal form. The dosage range is very wide and depends on each person’s constitutional background, sensitivity, and history.

Mineral Ascorbates

Mineral ascorbates (ascorbic acid combined with a mineral such as sodium) are water-soluble nutrients that have excellent extracellular anti-oxidative properties in quick release form. They are able to enter the mitochondria via facilitative glucose transporters and confer mitochondrial protection against oxidative injury as well, though at a much lower level. This allows them to reduce oxidative stress both within and outside the mitochondria.

Consider the combination of sodium ascorbate, calcium ascorbate, and magnesium ascorbate along with bioflavonoids and a small amount of ascorbic acid. They work well together. Not to be forgotten are important cofactors such as L-lysine, L-proline, malic acid, and citrus bioflavonoids. L-proline, L-lysine, and mineral ascorbates also support collagen synthesis. Malic acid helps to increase energy, and along with magnesium, helps to stabilize gastric intestinal irritation and relax tense muscles. Citrus bioflavonoids help make vitamin C more bioavailable to the cell.

Mineral ascorbates are best taken in conjunction with liposomal forms of vitamin C. Both forms work synergistically together for maximum sustained cellular delivery.

Dosage Recommendation: 500-2000 mg in powdered form.

Subclinical Mitochondrial Disease

Mitochondrial Disorder can affect Adrenal Fatigue and energy levelsOne does not need to have documented and diagnosable mitochondrial disease to suffer symptoms of mitochondrial weakness. Be on the look out for fatigue, a low energy state, insomnia, water retention, low body temperature, reduced thyroid function, reduced gastric assimilation, a weak urine stream, menstrual irregularity, constipation, dry skin, and an unstable mood. Signs and symptoms may be subtle, but they are clearly visible if you are on the alert. They point to a body that has reduced energy output from the mitochondria. These symptoms are similar to those experiencing hypothyroid or Adrenal Fatigue Syndrome. Viewed objectively, it is clear that the body is unable to go into overdrive when called upon. There is not enough fuel. It is like a car that moves slowly despite the gasoline pedal in full open throttle.

As AFS progresses from mild to severe, peripheral organ resistance frequently develops. Thyroid replacement becomes less effective, and organ resistance to cortisol surfaces. In order to achieve the same therapeutic effect, hormonal dosages must be increased. Not everyone can tolerate higher doses, which has many undesirable side effects, including anxiety, heart palpitations, and insomnia.

With organ resistance, fewer hormones are able to reach the mitochondria to facilitate its function. Less energy will be produced as a result. A state of subclinical mitochondrial disease is therefore an inescapable reality for many. Practically speaking, almost everyone in advanced stages of AFS will have certain degrees of mitochondrial weakness and lowered energy output, even if there is an absence of clinical diagnosable mitochondrial disease.

Without fortifying the mitochondria as the adrenals are healing, overall recovery from AFS is often slow and retarded. That is why mitochondrial fortification should be part of every comprehensive adrenal fatigue recovery program. The key is to know when to support the mitochondria, as bad timing can make AFS worse, especially in advanced stages.

Strategies for those with Adrenal Fatigue Syndrome

If you have mitochondrial disease and AFS concurrently with fatigue as the primary symptom, helping mitochondrial function should reduce fatigue in principal. This is true if AFS is in the early stages where fatigue is mild to moderate.

There are caveats, however. A significantly positive energy response with mitochondrial support may mask underlying unresolved adrenal problems. Energy levels can quickly reduce as mitochondrial support is withheld. It is important therefore that mitochondrial and adrenal support be concurrent but balanced. That way, when mitochondrial support is stopped, the adrenals are strong and well healed in order to continue unassisted and avoid any adrenal crashes. Failure to consider this two-pronged balanced approach is a common recovery mistake.

If you are in advanced stages of AFS when fatigue is moderate to severe, or if you are house bound and have little energy to do but basic chores of normal living, embarking on mitochondria supplementation should begin only after the adrenals are stable, internal toxin levels reduced, the liver decongested, and the extracellular matrix cleansed. Dosage should start at a very low dose and titrate upwards to reach therapeutic goals.

Due to the prevalence of paradoxical reactions in advanced AFS, do not be surprised if the body rejects any of these good nutrients, even at low dosages. The more advanced the AFS, the higher the risk. It is not unusual for paradoxical reactions to surface, where fatigue is worsening. Exaggerated positive responses may also surface, resulting in a sense of anxiety, irritability, insomnia, and heart palpitations. Both are undesirable and indicate dosage and delivery system adjustments are needed. Both occur when the mitochondria are overstressed or receptor site sensitivity increased. It is a sign that the body is not quite ready for mitochondrial support.

Catabolic State and Mitochondrial Support

Those who are in a catabolic state where the body is loosing muscle mass and protein and thus weight need to be extremely careful when it comes to mitochondrial support. Examples are those in very advanced stages of AFS, in post-surgery, with large open wounds. They are already in a fragile state within. Many have concurrent low body fluid volume, low blood pressure, temperature intolerance, electrolyte imbalance, delayed food sensitivity and intolerance, receptor sight disorders, liver congestion, extracellular matrix pollution, and severe fatigue.

The body is in a slow-down mode, with all nonessential functions, such as reproduction, shut off in order to conserve energy for survival. That is why most at this stage have low libido and irregular or absent menses. At the same time, the autonomic nervous system is activated and on full alert. As a result, the body is flooded in a sea of norepinephrine and adrenaline. The body is entrenched in a fight or flight mode at this time. The mitochondria is one of the last soldiers standing and working hard to put out the necessary ATP to keep the vital organs functioning, especially the heart, liver and kidneys. Already overworked mitochondrial cannot be stressed further. What the mitochondria needs is rest. It should not be driven to work harder by any nutrients even though they are supportive of mitochondrial function in normal situations.

Nutrients, no matter how good, administered at the wrong time will worsen the overall condition. Recognizing the proper timing is an art requiring extensive clinical experience correlating the state of the body with its ability to tolerate different kinds of nutrients. Failure to consider these factors is a common reason for AFS recovery failure.

Further ramping up mitochondrial function when the mitochondria is already at or close to peak output may lead to reduced marginal return over time at best. Energy output may go up for a short time and then plateau, while anxiety escalates quickly, leading to a state of wired anxiety. Those with AFS may experience adrenal crashes, with extreme fatigue and physical incapacitation. Many are bedridden for days and sometimes weeks.

Use natural compounds to help with a mitochondrial disorderTo avoid this, a better strategy is to reduce internal sympathetic tone and its hormones norepinephrine and adrenaline load first through stabilizing and healing the adrenals. This is best accomplished by a comprehensive recovery program using gentle and nurturing natural compounds. Herbs, glandular, and hormone should be avoided. The focus is on building and providing an alternative nutritional safety net for the body to dip into at times when it needs energy in order to stabilize and turn off the sympathetic alarm response. As the body regains its calm with this strategy, symptoms such as anxiety, fatigue, hypoglycemia, and insomnia reduces. Symptoms suggestive of sympathetic overtone commonly seen in advanced AFS such as heart pounding, postural hypotension, lightheadedness on arising, reactive hypoglycemia, and heart palpitations will resolve spontaneously. Once this is achieved, the next step is to make sure the extracellular matrix is cleansed and the liver is not congested. Only after these conditions are met should one proceed on mitochondrial support, which will yield results without the risk of decompensating adrenal crashes.

Summary

Mitochondrial disease is a category of different diseases grouped together. The common characteristic is the same—fatigue and low energy state from reduced mitochondrial ATP formulation. Fortunately, there are natural compounds with proven mitochondrial support. The most important nutrients include co-enzyme Q10, magnesium, glutathione, vitamin D, and arginine. Because the cell wall protects the mitochondria, a proper delivery system is of vital importance to ensure bioavailability for this key to any successful mitochondrial recovery program. Sufferers of Adrenal Fatigue Syndrome, especially in advanced stages, invariably have some level of mitochondrial weakness. Recovery faces special challenges with timing, dosage, and delivery system needed for mitochondrial support. Extensive clinical experience is required to avoid adrenal crashes and retarded recovery.

If you are suffering from mitochondrial diseases and have Adrenal Fatigue Syndrome, recovery needs to be personalized. An improper approach to recovery can complicate, deter, or even exacerbate your current state.

 
© Copyright 2015 Michael Lam, M.D. All Rights Reserved.