Healing is Voltage [Research Mirror]

JULY 2, 2014 by MARCO TORRESHealing Is Voltage

Maintaining an alkaline environment is a key to good health. As our voltage drops below a certain voltage, we begin to experience fatigue. As the voltage further drops (and thus the pH drops) we become prone to developing health problems. Cancer cells, for example, have a pH of about 6.3 and carry a specific voltage. By knowing that chronic disease is associated with low voltage, one might ask an obvious question; "What is my voltage?"

One can measure the body's voltage with a voltmeter that measures in millivolts. However, the voltage in the body pulses, making it difficult to get a true endpoint with a voltmeter. There are computerized devices that will measure the body voltage and impedance. 

These were developed in the 1950's before the FDA began to evaluate devices. The FDA has not approved these devices for measuring body voltage, but they have been in continuous use for this purpose around the world since 1951.

Electrons are needed for health and for healing. The optimal cellular pH of 7.35 = -20mv. pH is ultimately a measure of redox potential. Redox potential is a measure of whether electrons are available in surplus (and thus are “electron donors”) or whether electrons are deficient (and thus are “electron stealers”). When the voltage is an electron stealer, it is called plus voltage. When it is an electron donor, it is called a negative voltage. The voltage is converted to a logarithmic scale of 1-14 called pH. 

The minus sign means electrons are in surplus and are available to be donated. If cells are injured, -50 mv is needed for healing. In other words, for healing to take place, a more alkaline environment (with even more electrons available then normal) is needed. Antioxidants like vitamin C or glutathione are valuable because they are electron donors which help counteract oxidants (electron stealers). Some other electron donors are low level lasers, essential oils, homeopathic remedies, being grounded, and alkaline water (the next newsletter will be on this topic). Some electron stealers are root canals, mercury fillings, processed foods, acid water and carbonated beverages.

Cells are designed to run at a pH of 7.35 (-20 millivolts) to a pH of 7.45 (-25 millivolts). Cell membranes can achieve a temporary "action potential" of up to -90 millivolts.

We heal by making new cells. Making new cells requires -50 millivolts. 

We get sick when we cannot achieve -50 millivolts and thus cannot make new cells. We are thus stuck in chronic disease. All chronic disease is defined by having low voltage.

Chronic disease occurs when voltage drops below -20 millivolts.  As voltage drops, these things happen:

1. Cells dont have enough energy to work correctly.

2. Chronic pain is caused by low voltage.

3. As voltage drops, the amount of oxygen in cells drops, switching from aerobic (oxygen- available) metabolism to anaerobic (oxygen diminished) metabolism.

4. With anaerobic metabolism, one unit of fat makes only two molecules of ATP whereas with aerobic metabolism, one unit of fat makes 32 molecules of ATP.

5. With anaerobic metabolism, microorganisms begin to grow and put out toxins to dissolve our cells so they can eat us.

There are multiple sources where the body normally gets electrons (unprocessed food, alkaline water, sunshine, standing in the dirt, etc.). This creates a body pool of electrons. 

In the body, the tissue with the least resistance to the flow of electrons is fibrous tissue. Thus wherever there is fibrous tissue, it is serving two purposes: structural support and moving electrons.

The body has three "trucking systems" that move electrons down to the cells: ionically through the circulatory system, through the fibrous sheath surrounding nerves, and through the acupuncture system (the fascial system).

Cell membranes are made up of opposing phospholipids (fats). Because of their unique properties, this arrangement creates a capacitor, a unit designed to store electrons. Thus cell membranes are like small batteries.

Underneath the cell membranes are small power stations called mitochondria. Inside the mitochondria is a rechargeable battery system called ATP/ADP. When the battery is charged, it is called ATP. When it is discharged, it is called ADP.

ATP is the final power source for the proteins in the cell to move. This movement allows the cell to do whatever it is designed to do. As power is drained from the ATP battery, it becomes discharged and is called ADP. Electrons are then brought down from the cell membrane to recharge ADP back to ATP. ATP is also made by the Krebs Cycle. 

This process takes place about 70 times per day in every cell.
We have come to understand that chronic disease is accompanied by a loss of voltage. The image to the right is the "power grid" of the body. Thus you will usually find the cause of the loss of power by studying this image. If you can answer the question, "Why did I lose enough voltage to get sick?", you will know how to get well.

There are many things that can destroy your power grid. However, the four most common ones are eating trans fats, not having enough functional thyroid hormoneheavy metal poisoning, and dental infections.

Food manufacturers were losing money because of spoilage. The main thing that spoils is the fats turn rancid. They found that if they cook the fats for 5 hours at 350 degrees, it turns into something very similar to plastic. These "plastic fats" are called "Trans Fats" or "partially hydrogenated fats". Most of the food you will find in the grocery store contains these plastic fats because it increases the shelf-life and thus the profits of the food companies.

If you eat plastic fats, your cell membranes become like cellophane and won't hold a charge = you become a dead battery!

Canola Oil acts similarly to plastic fats and should also be avoided.

The total number of mitochondria (and thus the total number of rechargeable ATP/ADP batteries) you have is dictated by the amount of FUNCTIONAL thyroid hormone you have!

The pituitary gland makes thyroid stimulating hormone (TSH). This causes the thyroid gland to make thyroid hormones (T4 and T3). Doctors generally test the levels of each of these to determine if the thyroid is functioning normally. However, these tests are made invalid by fluoride.

The halogens are fluorine, chlorine, bromine, iodine, and astatine. Whenever an atom of fluorine is present, it will displace any of the other halogens.

T4 is a tyrosine protein with four iodines attached to it. When you consume fluoride in water, toothpaste, at the dentist, etc. it displaces the iodine on the thyroid hormone. It appears that the blood tests for thyroid hormones cannot tell the difference between the real hormone and the fake hormone. Thus many people are hypothyroid with normal blood tests! This is called Hypothyroidism Type II.

Heavy metals like lead, mercury, cadmium, etc. destroy mitochondria and thus lower your voltage. It only takes a piece of lead the size of a grain of salt to poison you. Lead was present in paint and gasoline until the 1950's. Lead is commonly found in items imported from China.

According to the World Health Organization, 80% of mercury in humans comes from their dental fillings. "Silver fillings" are mostly mercury. Mercury is so poisonous that you have to wear a biohazard suit to handle it---unless you put it into your mouth! Every time you get a flu shot, you get an injection of mercury!

Heavy metals do not stay in the blood very long. They quickly move down into your tissues. Thus if you find a heavy metal in your blood, it means you have a current source. To find chronic heavy metal poisoning, you must inject a chelating agent into the vein so it can pull the metal out of your tissue and dump it into the kidneys so it can be found.

Microorganisms like bacteria don't have a digestive system, so they secrete their digestive enzymes to dissolve our cells so they can have lunch. Of course this damage to our cells causes us illness.

If you think about it, the type of enzyme necessary for a bug to have lunch on a tooth has to be very strong compared to a Strept bacteria having lunch on your tonsils! These powerful enzymes (toxins) from bacteria that can live on teeth are called gliotoxins and thioethers. These poisons cause the mitochondria to shut down in cells far from your teeth!

Root canal surgery is performed by ripping the artery and nerve from a tooth, killing it. The dentists are the only physicians who purposely leave dead tissue in the body. All dead tissue, whether it is your tooth, your appendix, or you big toe, will become infected and harm you if you don't remove it. There are 2-3 miles of small tubules in a tooth, and it is impossible to sterilize these with lasers, medications or any other way.

Any infection, in a tooth, a root canal, or in the bone around a tooth must be aggressively dealt with or you will develop chronic disease elsewhere.

Comorbidity of hypercholesterolemia and Lyme disease [Research Mirror]


Borrelia burgdorferi is one of an increasing number of bacterial pathogens that can incorporate and metabolize cholesterol from the host. This organism requires cholesterol to grow but it lacks the metabolic machinery to synthetize it. In previous studies in our laboratory, we showed that cholesterol is key for maintaining the integrity and properties of the outer membrane of B. burgdorferi. Importantly, cholesterol is essential for pathogenesis of Lyme disease since cholesterol and cholesterol glycolipids form microdomains in the membranes of the spirochetes with all the hallmarks of eukaryotic lipid rafts, and that it may have important physiological functions. Despite the requirement for cholesterol, little is known regarding the effects of high cholesterol levels in serum, in tissues or in the accumulation of fat in tissues targeted by B. burgdorferi in Lyme disease patients. In a recent study [Toledo et al PNAS 2015], we showed that elevated levels of serum cholesterol, achieved with a short term high fat diet in cholesterol-transport deficient mice of two different genotypes [apolipoprotein E (apoE-), and low density lipoprotein receptor (LDLR-) deficient] resulted in increased arthritis as well as increased number of spirochetes in the joints. These results alerted us to the possibility that hyperlipidemias could be a comorbidity factor for: i. increased acute Lyme disease severity; ii. Increased persistence of spirochetes in tissue, and iii. dissemination to and colonization of tissues with high lipid concentrations. Based on the hyphotesis that B. burgdorferi can exploit the excess of serum cholesterol leading to enhanced acute and chronic infection, and that hyperlipidemias are comorbid factors for Lyme disease, we propose the following: 
Specific Aim 1. To determine whether chronic hypercholesterolemia affect the overall pathogenicity of B. burgdorferi in the murine model of Lyme disease with two subaims to determine whether acute or chronic infection of B. burgdorferi is enhanced by hypercholesterolemia in WT and LDLR- mice; 
Specific Aim 2. To evaluate the role of subcutaneous adipose and intra-abdominal fat in the dissemination of the spirochete.

Public Health Relevance

High levels of serum cholesterol are a common medical condition of adults and even some children. We have evidence that high serum cholesterol enhances the inflammation of mouse joints infected with the agent of Lyme disease. Considering that Lyme is a very frequent infection, we have thought that serum cholesterol could be a factor in enhancing susceptibility. In this application, the effects of high serum cholesterol an the acute and chronic stages of Lyme disease will be studied.

Influence of zinc on synthesis and the accumulation of collagen in early granulation tissue. [Research Mirror]




Chronic zinc deficiency causes a delay of reparative processes. The rate of repair is normalized by the administration of zinc. An acute lowering of the serum zinc level follows trauma. In a previous experimental study, it was demonstrated that the intramuscular administration of zinc beginning before trauma results in an increased collagen accumulation in early granulation tissue. In this study, the rate of collagen synthesis was determined to see if the higher amount of collagen found in early granulation tissue could be explained by increased collagen synthesis. The rate of collagen synthesis was studied by the determination of the incorporation of 14C-L-proline into collagen in vivo and in vitro. No difference was found regarding collagen synthesis in the granulation tissue of rats in the control and zinc treated groups. Specific activity of collagen, a measure of newly synthesized collagen in relation to the total amount of collagen, was found to increase markedly during the observation time. Further, the specific activity was found to be lower in the rats of the zinc treated groups than in the rats of the control groups on days 4 and 5, an indication that, after the administration of zinc there is more earlier synthesized, not labeled, collagen present. A possible explanation is that there is a concomitant synthesis and breakdown of collagen in granulation tissue and that the rate of breakdown is decreased by the administration of zinc.

Healing the Body With Celery Juice – Medical Medium [Research Mirror]


If people knew all the potent healing properties of celery juice, it would be widely hailed as a miraculous superfood. Celery has an incredible ability to create sweeping improvements for all kinds of health issues. 


Celery is truly the savior when it comes to chronic illness. I’ve seen thousands of people who suffer from chronic and mystery illness restore their health by drinking 16 ounces of celery juice daily on an empty stomach. That’s why long ago I started the movement of drinking pure, straight celery juice, and it’s why I want to be sure people know how to use this potent drink correctly and successfully. 

Celery juice is most powerful when you drink it solo. While it’s great to consume other green juices or vegetables juices and add in items like spinach, kale, parsley, cilantro, or apples, drink those mixed juices at a different time than your straight celery juice. These blends function differently than what I’m recommending as your greatest tool for recovering your health: pure celery juice taken on an empty stomach. If you drink your celery juice first thing in the morning, it will also strengthen your digestion of foods you eat for the rest of the day. 

We’ll get to more tips in a moment. First, let’s look at what makes this tonic a miracle juice.


Celery juice is teeming with powerful anti-inflammatory properties. This means it’s highly beneficial for people who suffer from chronic and mystery illnesses, including conditions labeled “autoimmune.” Hashimoto’s thyroiditis, rheumatoid arthritis (RA), fibromyalgia, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), Lyme disease, migraines, vertigo, celiac disease, irritable bowel syndrome (IBS), diabetes, psoriasis, eczema, acne, lupus, Guillain-Barré syndrome, sarcoidosis, Raynaud’s syndrome, Ménière’s disease, gastroesophageal reflux disease (GERD), gout, bursitis, bloating, intestinal cramping, distention, acid reflux, vertigo, constipation, restless leg syndrome, tingles, numbness—all of these symptoms and illnesses are mysteries to medical communities, even though they have names. Their true causes are not yet known by medical research and science. 

Celery is perfect for reversing inflammation, because it starves the pathogens, including unproductive bacteria and viruses such as Epstein-Barr (EBV), that create it. As I reveal in my book, Thyroid Healing: The Truth behind Hashimoto’s, Graves’, Insomnia, Hypothyroidism, Thyroid Nodules & Epstein-Barr, EBV is the actual cause of Hashimoto’s thyroiditis and many other diseases that medical communities call autoimmune. (More on the true cause of autoimmune conditions soon.) These pathogens lead to hundreds of different symptoms and conditions that go misdiagnosed. 


Celery is able to starve pathogens, plus it contains a multitude of undiscovered mineral salts that act together as an antiseptic. When these powerful mineral salts make contact with viruses such as Epstein-Barr, HHV-6, and shingles; bacteria such as Streptococcus; and other pathogens—troublemakers responsible for chronic illness—the salts begin to break down the pathogens’ cell membranes, eventually killing and destroying them. 

If you’re worried that the sodium in celery is a problem because you’ve heard that “salt is salt,” know that the sodium in celery is not just salt or the basic mineral sodium. Medical research and science have not yet discovered the different varieties of sodium in celery, nor how beneficial they are. Celery’s naturally occurring sodium actually helps stabilize blood pressure, bringing it down when it’s too high and up when it’s too low. Further, it won’t dehydrate your organs—instead, it clings to toxic, dangerous salts from poor-quality foods and helps draw them out of your body while replacing them with undiscovered cluster salts. 

These subgroups of sodium bond together as one and are infused with celery’s other critical chemical compounds and information that’s highly active in healing the body. Science has not yet deconstructed or studied these cluster salts. Eventually, research will reveal that these cluster salts work symbiotically and systematically to flush out toxins, dead pathogens such as viruses and bacteria, and pathogenic neurotoxins and debris from every crevice of the body. 

Neurotoxins, by the way, are created by viruses such as EBV feeding on toxic heavy metals, including mercury and aluminum. Medical science and research are not yet aware that viruses feed on certain fuel, let alone that they produce neurotoxins as waste. Neurotoxins create neurological symptoms, including burning skin, twitches, tremors, spasms, cold hands and feet, balance issues, vertigo, erratic heartbeat, insomnia, and body jerks, that confound doctors.

Now that you know that pathogens like EBV are responsible for chronic illness, you can understand just how critical the antiseptic function of celery’s cluster salts truly is. Your white blood cells use these cluster salts as both shield and weapon to go after viruses and unproductive bacteria—and that translates to relief from the numerous symptoms and conditions they cause. 


Mineral salts are critical for our bodies to function optimally. They keep your kidneys and adrenals functioning and raise your gut’s hydrochloric acid so your body can break down and assimilate what you eat—while they balance your pH as well as cleanse and repair your stomach, the rest of your digestive tract, and, most importantly, your liver. They also allow information to travel throughout your body so it can keep itself in balance no matter what’s occurring. 

The mineral salts specifically in celery are instrumental in the electricity that governs the body—they’re building blocks for neurotransmitter chemicals, they ignite electrical impulse activity, and they support neuron function. A brain with weak electrical impulses and weak neurotransmitters shuts down and goes into “low battery” mode—which makes celery juice, a battery charger for the brain, an answer to stop this from happening. Mineral salts keep the heart pumping and create the neurotransmitters needed to take information from point A to point B, that is, from neuron to neuron. (Picture a thought as a boat and mineral salts as the ocean: if the ocean dries up, the boat can’t go anywhere.)

That celery’s mineral salts are such an important support for the central nervous system means they are extremely healing for people who are struggling with depression, anxiety, brain fog, confusion, bipolar disorder, memory loss, Alzheimer’s disease, obsessive-compulsive disorder (OCD), attention-deficit/hyperactivity disorder (ADHD), and posttraumatic stress disorder (PTSD), as well as people who have difficulty with focus and concentration. 

Celery can really enhance the ability of supplemental GABA, glycine, and magnesium L-threonate to be absorbed by the brain and aid in neurotransmitter performance for sleep support. Celery also improves methylation, that is, the proper absorption and utilization of hundreds of nutrients, including B12 and zinc. 

The electrolytes in celery hydrate on a deep cellular level, lessening your chances of suffering from migraines, anxiety, panic attacks, and more. Celery also stabilizes and supports the adrenal glands, offers stress assistance, and repairs damaged cells inside the liver. 

And since celery’s mineral salts are antibacterial, they kill bacteria such as strep, and that encourages a healthy environment for “good” bacteria. Low-grade strep infections are often the actual cause of urinary tract infections (UTIs), chronic sinus infections, acne, IBS, and small intestinal bacterial overgrowth (SIBO), though at this time medical communities aren’t aware that strep infections are involved in these conditions. Now you know that celery juice and its antibacterial properties can help heal all of these conditions, too.

If you suffer from a thyroid condition, take note: celery has the ability to cleanse the thyroid of toxins and bolster production of the thyroid hormone T3. For more on the unknown true cause of thyroid problems like Hashimoto’s thyroiditis, Graves’ disease, thyroid nodules, cysts and tumors, enlarged thyroid, parathyroid disease, and much more, refer to Thyroid Healing.


Celery’s ability to break down and flush out viruses is life-changing news for anybody who has been told they have an autoimmune disease. Pathogens such as viruses, including EBV and shingles, are the true cause of the inflammation that’s mistakenly considered an autoimmune condition. Medical communities just aren’t aware of the real cause yet. 

The prevailing autoimmune theory is that the immune system is mistaking a part of the body for an invader and has begun attacking it, causing inflammation. This belief developed because by the 1950s, the medical world had become frustrated with not having an explanation for why conditions such as Hashimoto’s, Graves’, lupus, RA, Crohn’s disease, celiac, ulcerative colitis, and multiple sclerosis (MS) were leaving people ailing or even crippled. Close observation of some patients’ blood work revealed the presence of antibodies. A theory took off that the body had become confused and created antibodies to attack itself. It’s vital to remember that this was just one out of dozens of theories—it was never a definitive answer. The whole premise was an unproven hypothesis that the medical establishment came up with because they didn’t have the real answers for people’s suffering. So they pointed the blame at people’s bodies, which took the blame off of medical research and science, and unfortunately, the theory has stuck and become law. 

The autoimmune theory is not true. It’s critical to know what’s really happening with autoimmune issues: antibodies are present because your body is fighting a pathogen that scientific testing can’t detect yet. For example, in the case of Hashimoto’s, if antibodies are present, it’s because your body is going after the Epstein-Barr virus. It’s not that your body created antibodies that are attacking your thyroid gland. You can learn more about this in Thyroid Healing.

Again, contrary to current thinking, the body does not attack itself or turn against you. Your body only goes after pathogens, and only two factors cause inflammation: injury and invasion. Pathogens cause both. They’re invaders—foreign bodies in your body—and can also be injurers, sometimes damaging tissue in their travels through your system. (It doesn’t always take both factors to cause inflammation; for example, if you break your leg and it swells up, that’s solely an injury. It does always take at least one of these two causes.)

Sadly, the popular, incorrect autoimmune theory holds people responsible for their sickness. It leads people to believe that their body has betrayed them, turned against them, let them down. When you’re leaving the doctor’s office after being told that your body is attacking itself or attacking a specific organ, it can be emotionally damaging, and that belief itself hinders your immune system. Your body is loyal to you. It’s doing it’s very best to help you be whole and healed. It loves you unconditionally. Your own immune system will never harm you, it only works for you. Knowing this truth can kick-start the healing process for someone who previously believed their body was against them.

The autoimmune confusion is one of the greatest mistakes in modern medicine. It’s a prime example of why more than 250 million people in the U.S. alone are living with or suffering from mystery symptoms and conditions with no real relief. 

Which brings us back to why celery juice is such a big deal. As celery ushers pathogens out, your body will be much better able to handle whatever life throws your way. 


Why is it so beneficial that celery juice strengthens hydrochloric acid in your gut? Because hydrochloric acid is critical to digestion and to keeping your digestive system alkaline.

Although we can hear the word “acid” and think “bad,” gastric acids, including hydrochloric acid, are critical, helpful acids, not to be confused with having an acidic digestive system, which is detrimental to health. 

When you eat, food quickly travels down to your stomach to be digested with the help of hydrochloric acid. Although science hasn’t discovered this yet, hydrochloric acid isn’t just one acid—it’s actually a complex blend of seven acids. If hydrochloric acid levels are out of balance or low, your food won’t be sufficiently digested in your stomach. That means the food won’t break down enough for your cells to access the nutrients, and instead the food will just sit there and rot, causing bad acids to develop.


This gut rot, or putrefaction, creates ammonia gas, which has the ability to float, ghost-like, out of your digestive tract and directly into your bloodstream. It can also cross into organs such as your liver and brain. This is what I call ammonia permeability.

Millions of people walk around with digestive health problems, and one of the contributing factors is ammonia permeability, along with underlying sluggish liver issues. (The truth about ammonia permeability hasn’t yet been discovered. Similar though mistaken concepts are often referred to as “leaky gut syndrome” or “intestinal permeability.”) 

Another condition that worsens low hydrochloric acid and creates ammonia permeability is a sluggish, stagnant, fatty liver. Underlying liver conditions are extremely common. Medical communities don’t yet know how prevalent they really are or what’s behind these issues in the first place. A sluggish, stagnant, fatty liver causes lower bile production, which means the body can’t break down and disperse fats easily, and that also contributes to gut rot, causing even more ammonia permeability. It is vital to understand how to support your liver as almost everyone today has a sluggish liver which is at the core of countless symptoms, illnesses and premature aging and death. Thankfully, there are simple ways to support your liver’s health. I share these in detail in my book, Liver Rescue.

Here’s where our heroic celery juice comes in: It effectively rebuilds the stomach’s complex balance and supply of hydrochloric acid. It also strengthens the digestive system by helping to heal the liver, which leads to an increase in bile production, easing constipation and bloat. Plus by lowering levels of pathogens such as bacteria and viruses and invaders such as fungus and mold, it leads to strengthened intestinal linings. Celery juice is one of the most profound ways, if not the most profound way, to restore digestive health. It is that powerful. 


We tend to hold a lot of fear in our guts. Nervousness causes those sensations we know as tummy flips or butterflies in the stomach, and anxiety can run deep through the nervous system, putting our guts in knots. By restoring the entire digestive system, celery juice puts our minds and hearts at ease, too. Use it for its calming effects when you are feeling frightened, panicky, shocked, fretful, nervous, threatened, unsure, afraid, or defensive. 

I could go on and on about the benefits of celery juice for all manner of ills—mental, physical, spiritual, emotional. Celery juice is alkalizing, enzyme-rich, electrolyte-enhancing, liver-repairing, blood-sugar-balancing, antiseptic, and more. 

Don’t let the simplicity of humble celery mask it’s strength—it’s often the simplest of measures in life that gracefully work wonders in the most complex situations. Celery juice truly is a miracle juice. It’s one of the greatest healing tonics of all time.


If you want to heal and improve your health quickly and efficiently, follow this routine:

* Every morning, drink roughly 16 ounces of celery juice on an empty stomach. Make sure it’s fresh, plain celery juice with no other ingredients. Celery juice is a medicinal, not a caloric drink, so you’ll still need breakfast afterward to power you through the morning. Simply wait at least 15 minutes after drinking your celery juice before consuming anything else.

* If you’re sensitive and 16 ounces is too much, start with a smaller amount and work your way up.

* Use organic celery whenever possible. If you’re using conventional celery, be sure to wash it especially well before juicing. 

* If you find the taste of straight celery juice too strong, you can juice one cucumber and/or one apple with the celery. This is a great option as you get adjusted to the flavor. As you get used to it, keep increasing the ratio of celery; the greatest benefits come when celery juice is consumed on its own.


Plain, fresh celery juice is one of the most powerful healing juices available to us. This clean, green drink is the very best way to start your day. Make this juice a part of your daily routine, and soon you won’t want to go a day without it!

1 bunch celery

Rinse the celery and run it through a juicer. Drink immediately for best results.

Alternatively, you can chop the celery and blend it in a high-speed blender until smooth. Strain well and drink immediately.

I hope you will find a way to bring celery juice into your life soon—doing so will help bring you the healing you deserve. I wish you many blessings on your journey.  

Learn more about the miraculous healing powers of celery juice in the books Thyroid Healing & Liver Rescue 

5 Common Nutrient Deficiencies in Lyme Disease [Research Mirror]



People with chronic Lyme disease typically have multiple nutritional deficiencies. Replenishing the body’s stores of nutrients is essential for supporting the body during recovery, as the body relies upon these nutrients for proper functioning and to support the immune system as it is fighting Lyme.  In my 2012 book, Beyond Lyme Disease: Discovering the Underlying Causes of Chronic Illness in People with Borreliosis and Co-InfectionsI describe some of the most common nutritional deficiencies in people with Lyme and how to remedy those. While every person is unique and the nutrients that each person requires will vary from person to person, there are certain nutrients that doctors recommend almost universally for everyone. Following are five of the most important of these. (For more information on additional nutrients, I recommend reading Beyond Lyme Disease). 

·       Magnesium. Magnesium plays a role in over 300 enzymatic processes in the body. It is involved in energy production and transport, muscle contraction and relaxation, protein production, hormone regulation, and nerve conduction. It also plays an essential role in the maintenance and repair of all body cells.

It is readily depleted when the body is under stress and in chronic illness. Some researchers believe that Borrelia organisms and other microbes feed on and deplete magnesium. Many doctors believe that magnesium supplementation is therefore crucial for supporting the recovery process.

Magnesium is most effective when it’s taken via injection or intravenously; however, it is impractical for many people to do this, in which case transdermal magnesium crèmes and oils, or oral magnesium supplements, can be helpful for replenishing the body’s stores of this crucial nutrient. It’s important to choose a bioavailable form of magnesium that the body can readily use, such as magnesium citrate, malate or glycinate. Other forms have been shown to be less effective for people with Lyme. Ginger Savely, DNP, who has treated thousands of chronically ill Lyme patients, in Insights into Lyme Disease Treatment, recommends Peter Gilham’s Natural Calm products. Dosages may range from 350-1,000 mg daily, or more.

·       Vitamin D-3.  Most people in the United States are deficient in Vitamin D, and those with chronic Lyme disease perhaps even more so. Vitamin D comes from the sun but most of us don’t get enough sun nowadays and some people with Lyme have a genetic defect that prevents them from effectively synthesizing Vitamin D.

Yet Vitamin D plays a crucial role in many processes. It acts more like a hormone in the body rather than a vitamin, and plays a powerful role in immune system regulation and endocrine system health, including thyroid hormone utilization. Low levels of vitamin D-3 have been associated with high levels of inflammation in the body.  Vitamin D deficiency has also been linked to cancers of all kinds and given that some doctors believe that people with Lyme are more susceptible to cancer than the general population, Vitamin D-3 supplementation may be a good idea.

Most doctors recommend supplementation with anywhere from 5,000-20,000 IU daily, depending on their patients’ lab test results. Vitamin K is essential for proper utilization of Vitamin D in the body so choose a Vitamin D-3 product that also includes Vitamin K.

·       Zinc.  Lyme disease commonly causes zinc deficiencies. What’s more, many people with Lyme are deficient in zinc due to pyroluria, a condition in which the body fails to properly synthesize heme (a component of hemoglobin) and instead produces a heme byproduct, which binds with vitamins and minerals such as zinc and B-6 and excretes them from the body.

Zinc plays a vital role in immune function; white blood cells can’t function without it, so having a body depleted in zinc is like having white blood cells that have no ammunition to fight Lyme. Zinc also helps to prevent and combat heavy metal toxicity because it displaces metals in the body so that they can’t “lock on” to receptor sites on cells. Furthermore, zinc plays a role in neurotransmitter synthesis, particularly serotonin and GABA, as well as in the synthesis of the hormone melatonin. For this reason, zinc deficiency has been linked to depression and mental disorders of all kinds.

Zinc should be taken with food, as some people experience digestive upsets when they take it on an empty stomach. Effective doses depend upon many factors so always consult with your physician before taking zinc, especially since too high dosages can displace heavy metals in the body and cause symptoms of heavy metal toxicity.

·       Vitamin C.  As with the other nutrients described so far, people with Lyme disease tend to be universally deficient in Vitamin C. Some people with Lyme are so depleted in this vital nutrient that they may require dosages as high as 50-100 grams daily (note, this is grams, not milligrams).

The adrenal glands and brain utilize most of the body’s Vitamin C, and it may be the most important and abundant vitamin in the body for supporting immune function. In addition, the body uses it to make collagen and balance the pH; for detoxifying and repairing the body, supporting healthy gut bacteria production, destroying harmful bacteria and viruses, removing heavy metals and other environmental contaminants, and, as an antioxidant, neutralizing free radicals that result from inflammation.

Linus Pauling, a two-time Nobel Prize laureate, believed that everyone should take 10–20 grams (or 10,000–20,000 mg) of Vitamin C daily, just to maintain health. And it is not uncommon for people with Lyme to need at least 10-20 grams daily.

High-dose oral powdered formulas or liposomal products are an ideal way to get enough Vitamin C; the former because you can get concentrated doses of 4,000 mg (or 4 grams) per teaspoon; the latter because liposomal forms of Vitamin C are more readily absorbed by the body and so greater effects can be achieved with lower dosages. When choosing a Vitamin C product, it’s best to avoid GMO corn-derived Vitamin C (which is the most common type of Vitamin C in the United States) and to assess the bioavailability of different forms of vitamin C. For instance, ascorbyl palmitate is thought by some sources to be more effective in the body than ascorbic acid.

·       Probiotics.  The gut contains many hundreds of beneficial bacteria, many of which comprise an integral part of the immune system.  They defend the body against pathogens, which enter the body through air, food and water. In Lyme disease, the gut is commonly damaged and the beneficial bacteria depleted from Lyme infections, environmental pollutants and antibiotics.

Replenishing the bacteria is essential for helping to defend the body against infection; for food assimilation, and optimal gastrointestinal and brain health. However, not all probiotic products are created equal, so it’s essential to choose one that has a track record of success and which contains as many strains of beneficial bacteria as possible, especially L. acidophilus and bifidobacteria. L. acidophilus produces many compounds that inhibit the growth of nearly two dozen disease-causing pathogenic organisms. Bifidobacteria produces B-vitamins and eliminates many cancer-causing elements from the body.

Other strains of bacteria may also improve immune function, but L. acidophilus and bifidobacteria have been among the most widely studied for gut health. Many probiotic products contain strains of bacteria that have been destroyed by heat, so look for products that require refrigeration.

This list of nutrients is by no means exhaustive; it is not uncommon for people with Lyme to require other vitamins, minerals, essential fatty acids, amino acids and other nutrients, but these are among the most important and widely prescribed by doctors for their patients with Lyme disease. To determine what your body specifically needs, it’s best to work with your local doctor and do nutrient testing through a reputable lab like Spectra-Cell.Supporting your body’s nutrition is an important component to recovery from Lyme disease.

The Interplay between Magnesium and Testosterone in Modulating Physical Function in Men [Research Mirror]

Emboldened parts are important.



Marcello Maggio,1,2 Francesca De Vita,1 Fulvio Lauretani,1 Antonio Nouvenne,2 Tiziana Meschi,1,2 Andrea Ticinesi,1 Ligia J. Dominguez,3 Mario Barbagallo,3 Elisabetta Dall’Aglio,1,2 and Gian Paolo Ceda1,21Section of Geriatrics, Department of Clinical and Experimental Medicine, University of Parma, Via Gramsci 14, 43100 Parma, Italy
2Geriatric Rehabilitation Department, University-Hospital of Parma, Via Gramsci 14, 43100 Parma, Italy
3Department of Internal Medicine and Medical Specialties (DIMIS), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy

Received 24 November 2013; Revised 20 January 2014; Accepted 20 January 2014; Published 3 March 2014

Academic Editor: Lorenzo Maria Donini 

Copyright © 2014 Marcello Maggio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The role of nutritional status as key factor of successful aging is very well recognized. Among the different mechanisms by which nutrients may exert their beneficial effects is the modulation of the hormonal anabolic milieu, which is significantly reduced with aging. Undernutrition and anabolic hormonal deficiency frequently coexist in older individuals determining an increased risk of mobility impairment and other adverse outcomes. Mineral assessment has received attention as an important determinant of physical performance. In particular, there is evidence that magnesium exerts a positive influence on anabolic hormonal status, including Testosterone, in men. In this review we summarize data from observational and intervention studies about the role of magnesium in Testosterone bioactivity and the potential underlying mechanisms of this relationship in male subjects. If larger studies will confirm these pivotal data, the combination of hormonal and mineral replacements might be adopted to prevent or delay the onset of disability in the elderly.

1. Biological Role of Magnesium

Magnesium is an essential ion involved in multiple fundamental physiologic functions in humans [1]. As part of the activated MgATP complex, magnesium is involved in the pathways generating adenosine triphosphate (ATP) and energy in mitochondria, electron transport chain and complex subunits, and oxygen detoxification. Magnesium is also a cofactor in over 300 enzymatic reactions and biological processes, including protein and nucleic acid synthesis, and neuromuscular excitability [1].

Circulating magnesium exists in three forms. The metabolically active free ionized fraction (magnesium ion) is the most represented, accounting up to 60–70% of the total serum magnesium. Other main serum forms include the protein-bound (25% and 8% bound to albumin and globulin, resp.) and the chelated magnesium fraction (12%) [2].

The most represented reservoir of magnesium in human body is the mineral phase of the bone that accounts for about 64% of total magnesium. The remaining amount is located in the intracellular (34%) and extracellular spaces (1%). The intracellular magnesium concentration is fundamental to ensure the most important cellular and metabolic activities [3]. Indeed, the rapid requirements of this cation are usually met by intracellular stores that more quickly exchange magnesium with intracellular fluids.

Because of the lack of clinical tests available for assessing total-body magnesium content, the serum magnesium concentration remains the most clinically reliable test.

Adequate serum magnesium levels (normal ranges: 0.75–0.95 mmol/L or 1.7–2.5 mg/dL) seem to be critical in ensuring the normal cellular homeostasis [12]. Magnesium status is influenced by dietary intake, absorption in the gastrointestinal tract, renal excretion, and tissue uptake and utilization (e.g., cardiac and skeletal muscle tissue) [4]. To guarantee an optimal magnesium homeostasis the recommended intake from dietary sources is estimated in 420 and 320 mg/day for healthy men and women, respectively [5]. Food-rich magnesium sources are cereals, green leafy vegetables, seeds, nuts, cocoa, and seafood [6]. However, the definition of magnesium deficiency is notoriously complex. Magnesium serum concentrations below the laboratory reference range of <1.8 mg/dL are currently used to define some degree of magnesium depletion. However, this cut-off value could be not necessarily related to a pathophysiologic state of deficiency, because low intracellular magnesium has been documented even in patients with serum magnesium concentrations >1.8 mg/dL [7].

2. Magnesium and Muscle Function in Young Trained Individuals

Magnesium has been the most investigated mineral involved in muscle function. The beneficial effects of magnesium on skeletal muscle and physical performance are linked to its known actions on energetic metabolism (phosphorylation processes and reactions requiring ATP, energy utilization and transfer, and transmembrane transport) which have enormous implications in muscle contraction [1]. In fact, dietary magnesium deprivation is associated with increased oxygen requirements to complete submaximal exercise and reduced endurance performance [8].

Magnesium administration elicited the reductions in heart rate, ventilation, oxygen uptake, and carbon dioxide production during submaximal work [910]. In male athletes, 25 days of magnesium (390 mg/d), with a 3 wk washout, increased peak oxygen uptake and total work output during work capacity tests [11]. Similarly, in physically active collegians, magnesium supplementation significantly improved endurance performance and oxygen utilization [12]. In a depletion-repletion experiment in 10 postmenopausal women (aged 45–71), dietary magnesium (320 versus 180 mg/d) improved magnesium balance, erythrocyte and skeletal muscle magnesium concentrations, heart rate, and oxygen consumption during submaximal exercise [13].

It is not surprising that most of the current observational and intervention studies have been conducted on athlete subjects. In young men participating at 7-week strength training program, supplemental magnesium was capable of significantly improving muscle strength and power [14]. The gain in muscle strength occurred at dietary magnesium intake higher than 250 mg/d and was even more evident at 500 mg/d (exceeding the recommended dietary allowance, RDA) [14]. However, magnesium supplementation per se does not affect work performance in magnesium-replete trained individuals [15]. Dietary surveys reveal a magnesium intake equaling or exceeding the RDA for male athletes [16]. In female athletes it tends to be 60% to 65% of the current recommendation. Regardless of sex, athletes competing in sports requiring weight classifications or esthetic components tend to consume up to 30–55% of the magnesium RDA [17]. Serum magnesium levels may also be reduced during intense and/or long-term exercise [18] leading to latent fatigue and decreased endurance [19], similarly to what has been observed during the condition of zinc deficiency [20].

These lines of evidence led to consider magnesium as potentially limiting element for human physical performance, creating the rationale for the routine use of magnesium supplementation during intense endurance exercise.

3. Age-Related Changes in Magnesium Levels and Physical Performance

Suboptimal magnesium status is a frequent condition in older persons. The most common cause of magnesium deficit is the low dietary magnesium intake [21]. This is a well-represented phenomenon in older population, occurring in up to 10–15% of community-dwelling older subjects [22]. The typical western diet, highly rich in processed foods and deficient in green vegetables and whole grain, may also contribute to an inadequate magnesium intake.

The magnesium requirement for older population does not differ from young and adult subjects. However, data from the National Health and Nutrition Examination Survey (NHANES) III show an average daily magnesium intake dramatically below the recommended RDA, approximately of 225 mg/day in men and 166 mg/day in women [5].

A suboptimal magnesium status may also result from altered magnesium absorption and/or increased urinary loss [23]. Polypharmacotherapy (loop diuretics, digitals, and proton pump inhibitors) as well as a wide range of clinical conditions (HIV, type 2 diabetes, alcoholism, and cardiovascular diseases) plays additional important roles in lowering magnesium levels [2426].

However, the magnesium deficiency is more difficult to be detected in the elderly population. In fact the pauperization of intracellular stores is not usually accompanied by a parallel decline in magnesium serum concentrations that tend to remain more stable, within the normal range [27]. The deficiency of magnesium at cellular level and in the body stores is crucial for maintaining the skeletal muscle efficiency. It is very well known that sarcopenia (recently defined by consensus documents as the presence of both low muscle mass and low muscle function (strength or performance)) [2830] frequently leads to a condition of decreased physiological reserve, increased vulnerability to stressors, and adverse outcomes, known as “frailty” [31]. The frail status is a strong predictor of mortality, independent of traditional indicators of disease [32]. Despite the role of magnesium in muscle integrity and function, there are few data in this regard in the elderly. In a representative cohort of 1138 older men, Dominguez and colleagues [33] using data from the InCHIANTI Study showed a significant, independent, and strong positive relationship between circulating magnesium levels and measures of muscle performance (hand grip strength, lower-leg muscle power, knee extension torque, and ankle extension strength). These authors suggested the need of identifying serum magnesium cut-off values to attain the best possible physical function. These data suggest the potential contribution of low magnesium status, frequently observed in the elderly, to the reduced physical performance.

4. The Concept of Nutritional Modulation of Anabolic Hormonal Status in Older Men

In healthy adult subjects, changes in food consumption and utilization may induce homeostatic adaptations that redistribute nutrients without affecting muscle function and physical performance. During the aging process the body energy delivery system could be impaired because of the decline in physiological reserves and the disruption of metabolic pathways, and sarcopenia may arise. Physiological, psychological, and hormonal systems interact to determine the energy need. Macronutrients are essential to provide the body structure to perform work. Minerals are fundamental to enable the use of macronutrients for all physiological processes. In fact, an insufficient qualitative and quantitative nutrient intake is one of the multiple causes of loss of muscle mass, decreased physical performance, and adverse outcomes [34]. Anabolic hormones, whose levels decrease with age, play an important role in maintaining the optimal body energy delivery. In older persons, the occurrence of a single mild hormonal derangement is rarely observed. More frequently there is a simultaneous anabolic hormonal deficiency [Testosterone (T), Dehydroepiandrosterone (DHEA), estradiol (E2), growth hormone-Insulin-like Growth Factor-1 (GH-IGF-1), and vitamin D] which is part of “multiple hormonal dysregulation” [35]. These hormones interplay in ensuring overall anabolic state and induce the satellite cell activation together with exercise and muscle hypertrophy [35]. The simultaneous presence of low levels of Testosterone, together with DHEAS and IGF-1, has a strong effect on all-cause mortality in older men [36]. Experimental data confirm that hormonal therapies, singularly or in combination, may improve body composition and physical performance [3741]. The nutrients (especially the minerals magnesium, selenium, and zinc) and the anabolic hormones, especially T and IGF-1, seem to interact. The combination of nutritional and hormonal strategies in frail undernourished older people determines a more effective reduction in the number of hospitalizations, the time to hospital admission, and the days of hospital stay [4243]. The specific actions of both micronutrients and hormones at skeletal muscle level have led to the hypothesis of an interaction of these factors in ensuring optimal physical performance [44]. This novel concept could have important clinical implications in the elderly, who are more prone to a disruption of the anabolic/catabolic equilibrium and undernutrition. The use of specific mineral supplements may represent a sort of preventive measure of mobility impairment.

5. Changes in Testosterone Secretion with Age and Implications in Skeletal Muscle Function

Testosterone is the most important male sex steroid, synthesized by the Leydig cells of the testes (95%) and derived by peripheral adrenal androgens conversion for the remaining 5% [45].

In men, up to 44–65% of the circulating plasma T is bound to sex hormone binding globulin (SHBG) and 33–54% to albumin, and approximately 2-3% is available as a free form. The free fraction of circulating T plus albumin-bound T represents the amount of biologically active T (Bio-T) that more accurately reflects the clinical androgen state of the subject [46]. Total T levels progressively decrease from the age of 35, by 1% per year. The decline is more pronounced for Bio-T, 2% per year [45], especially in untreated depressed men [4748]. The causes of the age-related fall in total and Bio-T levels include a decrease in testicular function and a disruption of hypothalamic-pituitary axis. This peculiar phenomenon of the ageing process involves the GnRH secretion and activity (reduced amplitude of the peaks, attenuation of the circadian rhythm, and reduced sensitivity to negative feedback), the pituitary gland (reduced gonadotropin response to GnRH), and the Leydig cells (reduced response to human chorionic gonadotropin, HCG) [49].

Other mechanisms such as the increased SHBG levels and T aromatization (increased activity aromatase in adipose tissue) as well as the reduced bioconversion of T into dihydrotestosterone could also concur to impair T biological activity with age [5051]. Some authors hypothesize that the age-related decline in androgenic activity could be related to the reduced DHEA secretion, which is an important precursor of T [52]. Finally, qualitative changes in signaling transduction (reduced T receptors expression and/or impaired T binding capacity in the liver, brain, and prostate) should be also accounted for [5354].

The anabolic, anticatabolic, and neurotrophic effects of T administration on muscle are well known and extensively studied.

Observational studies on castrated animals [55] and adult men [5657] show that low T levels are associated with a reduction in lean body mass and muscle strength and other negative changes in body composition.

In a very recent cross-sectional analysis of 250 patients, 70 years or older, Ucak et al. [58] have found a negative impact of “compensated” or “subclinical” hypogonadism (defined as mild biochemical alterations accompanied by signs and symptoms of T deficiency) [59] on physical function, mood, cognitive, and nutritional status.

Intervention studies on elderly subjects have documented beneficial effects of T on counteracting the age-related changes of body composition and physical function [6062]. T exerts direct influence on lean body mass and strength [6364], whereas equivocal evidence is available on the effects of T on physical performance and quality of life [35].

The anabolic effects of T are even more evident in older subjects with mobility limitation.

In 209 community-dwelling men with low T levels (100 to 350 ng/dL [3.5 to 12.1 nmol/L]) from Testosterone in Older Men (TOM) with Mobility Limitations Trial, the daily T gel therapy for 6 months improved both leg-press and chest-press strength and stair-climbing power [65]. Testosterone may also influence muscle metabolism by improving haemoglobin levels in older men with mild anaemia [6667]. In women, skeletal muscle tissue seems to be sensitive to the anabolic action of androgens [68]. However, the impact of T administration on full physical function has not been fully studied. The precise molecular mechanisms underlying these observed physical changes in men are likely to include specific T effects on adipocytes and skeletal muscle cell receptors. The binding of T to its receptors could lead to the stimulation of lipolysis and protein synthesis [4169]. Finally, several lines of evidence support the hypothesis of permissive effects of T on the differentiation of the precursor stromal cells into muscular line [70].

6. The Interplay between Magnesium and Testosterone in Physical Function

The hypothesis of a link between magnesium and T has been tested in pivotal experiences using magnesium supplementation in adult subjects. Brilla and Conte investigated the combined role of magnesium supplementation and exercise on T levels [71]. A simple zinc-magnesium nutritional formulation (30 mg zinc monomethionine aspartate, 450 mg magnesium aspartate, and 10.5 mg of vitamin B-6) was able to improve T levels of athletes engaging in intense physical activity compared to placebo (132.1 to 176.3 pg/mL versus 141 to 126.6 pg/mL). The highest levels of T were found in those athletes both exercising and receiving magnesium supplementation. Moreover, significant differences in muscle strength via torque measurements and functional power were noted between the 2 groups (189.9 to 211 Nm at 180°/s and 316.5 to 373.7 Nm at 300°/s versus 204.2 to 209.1 Nm at 180°/s and 369.5 to 404.3 Nm at 300°/s). These data have been confirmed in a recent study performed on young subjects, where 4-week magnesium supplementation (magnesium sulfate 10 mg/kg/d) and exercise increase free and total T concentrations at exhaustion before and after supplementation compared to resting levels [7273]. There are limited data about the relationship between magnesium and T in study population, especially of older subjects. Maggio and colleagues [74] in 399 older men ≥ 65 years (mean age ± SD) from the InCHIANTI Study documented for the first time the strong and positive association between magnesium levels and total T and total IGF-1 levels. Interestingly, the relationship between magnesium and T was independent of body mass index, IL-6, DHEAS, SHBG, insulin, total IGF-1, grip strength, Parkinson’s disease, and chronic heart failure. Because of the cross-sectional nature of the study the authors could not establish a cause-effect relationship between magnesium and T levels. This finding led the authors to perform a pilot single-center, randomized, placebo-controlled, single-blind intervention study. 46 elderly hospitalized male subjects (21 in the treatment group), aged 65 years or older, with magnesium serum levels < 2.5 mg/dL, were randomly assigned to magnesium sulfate treatment (1 g/mL of ion Mg++ diluted in 250 cc of normal saline solution) or placebo (250 cc of saline solution) [75]. The active product or placebo was in a single intravenous dose administered in about 30 minutes. Testosterone, IGF-1, SHBG, and C-reactive protein (CRP) concentrations were evaluated before and after treatment. All measurements were performed at the Laboratory of the University-Hospital of Parma. Baseline characteristics between intervention and control groups were analyzed by -test. Paired -test was used to examine and to compare the response trends between the two groups at baseline and after treatment. As expected, magnesium sulfate administration induced a significant increase in serum magnesium levels (delta ) compared to placebo (delta ) (). Interestingly, total T levels remained substantially unchanged (delta ) in the intervention group while they were significantly decreased in the placebo group (delta ). The difference in total T levels between the 2 groups touched the statistical significance () (Figure 1). No differences were appreciated in bioavailable T (Bio-T), IGF-1, and SHBG concentrations. In this preliminary analysis no differences in CRP levels were observed between the two groups at baseline. The adjustment for CRP levels at baseline did not affect the relationship between magnesium and total T [75].

Interestingly, magnesium supplementation has been shown to have an apparent beneficial effect on male gonadal system, as observed in a very recent study performed on sexually mature male rats [76]. Chandra et al. evaluated the morphological, cytological, and functional changes in testis after magnesium administration. Interestingly, the authors showed significant enhancing in steroidogenic enzymes, namely, delta(5)3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase, activities at moderate and high dose of magnesium that resulted in increased serum T levels [76]. This phenomenon was followed by a progressive development in cytoarchitecture of genital organs without significant changes in quantitative spermatogenesis. The results were remarkably more evident in the groups treated for a longer period and at high doses of magnesium. In mice, dietary magnesium depletion seems to target apical cells within caput epididymis [77]. Moreover, in older male dromedary camel, the age-related decline in plasma T concentrations has been associated with a disruption of the mechanisms controlling normal cation distribution (including magnesium) in the testis, epididymis, and accessory glands [78].

7. The Role of Inflammation in the Interplay between Magnesium and Testosterone Levels

We can account for different factors influencing both T and magnesium concentration in adult and elderly men. Particular attention deserves the role of inflammation, which is a negative modulator of both these factors.

Inflammatory cytokines act as inhibitory factors at pituitary (on the secretion of LH) and testicular level (reduction of T secretion and sensitivity of T to LH) [79], contributing to the development of hypogonadism.

Higher levels of inflammatory markers and low T concentration are strong predictors of frailty, disability, and cardiovascular events [8081] that negatively influence the muscle mass [82].

In older men, there is a steeper decline of T levels during a proinflammatory postoperative status (also known as “acute postoperative frailty”) [83].

However, short-term T administration seems in turn to reduce systemic inflammatory cytokines including TNF-alpha, IL-6, and IL-1β [84] and to increase the anti-inflammatory cytokine IL-10 [85]. In a similar manner, magnesium seems to be fundamental in maintaining the threshold of antioxidant capacity and the control of oxidative stress [1]. Moreover, there is evidence of impaired overall antioxidant capacity and low-grade inflammation in magnesium-deficient cultured human and animals cells [86]. Inadequate intracellular magnesium may reduce the mitochondrial efficiency and increase the production of reactive oxygen species (ROS), determining structural and functional impairment of proteins [87] and DNA [88]. Interestingly, magnesium and T were found to be lower during systemic inflammation, and conditions associated with both increased ROS, oxygen-derived free radicals, oxygen peroxide production, and impaired antioxidant enzyme expression and activity [8990].

Multiple changes in physiological pathways could be identified as pathogenic factors in several age-related phenomena including sarcopenia, frailty, disability, or altered immune response and chronic diseases. Therefore, during the aging process, where lower anabolic hormones, increased proinflammatory cytokines, and impaired nutritional status frequently coexist, combined strategies could have important clinical implications [91] (Figure 2).

8. Biomolecular Mechanisms Underlying the Relationship between Magnesium and Testosterone

In the recent years biomolecular interactions between T, SHBG, and magnesium have been studied by high performance liquid chromatography (HPLC) [92]. Excoffon and colleagues [92] provided evidence of a magnesium-mediated variation in the T-SHBG affinity. The change in magnesium levels inside the biological serum concentration range (0.75–0.95 mM) could lead to an enhancement of the Bio-T. In fact, the affinity of T to SHBG seems to change slightly with the magnesium concentration. Magnesium binds SHBG in a nonspecific mode, leading to an uncompetitive inhibition with T in binding SHBG and to a subsequent enhancement of Bio-T availability. The binding is accompanied by a magnesium release (or uptake) with a corresponding heat effect around in magnitude 17 kJ/mol [92].

SHBG is a homodimer comprising 373 amino acid residues for each monomer that transports the sex steroids in the blood and also regulating their activity in target cells [93]. Interestingly, each monomer of SHBG contains three metal-binding sites, one calcium-binding and two zinc-binding, [9495], that are divalent cations as well as magnesium. This data supports, at molecular level, the role of magnesium in modulating T bioactivity.

Guillaume’s group investigated the role of magnesium on both the T-serum albumin binding process and the T displacement to its human serum albumin (HSA) binding cavity by DHEA. Serum albumin binds to T with low affinity [46]. In particular DHEA and T seem to bind to the same HSA site. DHEA has been shown to displace T to its HSA binding site. The authors observed in vitrothat adequate magnesium concentrations displaced T from its HSA binding site [9697] and hypothesized the opportunity of testing in vivo the effects of magnesium supplementation, during DHEA treatment, on the Bio-T rate.

9. Conclusions

The ageing process seems to be at least partly due to the defect of anabolic hormones, low-grade inflammation, reduced physical activity, and a poor quality of nutrition.The permissive role that several micronutrients, such as magnesium, might exert on the serum concentration and the biological activity of T could be of undoubted interest for future clinical approaches. Male individuals with impaired magnesium status and T deficiency (accurately assessed) could benefit from magnesium and/or T treatment targeting physical performance. Future randomized clinical trials adopting synergistic treatments could lead to improving the effectiveness of T treatment, in preventing mobility limitation and adverse outcomes in older men.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.


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Increasing Evidence Points to Inflammation as Source of Nervous System Manifestations of Lyme Disease [Research Mirror]


About 15% of patients with Lyme disease develop peripheral and central nervous system involvement, often accompanied by debilitating and painful symptoms. New research indicates that inflammation plays a causal role in the array of neurologic changes associated with Lyme disease, according to a study published in TheAmerican Journal of Pathology. The investigators at the Tulane National Primate Research Center and Louisiana State University Health Sciences Center also showed that the anti-inflammatory drug dexamethasone prevents many of these reactions.

“These results suggest that inflammation has a causal role in the pathogenesis of acute Lyme neuroborreliosis,” explained Mario T. Philipp, PhD, Professor of Microbiology and Immunology and chair of the Division of Bacteriology and Parasitology at Tulane National Primate Research Center (Covington, LA).

Lyme disease in humans results from the bite of a tick infected with the spirochete Borrelia burgdorferi (Bb). As Bb disseminates throughout the body, it can cause arthritis, carditis, and neurologic deficits. When the nervous system is involved, it is called Lyme neuroborreliosis (LNB). Clinical symptoms of LNB of the peripheral nervous system may include facial nerve palsy, neurogenic pain radiating along the back into the legs and feet, limb pain, sensory loss, or muscle weakness. Central nervous system involvement can manifest as headache, fatigue, memory loss, learning disability, depression, meningitis, and encephalopathy.

To understand further the neuropathologic effects of Bb infection, researchers infected 12 rhesus macaques with live B. burgdorferi; two animals were left uninfected as controls. Of the 12 Bb-inoculated animals, four were treated with the anti-inflammatory steroid dexamethasone, four with the non-steroidal anti-inflammatory drug (NSAID) meloxicam, and four remained untreated. Half of each group was studied for eight weeks postinoculation and the other half for 14 weeks.

The researchers examined the role of inflammation in the nervous systems of Bb-infected animals. Significantly elevated levels of the inflammatory mediators interleukin-6 (IL-6), IL-8, CCL2, and CXCL13 were observed, as well as pleocytosis (increased cell counts, primarily white blood cells) in the cerebrospinal fluid of all infected animals – except in those treated with dexamethasone.  “Chemokines such as IL-8 and CCL2 are known to mediate the influx of immune cells in the central nervous system compartment during bacterial meningitis, and CXCL13 is the major determinant of B cell recruitment into the cerebrospinal fluid during neuroinflammation,” explained Dr. Philipp.

Infection with Bb led to many histopathologic findings in infected animals not treated with dexamethasone, such as leptomeningitis, vasculitis, focal inflammation in the brain and spinal cord, and necrotizing focal neurodegeneration and demyelination in the cervical spinal cord. Evaluation of the dorsal root ganglia showed inflammation with neurodegeneration, along with significant apoptosis of neuronal and satellite glial cells (which surround sensory neurons), in all infected animals with the exception of those treated with dexamethasone. Researchers were able to quantify the protective effect of dexamethasone treatment in protecting both satellite glial cell and neuronal apoptosis; in contrast, meloxicam treatment was only effective in protecting against satellite glial cell apoptosis and only after prolonged administration. 

The dorsal roots of animals infected with live Bb (but not treated with dexamethasone) showed the presence of abundant lymphocytes and monocytes.  Interestingly, reactions near the injection sites were histologically different from the more diffuse inflammation found along the spinal cord. The pathology found in the dorsal root ganglia and sensory nerves may explain the localized pain and motor deficits that Lyme disease patients experience close to the origin of the tick bite.

Some patients with Lyme disease also show evidence of demyelinating neuropathy and slowing nerve conduction. Nerve conduction studies in motor and sensory nerves of the macaques showed that the Bb infection resulted in specific electrophysiological abnormalities (increased F wave latencies and chronodispersion) that could be prevented with dexamethasone.

Although antibiotics are the standard and necessary first-line treatment for Lyme disease, the results show the potential therapeutic impact of anti-inflammatory or immune-modulatory agents for Lyme-related neuroborreliosis. Most of the neuropathological changes produced by Bb infection were prevented by dexamethasone, a broad-spectrum steroidal anti-inflammatory drug, whereas the non-steroidal anti-inflammatory drug meloxicam was generally ineffective or only partially effective. Analyses of the differences in the mechanisms of action of both drugs may provide a blueprint for the development of new adjuvant treatments for LNB.

“Importantly, we found necrotizing myelitis and degeneration in the spinal cord, neurodegeneration in the dorsal root ganglia, and demyelination in the nerve roots only when lymphocytic inflammatory lesions were also observed in both the central nervous system and peripheral nervous system,” stated Dr. Philipp. “Our results suggest that ongoing cytokine activation in the nervous system can contribute to the persistent symptoms of fatigue, pain, and cognitive dysfunction that patients sometimes experience despite having been treated for Lyme disease.”

ALA, ALCAR, & NAC – A Key Triad of Mitochondrial Support Nutrients [Research Mirror]


Since the early 1970`s, scientists have postulated that a lifetime of exposure to toxic chemicals, poor diet, and harsh pharmaceutical medications leads to increased free radicals, decreased cellular energy production and chronic disease. Excess accumulation of free radicals causes changes in mitochondrial structure and function that we now know leads to a variety of medical conditions (fibromyalgia, chronic fatigue syndrome (CFS), diabetes, Alzheimer’s disease, coronary artery disease, and Parkinson’s disease). This progression is frequently referred to as the “Mitochondrial Theory of Ageing and Disease”.

Scientific support for the use of micronutrient-based mitochondrial support as a means of protecting cells from progressive oxidative damage is accumulating. Such therapies are intended to scavenge for toxic free radicals and aid critical enzyme reactions in performing their important functions.

Studies have shown that patients suffering with chronic fatigue caused by mitochondrial dysfunction have improved with supplementation of mitochondrial nutrients and antioxidants, including acetyl-L carnitine, alpha-lipoic acid, and N-acetyl cysteine (NAC). This triad has been shown to reduce damage to mitochondrial membranes, restore mitochondrial energy production, protect cellular structures from oxidative damage, and decrease fatigue.

The Key Triad

Acetyl-L Carnitine (ALCAR)

Acetyl-L-carnitine is an amino acid, which plays a critical role in energy production by transporting long-chain fatty acids into the mitochondria so they can be metabolized to produce energy. This key amino acid also transports toxic compounds out of this cellular organelle to prevent their accumulation. ALCAR is commonly supplemented in combination with other vitamins and cofactors.

Research in aged rats has found that supplementation with high doses of acetyl-L-carnitine and alpha-lipoic acid (an antioxidant) improved oxidative stress levels, restored mitochondrial functioning, lowered neuron RNA oxidation, and increased rat ambulatory activity and cognition (as assayed with the Skinner box and Morris water maze).

A meta-analysis of double-blind, placebo-controlled studies suggests that supplements of acetyl-L-carnitine may improve mental function and reduce deterioration in older adults with mild cognitive impairment and Alzheimer’s disease. Additionally, acetyl L-carnitine has been shown in studies to improve memory and brain function in people who are suffering from type 2 diabetes

Alpha-Lipoic Acid (ALA)

Alpha-lipoic acid acts as an enzymatic “cofactor” and is essential for healthy mitochondrial function. First, alpha-lipoic acid helps support  enzymes that are vital for transforming foods in the form of sugars, proteins, and fats into usable cellular energy (ATP). Second, as a potent antioxidant, ALA scavenges free radicals and peroxides that cause widespread oxidative stress and cellular damage. Finally, alpha-lipoic acid blocks inflammatory signals and boosts levels of pro-oxidant destroying molecules.

Studies have shown that ALA supplementation improves energy expenditure in aged mice. Researchers examined aging mice that were broken into two groups: one supplemented with alpha-lipoic acid and the other served as a control group for a period of 30 days. Both groups were tested for metabolic functions relating to glucose metabolism, energy production and antioxidant status. Results showed that the alpha-lipoic acid supplemented group experienced mitochondrial biogenesis, a process that replaces damaged and aging mitochondria.

N-acetyl cysteine (NAC)

N-acetyl cysteine (NAC) replenishes intracellular levels of the natural antioxidant glutathione (GSH) that is often deficient in ageing individuals and those with chronic illness. This critically important precursor to glutathione synthesis also helps restore cells’ ability to fight free radical damage and protect mitochondrial proteins.

NAC has also been in clinical use for the treatment of acetaminophen (Tylenol©) overdose and liver failure for many years.

Broad-Spectrum Supplementation

Mitochondrial enzymatic reactions require a wide range of vitamins and mineral cofactors to function. Therefore, when attempting to support mitochondrial health and energy production, all micronutrients required for increased mitochondrial metabolism may need to be supplemented in a broad-based fashion to achieve optimal results. In addition to taking a high-potency multivitamin, the addition of therapeutic dosages of this key triad – NAC, alpha lipoic acid and acetyl-L-carnitine – have solid research supporting their use as part of an effective mitochondrial support supplement program.

Top 18 Proven Heavy Metals Detoxes For Safe Chelation [Research Mirror]


How to Safely Chelate and Detoxify Heavy Metals

The overall goal in chelating and detoxifying heavy metals is to bind them with a strong chelator and then excrete them safely out of the body without redistributing them to other organs.

1) Supplement with Essential Minerals

During this process, supplementation with zinccalciumiron, and magnesiumis recommended, as these nutrients reduce the absorption of toxic heavy metals and their depletion results in enhanced toxic metal uptake from the gut [RRRR].

2) Remove Sources of Heavy Metal Exposure

The first step in reducing the body burden of heavy metals is to reduce or remove the source of exposure, if possible. This may mean reducing consumption of high mercury seafood, testing and filtering drinking water, or quitting smoking.

3) Ensure that Excretory Organs Function Correctly

If you will use chelation to remove toxic heavy metals, it is important to ensure that your excretory pathways are open and not overburdened in order to allow the metals to pass out safely. Constipation, leaky gut, or kidney and liver diseases will prevent metals  [R].

4) Bind (Chelate) Heavy Metals

The next step is to bind heavy metals where they are stored in the body, escort them into the bloodstream, and excrete them through the liver via bile in the feces, through the kidneys via urine, or through the skin via sweat [R].

5) Detoxify Slowly or Pulse the Chelation Process

It is important to detoxify from heavy metals slowly to prevent redistribution through the body and therefore it is recommended to temporarily discontinue or lower dosages of chelating compounds if symptoms worsen and allow the body’s detoxification and excretory systems to “catch up” [R].

Moreover, it is generally advised to pulse the chelation process and to work with a qualified physician during this time.

Supplements that Help with Heavy Metal Chelation and Detoxification

1) Glutathione Protects Against Mercury Toxicity

Glutathione is a powerful antioxidant that is produced from three amino acids: cysteine, glutamic acid (closely related, but not to be confused with glutamine), and glycine.

Glutathione contains sulfur components that readily bind with mercury, lead, and cadmium [R].

Other compounds that have thiol groups include the amino acid cysteine, albumin, and metallothioneins. Mercury has a high affinity for thiol groups and will readily bind to the thiol-containing compound (usually glutathione) in the highest concentration [R].

Higher levels of glutathione protect against mercury accumulation [R].

Mercury has been shown to deplete glutathione levels in brain cells, red blood cells, and kidneys [RRR].

Glutathione protects against mercury in 4 ways:

  1. Binding to it and preventing it from causing damage to enzymes and cells [R]

  2. Preventing the mercury from entering the cell where it does the most damage [R]

  3. Helping transport and eliminate it from the body [R]. Indeed, glutathione mercury complexes are the most abundant form of mercury in both bile and urine [R].

  4. Serving as an antioxidant that neutralizes the free radicals such as hydrogen peroxideand lipid peroxides that are produced by mercury [R].

You can learn how to increase your glutathione levels in this post.

2) Alpha-Lipoic Acid Protects Against Arsenic, Cadmium, and Mercury Toxicity

Alpha-lipoic acid (ALA) is another strong antioxidant with the ability to penetrate the cell membrane as well as cross the blood-brain barrier to chelate heavy metals stored there [RR].

This is important as lead and mercury easily accumulate in the brain [RR].

Alpha-lipoic acid decreases damage to cell membranes (lipid peroxidation), which can be caused by heavy metals [R].

Alpha-lipoic acid has also been shown to increase glutathione levels both inside and outside of the cell by regenerating used glutathione to make it active again [RR].

Additionally, alpha-lipoic acid increases the production of glutathione by increasing the uptake of cysteine, the rate-limiting component of glutathione, into the cell [R].

Although no clinical trials have investigated the use of alpha-lipoic acid in chelating heavy metals, animal studies show that the compound reduces uptake of cadmium into liver cells and prevents absorption of arsenic in the intestines [RR]

Of note, animal studies have also shown that alpha-lipoic acid has the potential to redistribute heavy metals, however, these studies have administered the compound intravenously, which may cause alpha-lipoic acid to combine with glutathione in the liver and prevent the glutathione from carrying heavy metals out of the body [R].

This effect has not been seen in human trials with alpha-lipoic acid and the vast amount of evidence strongly suggest that it can prevent the damage caused by heavy metals as well as help glutathione bind to and excrete metals [RR, ].

Oral doses of as much as 1,800 mg/day of alpha-lipoic acid are well-tolerated with no side effects in clinical trials [R].

3) Modified Citrus Pectin Increases Lead, Cadmium, and Arsenic Excretion

Pectin is a fiber in plants. Modified citrus pectin (MCP) is a form of pectin that has been altered to be more digestible.

In children with high blood levels of lead, 15 grams of MCP a day for 28 days decreased lead in the blood, while urine lead levels increased by more than 132% (indicating lead removal) [R]. No side effects were reported.

Another study found that 15 grams of modified citrus pectin a day for five days increased urinary excretion of arsenic (130%), cadmium (150%), and lead (560%) [R].

Note: the studies were performed by the creator of MCP.

4) Sauna/Sweating Increases Arsenic, Cadmium, Lead, and Mercury Excretion

Sauna use increases the circulation throughout the skin and induces sweating, with blood flow to the skin increasing from 5-10% of the amount of the blood pumped through the heart at rest to 60-70% [R].

Sweating, caused by either exercise or sauna use, has been shown in many studies to excrete clinically meaningful levels of arsenic, cadmium, lead, and mercury, in some cases surpassing the amount excreted in urine [RRRR].

Beneficial metals, vitamins, and electrolytes, such as zinc, coppermanganesevitamin E, sodium, and chloride, are also lost during sweating. Therefore, it is crucial to consume a diet sufficient in these nutrients to counteract any loss due to sweating.

5) Vitamin C Protects Against Lead Toxicity

Low vitamin C levels have been associated with decreased glutathione levels and increased oxidative stress [R].

Vitamin C increases glutathione levels by recycling used glutathione, as in human red blood cells (DB-RCT) [R].

In rats, vitamin C supplementation increases lead excretion in the urine and feces and prevent lead absorption in the intestine [R].

Lead toxicity can lead to damage to the membranes of red blood cells, impairing their function. In 15 workers exposed to lead, one year of vitamin C (1 g/day) and E supplementation (400 IU/day) reduced lipid peroxidation in red blood cells between 47.1% and 69.4%, comparable to 19 non-lead exposed workers [R].

Dosages between 500-1500 grams a day are often used in clinical research settings, however many users greatly exceed these levels, with few adverse effects beyond diarrhea.

6) Selenium Increases Mercury Excretion

Selenium is a crucial nutrient when it comes to chelating heavy metals.

The mineral increases the activity of glutathione, and increased levels of selenium are associated with increased levels of glutathione in the blood [RR].

In rats exposed to mercury, selenium prevented the destruction of neurons and suppression of protein synthesis caused by mercury and helped repair damaged tissue that helps conduct nerve signals (myelin sheath) [R].

In 103 mercury-exposed villagers in China, 100 micrograms of selenium daily in the form of enriched yeast increased mercury excretion and as well decreased markers of inflammation and oxidative stress compared to controls who were given the yeast without selenium [R].

Brazil nuts are often mentioned as important food to chelate heavy metals. Any chelating effect is likely due to its high concentration of selenium, with one nut containing 68-91 mcg of selenium.

7) N-Acetylcysteine Reduces Mercury and Lead Levels

N-Acetylcysteine (NAC) is a form of cysteine that increases the production of glutathione.

In mice, N-Acetylcysteine enhanced excretion of mercury by 400% in comparison to control animals [R].

In 171 workers exposed to lead, N-Acetylcysteine reduced blood levels of lead and increased glutathione concentrations, while at the same time decreasing oxidative stress [R].

8) Zinc Prevents Cadmium and Lead Absorption and Increases Cadmium Excretion

Zinc competes with cadmium and lead for the binding sites on proteins, and zinc deficiency can lead to greater absorption of cadmium and lead [RR].

Zinc supplementation also increases synthesis of metallothionein, a protein that binds cadmium and helps detoxify it from the body [RR].

Moreover, supplementation with zinc protects the activity of an enzyme called δ-aminolevulinic acid dehydratase (ALAD) that is very sensitive to lead [R].

9) Calcium Disodium EDTA Increases Lead Excretion

Calcium Disodium EDTA (CaNA2EDTA) is effective in chelating lead from the body [R]. Because it is poorly absorbed orally, EDTA must be administered intravenously.

Caution is needed when chelating with CaNA2EDTA as it tends to deplete essential minerals, particularly zinc, copper, and manganese [R]. It should not be used during pregnancy or in people with kidney or liver diseases [R]

10) DMSA Increases Lead, Mercury, Arsenic and Cadmium Excretion

Dimercaptosuccinic acid (DMSA) is a water-soluble pharmaceutical chelator that contains two thiol groups, making it an especially strong chelator of heavy metals.

It can be administered orally, intravenously, or through the skin.

Chelation therapy is the use of intravenous pharmaceutical chelation agents such as DMSA, dimercaptopropane sulfonate (DMPS), or ethylenediaminetetraacetic acid (EDTA) to pull heavy metals out of the blood in cases of acute toxicity [R].

Chelation therapy is also used to treat cardiovascular disease, but a systematic review found that evidence does not support its use for such diseases [R].

Oral supplementation with DMSA has been shown in many studies to significantly and greatly increase urinary excretion of lead, mercury, arsenic, and cadmium [RRRR].

In 17 lead-poisoned adults, DMSA increased urinary lead excretion by a factor of 12 and rapidly reversed symptoms related to lead toxicity [R].

Caution is warranted with DMSA, as it has also been shown to excrete beneficial metals like zinc, iron, calcium, copper, and magnesium as well, so it strongly advised to supplement with these after therapy [R].

11) DMPS Increases Lead, Mercury, Arsenic, and Cadmium Excretion

Dimercaptopropane sulfonate (DMPS) is another pharmaceutical chelator, like DMSA, with two thiol groups.

Oral absorption of DMPS is about 40% higher than that of DMSA [R].

Like DMSA, DMPS increases excretion of arsenic, cadmium, lead, and mercury in the urine, with the former more effective in excreting mercury from the brain and the latter more effective in excreting mercury from the kidney [RRRR].

In mice, DMSA was more effective in removing cadmium than DMPS [R].

Also like DMSA, DMPS increase urinary excretion of necessary nutrients like copper, selenium, zinc, and magnesium, necessitating supplementation with them before or after treatment [R].

In one trial with autistic patients, a few children developed worsening of symptoms [R]. The researchers thought that this was likely due to the redistribution of recently mobilized metals without the ability to excrete them sufficiently [R].

In addition, adequate hydration and bowel regularity are essential, as during chelation therapy, mobilization and chelation of metals should not exceed the ability to excrete them, otherwise they will be redistributed throughout the body where they have the potential to cause more harm than their initial storage site.

Chelating Compounds With Non-Human Evidence

12) Garlic

Garlic has been shown to protect against the damaging effects of heavy metals and help with their excretion.

When rats were given garlic at the same time as cadmium and mercury, accumulation of the heavy metals in the liver, kidneys, bone, and testes was decreased and the activity of certain key enzymes was partially restored [R]. In addition, cadmium excretion was increased.

In rats given mercury, cadmium, and lead in addition to 7% raw garlic in their food, accumulation of the heavy metals was decreased in the liver, with the greatest effect seen for cadmium [R].

13) Chlorella

In mice, diets consisting of 5% and 10% of Chlorella significantly increased urinary and fecal excretion of mercury, and decreased mercury levels in the brain and kidneys, without affecting glutathione levels [R].

14) Cilantro

In mice, cilantro supplementation alongside lead administration resulted in significantly fewer lead deposits in the bones [R].

In humans, a study (RCT) on 32 children aged 3-7 years with lead-exposed parents found that cilantro extract given for 14 days decreased lead concentration in blood while increased its excretion in urine. However, it didn’t increase significantly more than the placebo group [R].

15) Activated Charcoal

While there are studies showing activated charcoal’s ability to bind mercury, lead, and nickel in industrial waste, no studies that have measured its chelation abilities in the human body [R].

16) Methionine

Methionine may help with chelating metals because of its sulfur group.

When methionine was added to the diet of rats, it significantly increased fecal excretion of lead [R].

17) Taurine

Taurine is a sulfur-containing compound.

When taurine was given to mice, it protected against oxidative damage in the brain caused by cadmium and improved the antioxidant status in the animals [R].

Another study in rats found that taurine supplementation prevented damage of brain tissue due to arsenic [R].

Taurine has also been shown to protect against lead toxicity in rat ovaries and mercury toxicity in the hearts and livers of rats, without affecting excretion of either metal [RRR].

18) Carnosine

Carnosine is a molecule made of the amino acids beta-alanine and histidine with strong antioxidant properties [R].

Carnosine is able to chelate cadmium and mercury and prevent heavy metals from harming cell membranes [R].

In rats, carnosine supplementation was able to prevent kidney damage from lead and increased glutathione levels [R].

Other Supplements That May Be Effective:

Experiences of People who Removed Heavy Metals from their Bodies

Many users have reported that N-Acetylcysteine supplementation improves symptoms of depression, reduces brain fog, and provides a slight energy boost. I supplement with N-Acetylcysteine regularly, but I do not exceed 1 g/day as I tend to experience gastrointestinal discomfort and headaches beyond this dosage, which I suspect are due to increased mobilization of metals exceeding my ability to excrete them.

Users report mixed results when supplementing with alpha-lipoic acid, with some noting increased energy and feelings of general well-being and reduction in nerve pain, while others report an increase in fatigue and mental fogginess, to which some attribute to redistribution of mercury.

One individual claimed to have removed heavy metals by taking 1 g/day of DMSA (in addition to N-Acetylcysteine and alpha-lipoic acid) for 3 days every 2 weeks, which eliminated chronic Candida infections and persistent anxietyand brain fog. Another DMSA user noted that just 50 mg of DMSA resulted in psychosis lasting for a month.

Info on Systemic Enzymes [Research Mirror]


Systemic Enzymes – What are They?

When we hear the word enzymes we normally think of digestive enzymes, and while they are crucial for breaking down our food, they are not “systemic,” but are in fact utilized in the GI tract. For some people adding digestive enzymes makes all the difference in their health. If you suffer from GERD, for instance, adding digestive enzymes will revolutionize your health. Food enzymes are found in raw food. And by raw food, I mean uncooked. Systemic enzymes, on the other hand, are used all over the body and have been found to help many disease processes, and in fact, can be downright miraculous.

http://www.globalhealingcenter.com/natural-health/difference-systemic-enzymes-digestive-enzymes/  Enzymes are proteins used by every cell in the body that help chemical reactions within our body. We produce these enzymes but as we age, they decline like everything else.  If you think about it, this means every chemical reaction in our body is affected. These systemic enzymes help break down mucus, fibrin, toxins including viruses, allergens, and clotting factors. These are key areas to address for MSIDS (multi systemic infectious disease syndrome) patients. Unlike NSAIDS, enzymes do not hurt the liver and they also help white blood cell efficiency. And get this – they help manage yeast overgrowth. They also help you absorb vital nutrients and improve your performance.

http://www.newswithviews.com/Howenstine/james174.htm   According to Dr. Howenstine, enzymes cannot be patented, which means mainstream medicine doesn’t promote their usage. In Europe, large doses of enzymes are used in cancer therapy.They have an enteric coating so they are not dissolved in the stomach, making them able to get into the blood without being destroyed. Systemic enzymes are also able to remove the thick layer of fibrin around cancer cells. The thick fibrin cloaks malignant cells so they are able to get by the killer immune cells. Enzymes remove this coating as well as stimulate immune cells to increase more tumor necrosis factor to attack tumors and viruses. Dr. Wyba states that one-third of pancreatic cancer cases have been cured using Wobenzyme a specific patented systemic enzyme. The patient takes up to 30 pills three times a day for life or the cancer returns.

Many MSIDS patients suffer with hyper coagulation, or thick blood, often due to infection. There are numerous factors for this but one is high levels of parasites in the blood and biofilms. Systemic enzymes dissolve blood clots and therefore lessen coagulation. The only contraindication is for those with hemophilia and those on anticoagulant drugs as they may have thinner blood with enzyme therapy. Make sure to work with your health care professional if you have either of these issues as extra precautions will need to be taken.

Regarding viruses, enzymes eat the exterior coating, rendering the virus permanently incapacitated. You have to take enough to get ahead of rapid viral replication, requiring 5-10 capsules three times a day or more. It was also discovered that those with prosthetics often need these parts replaced as bacteria are able to prevent antibiotics from killing infection due to biofilm formation. MSIDS patients have the same problem.The enzyme serrapeptase enhanced Ofloxin in cultures by preventing biofilms. Systemic enzymes could be the magic bullet to help break down biofilms in MSIDS patients.  Regarding allergens, a low dose of 2-3 caps a day should prevent asthma attacks – if taken as maintenance. Enzymes thin and decrease secretions as well as alleviate symptoms of hay fever and other allergies.

Regarding pain, enzymes have helped headaches, arthritis, bursitis, and synovitis – all symptoms that are frequent with MSIDS. It is also a promising therapy for sarcoidosis. Safer than cortisone, regular enzymes will reduce fibrosis.

The truly miraculous effects of systemic enzymes is their ability to remove necrotic(dead cells) debrisreduce inflammation, balance the immune system, and remove viruses and toxins, all issues faced by the MSIDS patient.

http://www.newswithviews.com/Howenstine/james175.htm   He also states they can benefit fibromyalgia patients. Mycoplasma, anaerobic bacteria, fungi, and borrelia have all been found in FM patients with high-resolution microscopy. Several FM patients have recovered by taking nattokinase – another enzyme that lessens fibrin production, improving blood circulation. Kidney diseases can be helped by systemic enzymes by their ability to lower swelling, inflammation, scarring (fibrosis), and immune complexes. Other conditions such as fibrocystic breasts, uterine fibroids, endometriosis, PCOS, benign prostatis hypertrophy, breast, prostate, and uterine cancers, are all estrogen excess states, producing fibrosis – which for those having these conditions correctly equate with PAIN. Endometriosis may require five or more caps three times a day until pain disappears. Fibrocystic breast disease patients should stay on enough enzymes to prevent symptoms. Taking systemic enzymes after surgery or injuries prevents excessive scar formation. All of these conditions can be helped with systemic enzymes.

**Please read Dr. Howensteine’s article in the link above if you suffer with any of these estrogen dominant diseases as he discusses in far more detail the interaction of various hormones and why these disease states are becoming more prevalent. I feel there is a desperate need for this information as this issue is far more common than not. Also, for more information regarding the use of bioidentical hormones please listen to PhD Kathy Lynch from Women’s International Pharmacy: https://madisonarealymesupportgroup.wordpress.com/2015/06/10/audio-on-hormones-and-adrenal-support/

**Do not take systemic enzymes 24-36 hours before elective surgery and do not resume until 24-36 hours after the operation as they could prevent normal clotting in small blood vessels.

Here’s what’s in systemic enzymes and what each ingredient does:

Rutin: a bioflavinoid that strengthens and controls the permeability of blood vessels and capillary walls, lowering blood pressure and slowing aging.
Serrapeptase: anti-inflammatory, anti-edema, and fibrinolytic properties. Less swelling after surgery, less breast pain for fibrocystic patients, electrophysiologic proof of recovery in carpal tunnel syndrome patients.
Protease: http://www.enzymeessentials.com/HTML/protease.html: breaks down proteins and are important to digestion as they liberate needed amino acids. Helps with inflammation, immune regulation, breaking down cellular debris including toxins in the blood, freeing up the immune system to concentrate on bacterial, parasitical, and viral infections. Those with a protease deficiency have excess alkalinity which can cause anxiety and insomnia, arthritis, osteoporosis and other calcium-deficient diseases. Inadequate protein digestion results in hypoglycemia, which means moodiness.

Amylase: http://www.enzymeessentials.com/HTML/amylase.html: breaks down sugar and starch, and also digests dead white blood cells. Involved in anti-inflammatory reactions such as those caused by the release of histamine. The amylase deficient may have issues with psoriasis, eczema, hives, insect bites, allergies, atopic dermatitis, all types of herpes, and lung problems such as asthma and emphysema.
Papain: found naturally in unripe papayas, it has been used as a meat tenderizer as it breaks down the fibers in muscle tissue, as well as in preparation of cell cultures due to its ability to dissolve bonds between cells. It helps break down foods for digestion.
Trypsin: also breaks down protein into amino acids for absorption in the blood stream, as well as breaking down casein in milk, dissolving blood cloths in its microbial form, and treating inflammation in its pancreatic form. Atlantic cod trypsin in an oral spray was found to protect those inoculated with rhinovirus.
Lipase: http://www.enzymeessentials.com/HTML/lipase.html: breaks down fats into fatty acids and glycerol. Helps control appetite and healthy cholesterol and triglyceride levels. Those deficient in lipase have decreased cell permeability which means nutrients cannot get in and waste cannot get out, as well as muscle spasms, and spastic colon.
Chymotrypsin: http://www.encyclopedia.com/topic/chymotrypsin.aspx: Also breaks down proteins to produce enzymes for digestion and absorption of food. Also is anti-inflammatory. The presence and amount in stool is measured as a test of pancreatic function. Used for those with pancreatic insufficiency (impaired digestion, malabsorption and passing of undigested food in stool, gas, abdominal bloating, and nutrient deficiencies. Incomplete digestion of proteins may result in allergies and the formation of toxic substances. Helps keep the small intestine free from parasites such as bacteria, yeast, protozoa, and worms. Used to treat shingles, acne, age spots, sun damage, ulcerations and abscesses, arthritis and other autoimmune diseases, infections, injuries, and possibly cancer.
Bromelain: http://umm.edu/health/medical/altmed/supplement/bromelain: found in pineapples, it too digests protein. Used for indigestion and inflammation. When used on the skin it may be useful for removing dead tissue from third-degree burns. May reduce cough and nasal mucus as well as pain. It can kill some viruses and bacteria, and has anti-tumor properties and may help the effectiveness of certain chemotherapy drugs.
Quercetin Dihydrate: http://www.globalhealingcenter.com/natural-health/health-benefits-of-quercetin/: a bioflavonoid (plant pigment) found in fruits, vegetables, grains, and leaves. It is an anti-oxidant, anti-carcinogenic, neuroactive, anti-artherogenic, supports cardiovascular health, balanced blood pressure, protects against stress, and has an antihistamine effect.
Questions about Systemic Enzymes

“When is the best time to take a protease supplement?
For maximum systemic benefit, it is best to take proteases between meals as this allows for faster absorption into circulation. However, if this is not realistic for your patient, then it is ok to take proteases with meals knowing that some of the protease enzymes may be used to digest food proteins. Also, it is better to take small doses several times throughout the day rather than one or two large doses in a day. Common dosing times are first thing in the morning, mid-morning, mid-afternoon, and bedtime.
Can protease enzymes be taken with NSAIDS and/or prescription medications?
Digestive enzymes function by breaking down specific chemical bonds in foods. In most cases digestive enzymes can therefore safely be taken with medications. However, it is of course always recommended to let your health care provider know what you are taking.
Can protease enzymes be taken with prescription blood thinners?
One area of caution is with prescription blood thinning agents. These types of prescription drugs interfere with the natural blood clotting mechanisms, while proteases break down fibrin allowing for better blood flow. They can be taken in conjunction, but it is recommended to dose them about four hours apart and monitor lab work closely. We recommend notifying and working with the doctor prescribing the medications.
Can you take protease enzymes when taking prescription “protease inhibitors”?
More often than not, the term “protease” that describes proteolytic enzymes is used in very general terms. There are many metabolic proteases in our body, each with many different functions. The medications that are designed as protease inhibitors are targeting a very specific viral protease. The supplemental digestive proteases are very different and will not interfere with the medication. In fact, oral supplemental digestive enzymes can be very supportive to those patients with auto-immune disorders.”

How to choose the best systemic enzymes: http://www.wisegeekhealth.com/how-do-i-choose-the-best-systemic-enzymes.htm

Some examples of Systemic Enzymes:

Wobenzym:  http://www.wobenzym.de/en/background/enzymes-in-wobenzym/

Vascuzyme:  http://www.orthomolecularproducts.com/vascuzyme/

Zymeessence:  http://www.drwongsessentials.com/Zymessence-p/zy180.htm

Heal-n-Soothe:  http://www.losethebackpain.com/proteolyticenzymes.html

I’m sure there are many more types out there.  Do a google search and more will crop up.  I personally have used WobenzymN as well as Vascuzyme with great success.  The WobenzymN was expired by two years and still worked.  I switched to Vascuzyme by Ortho Molecular as it was stronger and my LLMD sells it in his office.  Make sure to read about the different types as they have different ingredients, dosages, and strengths.

**As you read above, please consult with your health care professional – particularly if you are taking blood thinners or have a blood disorder.  One site also stated that you SHOULD NOT take systemic enzymes if you are also taking antibiotics.  Discuss all of this with your practitioner.

My husband and I both tried WobenzymN while in antibiotic treatment and felt nothing.  After we quit antibiotics due to not herxing any longer and being fairly symptom-free for 3-4 months (except the excruciating pain in my head/neck/spine and his itching and fatigue) we started an herbal program for maintenance.  After 4 months of this with the pain still there, I retried the WobenzymN and within the first dose it took 70% of my pain away.  Since then, a month later, the pain is 99% gone.  All I take is 3 capsules each morning on an empty stomach.  For some of you, this may be the thing that will help you turn the corner and is certainly worth considering.

*Although you can buy these over the counter, make sure to run this and all supplements by your health practitioner as there are cross reactions with certain medications.

Adverse Effects of Sleep Deprivation on Performance and Longevity [Research Notes & Mirror]

Notes taken from a Brandon Marcello, Ph.D. seminar: 

  • Not getting enough sleep leads to increased risk of injury and reduced pain threshold; greater susceptibility to sickness; reduced physical and psychological performance; reduced motivation, learning ability, and memory; increased anxiety, irritability, and mistakes; increase in body fat percentage; reverting to old habits; poor justment of distance, speed, and/or time.

  • Most of the Rapid Eye Movement (REM) cycle occurs in the final 2-3 hours of a night’s rest. Missing ~25% of your total sleep one night may have a larger than 25% negative impact on your mind and body. 

  • Getting enough sleep improves motivation; recovery of muscle strength; sprint speeds; muscle glycogen (stored energy in muscle); cortisol (stress) regulation; motor skill development; memory consolidation.

  • Sleep debt simplified: if you need 8 hours and get 7 hours, that means you accrue 1 hour of sleep debt. Need to get 9 hours to repay that 1 hour of debt. Sleep debt can build up over time to (30 hours? I failed to write this down).

  • After extending time in bed to 10 hours per night for several weeks, collegiate swimmers showed improvements of +8% 15meter sprint speed; +20% reaction time off the block; +10% turn time efficiency; +19% kickstrokes.

  • During sleep, the brain will get rid of waste products and clean out toxic proteins which can impair healthy aging of the brain and cause brain related diseases such as Alzheimer’s and other neurological disorders.

  • Sleep Myths: you can get too much sleep; naps are bad; 8 hours of sleep is ideal (everyone is biologically wired to require different amounts of sleep); older people don’t need as much sleep (they need more because they usually awaken more frequently); storing up sleep for the week ahead; alcohol helps you sleep.

  • Sleep/Nutrition Interaction: sleep deprivation alters the ability of the body to metabolize and store carbohydrates for recovery, as well as use for a later time; reduces glycogen levels.

  • Ask yourself: what is detracting from your sleep quality? Noise? Light? Pain? Temperature? Priorities? Stress? Alcohol/Drugs/Food?


Studies: Predicting Major League Baseball (MLB) Player Career Longevity via Sleepiness Measurements, Validation of a Statistical Model Predicting Possible Fatigue Elementas in Major League Baseball, Chronic lack of sleep is associated with increased sports injuries in adolescent athletes, Sleep patterns of U.S. Military academy cadets (2003), Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men
Seminars: One More Reason to Get a Good Night’s Sleep (Jess Iliff), Why Do We Sleep? (Russell Foster)
Books: The Promise of Sleep (William Dement, M.D., Ph.D.), Take a Nap! (Sara Mednick, Ph.D.), The Sleep Revolution (Arianna Huffington)

Info from Joe Rogan Experience interview with Dr. Matthew Walker (Source)

  • Lack of sleep and physical performance

    • If you’re getting 6 hours of sleep or less, your time to physical exhaustion drops by up to 30%

    • Lactic acid builds up quicker the less you sleep

    • The ability of your lungs to expire CO2 and inhale oxygen decreases

    • The less sleep you have

      • The lower your peak muscular strength, lower your vertical jump height, and lower your peak running speed

    • A higher injury risk

      • One study showed a 60% increase in probability of injury comparing people who get 9 hours of sleep a night, to those who get 5

      • Your stability muscles fail earlier when not getting enough sleep

  • We need 7-9 hours a night

    • Once you get below 7, we can measure impairments in the brain 

    • There is a small fraction of <1% of the population, that has a certain gene that allows them to survive on 5 hours of sleep

      • You are more likely to be struck by lighting than have this gene

      • The gene promotes wakefulness chemistry in the brain

  • The shorter your sleep on average, the shorter your life

    • Short sleep predicts all cause mortality

  • Wakefulness, compared to sleep, is low level brain damage. Sleep offers a repair mechanism for this.

    • During deep sleep at night, there is a sewage system in the brain that cleanses the brain of all the metabolic toxins that have accumulated throughout the day

      • One of those toxins is beta amyloid – which is responsible for the underlying mechahism of Alzheimer’s disease

      • The less you sleep – the more this plaque builds up

      • Insufficient sleeps is the most significant lifestyle factor for determining whether or not you’ll develop Alzheimer’s Disease

  • Insufficient sleep is linked to bowl, prostate, and breast cancer

    • The WHO has decided to classify any form of nighttime shift work as a probable carcinogen

    • Shift workers have higher rates obesity, diabetes, and cancer

  • Leptin and ghrelin

    • Both control appetite and weight

    • Leptin tells our brain we’re full

    • Ghrelin does the opposite, it’s the hunger hormone

    • With less sleep, leptin gets suppressed, and ghrelin gets ramped up

      • People sleeping 4-5 hours a night will on average eat 200-300 extra calories each day (70,000 extra calories each year which translates into 10-15 lbs. of body mass)

      • You also eat more of the wrong things

    • Lack of sleep if a critical factor of the obesity epidemic

  • 1 out of every 2 adults in America are not getting the recommended 8 hours of sleep

    • 1 out of 3 people are trying to survive on 6 hours or less of sleep

    • The average American adult is sleeping 6 hours and 31 minutes during the week (it used to be 7.9 hours in 1942)

    • “The number of people who can survive on 6 hours of sleep or less, rounded to a whole number, and expressed as a percentage of the population is 0”

    • “You don’t know you’re sleep deprived, when you’re sleep deprived”

  • Under slept employees will take on fewer work challenges, are more likely to slack off in groups, and are less likely to come up with creative solutions

  • Less sleep does not equal more productivity

How Lyme disease bacteria spread through the body [Research Notes]


Summary: Researchers have developed a live-cell-imaging-based system that provides insights into how Lyme disease bacteria latch onto and move along the inside surface of blood vessels to reach key destinations in the body where they may be able to persist longer and avoid treatment. Ironically, the same strategies that these bacteria use to spread through the body are also used by immune cells to protect against infectious disease.

Researchers have developed a live-cell-imaging-based system that provides molecular and biomechanical insights into how Lyme disease bacteria latch onto and move along the inside surface of blood vessels to reach key destinations in the body where they may be able to persist longer and avoid treatment. Ironically, the same strategies that these bacteria use to spread through the body are also used by immune cells to protect against infectious disease. The study appears August 25 in Cell Reports.

“There is very little known about the biomechanics of bacterial-vascular interactions, even though understanding this is really important for understanding how bacteria spread through the body via the cardiovascular system, and for developing methods to block bacterial dissemination,” says senior study author Tara Moriarty of the University of Toronto. “Our in vitro live-cell-imaging-based system will permit more efficient dissection of the underlying interaction mechanisms and more rapid screening for inhibitors of bacterial-endothelial interactions and dissemination.”

Moriarty and her team developed a flow chamber system and real-time tracking methods that enabled microscopy analysis of bacterial interactions with human endothelial cells lining the surface of blood vessels. Using genetically modified strains of the Lyme disease bacterium (Borrelia burgdorferi), the researchers discovered that a cell-surface adhesion protein called BBK32 plays an important role in stabilizing and strengthening bacterial-vascular interactions under flow. By calculating the displacement of bacteria from the endothelial cells, the researchers also found that the microbes use bungee-cord-like tethers to stabilize and strengthen these bonds.

Using their imaging-based system, the researchers went on to discover that bacteria move along endothelial surfaces under flow by transferring mechanical load along a series of successively formed and broken bonds. Similar to children swinging on monkey bars, the bacteria transferred force from one bond to the next without fully detaching, slowing down every time they established a new bond and accelerating when they broke a bond and transitioned to the next one. This repeating cycle allowed the bacteria to stably move over the endothelial surface at a constant overall speed, similar to the way immune cells called leukocytes move through blood vessels.

Additional calculations revealed that the propulsive force generated by bacterial motility is stronger than the forces imposed on bacteria by flow, suggesting that the microbes may use rotating internal structures called flagella to actively migrate along blood vessel walls and exit the vasculature to reach specific tissues, even under the force conditions generated by blood flow. The entire process is similar to humans swimming down a river, using their legs to move toward trees lining the bank, grabbing onto a series of branches to slow down, and eventually pulling on the branches while kicking to exit the river and reach dry land.

“The ability of Lyme disease bacteria to disseminate using the network of rivers and streams provided by the bloodstream, and the ability to catch onto the banks of these rivers and streams, would likely be very important for spreading throughout the body, because they can overcome the barrier to dissemination caused by blood flow,” says first author Rhodaba Ebady of the University of Toronto. “It’s likely that this property helps the bacteria get to sites where they might be able to persist longer, and this property might therefore make it harder to treat infections caused by these bacteria.”

The findings also suggest that drugs targeting BBK32 or as-yet-unidentified endothelial receptors could help to prevent or slow down the spread of Lyme disease bacteria to joints, the heart and the nervous system, thereby eliminating or reducing the severity of symptoms such as arthritis, heart inflammation, facial paralysis, and nerve pain. Because BBK32-like proteins are also produced by pathogens such as Staphylococcus aureus and Streptococcus pyogenes as well as certain Borrelia species, the findings could also be relevant to other serious conditions caused by blood-borne spread of bacteria, including pneumonia, relapsing fever, and inflammation affecting the heart, bones, and nervous system. Moreover, currently available drugs that inhibit leukocyte-vascular interactions for the treatment of autoimmune and inflammatory diseases could potentially be repurposed for Lyme disease and potentially other infectious diseases.

In future studies, the researchers will attempt to identify the endothelial receptors that BBK32 interacts with, assess the biomechanical role of bacterial flagella in vascular interactions and dissemination, and try to determine how bacteria target specific endothelia associated with different tissues. More broadly, their cell-imaging approach could be used to study how other pathogens spread through the body. “We really hope that other labs can use some of the approaches we’ve established to study other bugs and will be glad to help other groups do this,” Moriarty says. “There’s so much to do, and all we’ve seen so far is the very tip of the iceberg.”

Lipid Exchange between Borrelia burgdorferi and Host Cells [Research Mirror]



Borrelia burgdorferi, the agent of Lyme disease, has cholesterol and cholesterol-glycolipids that are essential for bacterial fitness, are antigenic, and could be important in mediating interactions with cells of the eukaryotic host. We show that the spirochetes can acquire cholesterol from plasma membranes of epithelial cells. In addition, through fluorescent and confocal microscopy combined with biochemical approaches, we demonstrated that B. burgdorferi labeled with the fluorescent cholesterol analog BODIPY-cholesterol or 3H-labeled cholesterol transfer both cholesterol and cholesterol-glycolipids to HeLa cells. The transfer occurs through two different mechanisms, by direct contact between the bacteria and eukaryotic cell and/or through release of outer membrane vesicles. Thus, two-way lipid exchange between spirochetes and host cells can occur. This lipid exchange could be an important process that contributes to the pathogenesis of Lyme disease.

Author Summary

Lyme disease, the most prevalent arthropod-borne disease in North America, is caused by the spirochete Borrelia burgdorferi. Cholesterol is a significant component of the B. burgdorferi membrane lipids, and is processed to make cholesterol-glycolipids. Our interest in the presence of cholesterol in B. burgdorferi recently led to the identification and characterization of eukaryotic-like lipid rafts in the spirochete. The presence of free cholesterol and cholesterol-glycolipids in B. burgdorferi creates an opportunity for lipid-lipid interactions with constituents of the lipid rafts in eukaryotic cells. We present evidence that there is a two-way exchange of lipids between B. burgdorferi and epithelial cells. Spirochetes are unable to synthesize cholesterol, but can acquire it from the plasma membrane of epithelial cells. In addition, free cholesterol and cholesterol-glycolipids from B. burgdorferi are transferred to epithelial cells through direct contact and through outer membrane vesicles. The exchange of cholesterol between spirochete and host could be an important aspect of the pathogenesis of Lyme disease.


Borrelia burgdorferi, the causative agent of Lyme disease [1][2], is unusual among prokaryotes in that in addition to phosphatidylcholine, phosphatidylglycerol [3][7] and many different lipoproteins [4][5][8][10], it has free cholesterol and cholesterol-glycolipids in its outer membrane (OM). The glycolipids of B. burgdorferi are mono-α-galactosyl-diacylglycerol (MGalD), which does not contain cholesterol; cholesteryl-β-D-galacto-pyranoside (CGal); and cholesteryl 6-O-acyl-β-D-galactopyranoside, or cholesteryl 6-O-palmitoyl-β-D-galactopyranoside (ACGal/Bb-GL-1), which contain cholesterol [3][11][14]. The cholesterol-glycolipids constitute a significant portion, 45% [11], of the total lipid content [3][5][12][13][15][18]B. burgdorferi does not have the biosynthetic ability to synthesize cholesterol or any long-chain-saturated and unsaturated fatty acids that are required for growth [6]. As a result, the lipid composition of B. burgdorferi reflects that of the culture medium or host animal fluids or tissues [6]. Furthermore, it has been hypothesized that in addition to the activity of galactosyltransferase bb0454, other uncharacterized spirochetal transferases could be responsible for constructing the cholesterol-glycolipids [18]. Important to the pathogenesis of B. burgdorferi, ACGal, and to a lesser extent MGalD and CGal, are antigenic [13][15][17][19]. These glycolipids induce antibody responses throughout all stages of Lyme disease, being most prominent in the late stages [9][11][12][20][21]. Additionally, we demonstrated that antibodies to the cholesterol-glycolipids cross-react with host gangliosides and antibodies to the gangliosides cross-react with the glycolipids [22][23]Borrelia lipid antigens can also be presented in the context of CD1d on NKT cells [24][29].

Using ultrastructural, biochemical, and biophysical analysis, we previously determined that the cholesterol-glycolipids in the OM of B. burgdorferi are constituents of eukaryotic-like lipid raft domains [30]. In eukaryotic cell membranes, lipid rafts are microdomains that are rich in sterols, sphingolipids, and phospholipids with saturated acyl tails that allow for tight packing of these lipids into ordered domains [31][32]. These cholesterol-rich domains segregate from the disordered membrane domains that contain mostly unsaturated lipids [31][33]. In addition to the enrichment of specific lipids, lipid-anchored proteins such as glycosyl phosphatidylinositol (GPI) proteins and proteins covalently linked to saturated acyl chains are targeted to lipid rafts [34]. Lipid rafts are important for the segregation of plasma membrane proteins [31][33][35][38], and contribute to endocytosis, exocytosis, vesicle formation, and budding [39][43]. Furthermore, lipid rafts have been identified as important platforms in cell signaling [33].

The presence of free cholesterol and cholesterol-glycolipids with saturated acyl chains in B. burgdorfericreates an opportunity for lipid-lipid interactions with constituents of the lipid rafts in eukaryotic cells. This is of particular interest since B. burgdorferiadheres to many different cell types [44][45]. Lipid-lipid interactions could also facilitate the ability of the spirochete to adhere to many different types of cells [46][49] and to cellular and matrix proteins [50][52]. Furthermore, exchange of lipids between spirochetes and host cells could be important for cholesterol acquisition by the spirochetes, acting as an important nutritional source. Additionally, acquisition of spirochetal antigens by the cells could result in presentation of these antigens in a manner that would be recognized by the immune response leading to a potential mechanism for cellular damage.

The requirement for cholesterol is important for other bacteria. The presence of a cholesterol glucoside in spirochetes was first identified in B. hermsii [53], an agent of relapsing fever. In addition, cholesterol has been documented in the membranes of HelicobacterMycoplasmaEhrlichiaAnaplasma, and Brachyspira[54][60]. It is unknown whether raft-like structures similar to that in B. burgdorferi form in these other bacteria. However, acquisition of cholesterol from the plasma membrane of host cells has been documented with H. pylori, another prokaryote that has cholesterol in its OM [61], and this organism associates with cholesterol rich areas of the eukaryotic cells [61][62].

We show here that there is a two-way exchange of lipids between B. burgdorferi and eukaryotic cells and that this exchange is accomplished through direct contact with the spirochete as well as contact with outer membrane vesicles (OMV).Go to:


B. burgdorferi attach to HeLa cells and acquire cholesterol

We first investigated whether B. burgdorferi acquires cholesterol through direct contact with HeLa cells using BODIPY-cholesterol. BODIPY-cholesterol is an environment sensitive, lipophilic probe that only fluoresces in hydrophobic, but not aqueous environments [63][65]. When B. burgdorferi were incubated with HeLa cells labeled with BODIPY-cholesterol at a multiplicity of infection (MOI) of 40∶1, we observed colocalization (yellow) between the BODIPY-cholesterol and B. burgdorferi outer membrane protein OspB on the spirochete and at the point of attachment with the HeLa cell (Figure 1S1 for additional images). Colocalization of BODIPY-cholesterol and the spirochetes was demonstrated in single 0.5 µm Z-slices and showed the uptake of cholesterol by adherent B. burgdorferi (Figure 1S1). Furthermore, BODIPY-cholesterol labeling extended outward from the point of attachment along the length of the spirochete (Figure 1S1). Acquisition of BODIPY-cholesterol is not detected at the start of the experiment (Figure 1, 0 min panels). HeLa cells do not release BODIPY-cholesterol into the supernatant over the course of the 1 hr coincubation (data not shown); therefore, B. burgdorferi most likely acquired BODIPY-cholesterol directly from the labeled HeLa cells and not the supernatant.

Neurotransmitters, Amino Acids, and their interaction with Borrelia Burgdorferi/Lyme Disease [Research Notes]


Functions of Neurotransmitters: 

Acetylcholine – First known neurotransmitter (1920)  Nerve-muscle connections for all the voluntary muscles of the body and many involuntary muscles. In the presence of water acetylcholine is broken down to acetic acid (5% acetic acid is vinegar) and choline. An enzyme (acetylcholinesterase)  does the breakdown. The acetylcholine is absorbed on the post synaptic membranes and the impulse travels down the neuron, releasing acetylcholine which is absorbed by another post synaptic membrane.  This continues until the muscle or endocrine gland is stimulated.  Poisons which inhibit the acetylcholinesterase cause death by paralysis. Examples: curare, nerve gases (Sarin)

Thyroxine – Produced by the thyroid gland.  It comes from the amino acid phenylalanine and requires iodine for its structure.  It regulated basal metabolic rate (BMR).  Too little – lethargy.  Too much – hyperactivity.  Was once used as a diet supplement to increase the BMR which results in weight loss.

Dopamine – Produced by the substantia nigra structure in the brain. It is synthesized from the amino acid phenylalanine. Dopamine is involved in 1) movement control; 2) emotional responses; 3) Experience of pleasure or pain.  Oversupply results in schizophrenia.  Undersupply results in Parkingson’s disease. Dopamine plays a role in the brain’s reward system. Methamphetamine releases huge quantities of dopamine from the vesicles giving a euphoric feelings.  The vesicles get depleted and that high becomes more difficult to re-acheive. Cocaine blocks the re-uptake of dopamine – leaving it in place for the experience of pleasure. DOPA cannot pass through the blood brain barrier so L-DOPA is used.

Epinephrine (Adrenalin) – Norephrine  – The fight or flight hormones produced by the adrenal glands  which sit on top of the kidneys. It is syntesized from the amino acid phenylalanine. Gives unsual strength or energy.  Epinephrine can cause heart arrhythmias and beta blocker drugs (Inderol) are used. They are specific for certain cells.

Serotonin – Is synthesized from the amino acid tryptophan.  Serotonin affects the perception of pain, thermo-regulation and sleep.  Low levels result in depression, bulermia, anorexia nervosa, season adjustment disorder (SAD).  High levels produce a manic state. Bipolar disorder can be managed by controlling the the levels of serotonin. Psychoactive drugs have actions on serotonin metabolism.  LSD, an analog of serotonin, produces hallucinations.  Low levels of a metabolite of serotonin (5 HIAA) is found in spinal fluids of suicide victims.  High levels of 5 HIAA are found in small bowel tumors. 
Mechanism: Nerve impulses release serotonin which goes to the receptor cells.  Drugs can 1) increase the serotonin release; 2) prevent the re-uptake of the serotonin, leaving it there longer; or 3) inactive the enzymes which breakdown the serotonin.  

Melatonin  – Is synthesized from the amino acid tryptophan. Serotonin is converted to melatonin.  Melatonin is involved in the wake/sleep cycle.

GABA  (gamma amino butyric acid)  – Is synthesized from the amino acid glutamic acid.  GABA is the chief inhibitory neurotransmitter in the brain. The off switch of the brain.  Vitamin B6 (pyridoxine) is needed to convert glutamic acid to GABA.  In 1950’s a screw up on baby formula omitted B6  and the infants had seizures.

Glycine – Is the simpliest amino acid.  It is the major inhibitory neurotransmitter in the spinal cord.

Glutamate – Is the chief excitatory amino acid in the brain.  MSG is monosodium glutamate, the flavor enhancer.  Some people cannot tolerate MSG – it makes them hyperactive and anxious.

Nitric Oxide  NO  – Is formed from the amino acid arginine. Diffuses readily into the cell and is gone in 8 to 12 seconds. NO dilates blood vessels and lowers blood pressure.  The heart drug nitroglycerin worked by releasing NO which resulted in lowering the blood pressure.  Viagra works by dilating the blood vessels and relaxing the muscle cells.  

Histamine – Is formed from the amino acid histine.  Histamine goes to the receptor sites on the cells of the respiratory tract giving redness, swelling and itching. Antihistimines block the histamine receptors on the cells.  Some antihistamines cross the blood brain barrier and acts on cells controlling sleep.

MTHFR & Aminos 

The MTHFR gene provides instructions for making an enzyme called methylenetetrahydrofolate reductase. This enzyme plays a role in processing amino acids, the building blocks of proteins. Methylenetetrahydrofolate reductase is important for a chemical reaction involving forms of the B-vitamin folate (also called folic acid or vitamin B9). Specifically, this enzyme converts 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. This reaction is required for the multistep process that converts the amino acid homocysteine to another amino acid, methionine. The body uses methionine to make proteins and other important compounds.

Methionine is one of the essential amino acids needed for good health but cannot be produced in the body, and so must be provided through our diet. 


Ability to be a supplier of sulfur and other compounds required by the body for normal metabolism and growth. Without an adequate intake of sulfur, our body will not be able to make and utilize a number of antioxidant nutrients.
Used to treat depression, inflammation, liver diseases, and certain muscle pains.
Methionine is an especially important nutrient beneficial for those suffering from estrogen dominance, where the amount of estrogen in the body is excessively high when compared to its opposing hormone called progesterone. Since estrogen is cleared through the liver, an enhanced liver function will reduce the body’s estrogen load. Specifically, methionine converts the stronger and carcinogenic estradiol (E2) into estriol (E3) which is the “good” estrogen as compared to estradiol.  
Loss of methionine has been linked to senile greying of hair. Its lack leads to a buildup of hydrogen peroxide in hair follicles, a reduction in tyrosinase effectiveness and a gradual loss of hair color.
Methionine is also responsible for the reduction of the level of histamine in the blood, which is why it can positively affect the symptoms of allergies. In addition, it is important for the regulation of the acid-base balance and provides sulphur atoms for various chemical processes.
Contributes to the detoxification of heavy metals (such as mercury from dental fillings) through the formation of complexes and of cartilage.
Prevents Urinary Tract Infections
Can reduce the severity of depression or Parkinson’s and otherwise improve the quality of life of those suffering from such conditions.

If you have MTHFR mutations this process can be interrupted (called homocystinuria). 

At least 40 mutations in the MTHFR gene have been identified in people with homocystinuria. Most of these mutations change single amino acids in methylenetetrahydrofolate reductase. These changes impair the function of the enzyme, and some cause the enzyme to be turned off (inactivated). Other mutations lead to the production of an abnormally small, nonfunctional version of the enzyme. Without functional methylenetetrahydrofolate reductase, homocysteine cannot be converted to methionine. As a result, homocysteine builds up in the bloodstream, and the amount of methionine is reduced. Some of the excess homocysteine is excreted in urine. Researchers have not determined how altered levels of homocysteine and methionine lead to the health problems associated with homocystinuria. MTHFR is VERY complicated and too much to cover in this post. I have posted on MTHFR previously here.

Lyme, Mitochondria, Cells and Aminos

What are Mitochondria? In a nutshell Mitochondria are the cell’s power producers. They convert energy into forms that are usable by the cell. Located in the cytoplasm, they are the sites of cellular respiration which ultimately generates fuel for the cell’s activities. Mitochondria are also involved in other cell processes such as cell division and growth, as well as cell death. When cells become damaged or undergo some type of infection, they die. One way to remove these cells without causing harm to other cells is through apoptosis. During apoptosis, a cell triggers a process that will allow it to “commit suicide.” In this process, the cell undergoes a reduction in size as its cellular components break down and condense. 

The Journal of Neuroinflammation (published on 18 July 2013) states that the Lyme disease spirochete Borrelia burgdorferi induces inflammation and apoptosis in cells. In plain English, Lyme causes your cells to “commit suicide.”

Other preliminary studies state: Apoptosis plays an important role in the control of the immune system, and its impairment may be associated with autoimmune responses. Different bacterial and viral pathogens interfere with the regulation of apoptosis. This may take place in Lyme borreliosis, in which pathological autoimmune reactions are likely to occur.

As I said before, generally amino acids serve five functions in the body:

They furnish the material from which proteins are synthesized by various cells.
They are used by the cells in manufacturing enzymes, hormones and other nitrogenous products.
They are used in constructing blood protein.
They may furnish a source of energy, with some of the amino acids being transformed into glucose and glycogen.
They aid the body in performing many functions as described in their individual descriptions.

We NEED Aminos for our Mitochondria to function properly! 

Amino Acids—Essential and Non-Essential
Amino acids can be placed in the category of either essential or non-essential. The name is self explanatory. Essential amino acids are those that are “essential” in the diet. In other words, we cannot create them through our own metabolism. Therefore, we need to obtain them through foods containing them. Fortunately, protein-containing foods contain varying degrees of the essential amino acids. During times of starvation, our body relies on its own protein stores, such as pre-albumin, albumin, and ultimately protein from sources that it normally shouldn’t have to utilize (e.g., muscle tissue, etc.)

Non-essential amino acids are those which can be produced from other amino acids and substances in the diet and metabolism. During times of need, the metabolism can shift into producing the amino acids that it requires for synthesizing proteins essential to our survival.

Below is a list of essential and non-essential amino acids.

essential amino acids

non-essential amino acids

Dr. Vickery’s Work With Aminos on Treating Bacterial, Yeast/Fungus, Parasites, and Toxic Metals
In an earlier post I talked about the work of Dr. Vickery and his healing of thousands of people (including Lyme patients) with Amino therapy. You can read more on him and his work here.

He states that protein deficiency will allow yeast or fungal infections to begin to cause problems all over the body,showing up as rashes, constipation, poor concentration, and sinusitis. It is his observation that many auto immune conditions such as, rheumatoid arthritis, lupus, and fibromyalgia occur as a result of chronic infections, which the body is not equipped to 
control. Overwhelmed, the body becomes confused and begins to produce T-cells that are programmed to attack live healthy cells, In other words without the necessary protein to act as our body’s general system manager, chaos ensues and we respond with an allergic reaction to ourselves! Correct the protein/enzyme issue, heal the body.

Aminos & Pathogens
A research scientist from the Fraunhofer Institute for Cell Therapy and Immunology IZI in Leipzig, Germany, has discovered that simple, natural amino acids work better than antibiotics at treating infections, and they do not cause harm to healthy cells in the body. For their study, Dr. Andreas Schubert and his colleagues from Fraunhofer tested the effects of amino acids in vitro and found that they broke through bacterial membranes and penetrated them quicker and with less of a required concentration than antibiotic drugs. And the best part of all was that the amino acids caused no cell damage, unlike antibiotics which kill off beneficial bacteria in the system as well as harmful bacteria.

“Antibiotic peptides (from amino acids) unlock their microbicidal effect within a few minutes. They also work at a concentration of less than 1 microliter, compared with conventional antibiotics which require a concentration of 10 microliters,” said Schubert as part of his test results. “The spectrum of efficacy of the tested peptides includes not only bacteria and molds but also lipid-enveloped viruses. Another key factor is that the peptides identified in our tests do not harm healthy body cells.”

The findings are revolutionary, because they show that amino acids work on virtually every infection, including even MRSA and CRKP. And because amino acids occur naturally in various foods like nuts, grass-fed meats and dairy products, beans, seafood, eating more of these foods regularly can help boost levels of these vital nutrients without the need for drugs. Amino acids supplements are also a great way to boost amino acid levels to optimal levels in order to prevent or treat infections.

“We have already identified 20 of these short chains of amino acids which kill numerous microbes, including enterococci, yeasts and molds, as well as human pathogenic bacteria such as Streptococcus mutans, which is found in the human oral cavity and causes tooth decay,” said Dr. Andreas Schubert, group manager of Fraunhofer. “Even the multi-resistant hospital bug Staphylococcus aureus is not immune, and in our tests its growth was considerably inhibited.”


Because of arginine’s powerful boost to the immune system, people suffering from a great variety of ailments may be tempted to experiment with it. Before doing so, make sure you do not have an acute or chronic virus, such as Epstein-Barr Virus (EBV), Cytomegalovirus (CMV) or Human Herpes Virus VI (HHV6), Herpes Simplex I or II. Arginine will speed up the rate of viral growth, which can prove to be dangerous. Theamino acid, Lysine, has the opposite effect on viruses, slowing down their growth. – Dr. Dennis Gersten

Myelination [Research Notes]

Notes from Headstrong by Dave Asprey

How Your Neurons Can Perform Better

As you know, all cells have a membrane made primarily of fat, but myelin is a special, thicker fat layer that is essential for your brain to function; without it, the signals between neurons would simply be lost.

We are born with very little myelin, and the process of producing it (called myelination or myelinogenesis) occurs rapidly during infancy. This is the main reason babies develop so quickly from adorable little lumps to walking and talking humans. On the opposite end of the spectrum, demyelination, or the loss of myelin along the cells; axons, is responsible for many neurodegenerative diseases, such as multiple sclerosis.

Researchers have learned a lot about how myelin is created (and destroyed) by studying patients with MS. While the majority of us are unlikely to develop MS, we can all benefit from this research by looking at the methods doctors are using to treat neurodegeneration. It takes a lot more work to restore failed myelin than it does to keep yours strong, but the methodology is the same.

A type of brain cell called oligodendroglia does the work to form your myelin. Throughout adulthood these cells constantly generate new myelin and replace segments of myelin that break. Just as the electric company maintains power lines to ensure smooth signals across a network, so, too, do these specialized cells conduct myelin maintenance throughout your neural networks. And your maintenance worker cells rely on a proper balance of hormones – particularly thyroid hormones and progesterone – to do their job well.

Research shows that thyroid hormones are also crucial for the health and survival of oligodendroglia cells and therefore for the constant rebuilding of healthy myelin. This is one more reason to stay on top of your thyroid health and get your levels checked once a year or more often if you are feeling tired a lot.

Researchers have found that the hormone progesterone signals oligodendroglia to initiate the process of demyelinating neurons. In one study, mice that were treated with progesterone had more oligodendroglia that were able to repair more myelin.

ATP: The Fuel that Powers Our Cells [Research Mirror]


What is ATP?

ATP or adenosine triphosphate is an organic molecule used in many cellular reactions. Many call it the energy “currency” of our cells, and the “transactions” are metabolic reactions.
When our body turns calories into energy for our cells, enzymes convert carbohydrates into glucose, and our liver converts fatty acids into ketones. These are two of the substrates that our mitochondria turn into ATP. Many people say that the mitochondria are like little power plants in our cells.
I liken mitochondria to little battery factories because ATP is a way that our body can store energy, transport it to another area in the cell, and then use that energy there to power a chemical reaction. For this reason, ATP is often known as a co-enzyme because it works with other compounds.

3D Model of ATP Molecule

What are Free Radicals and Reactive Oxygen Species?

Most people hear free radicals, and think of them as the “bad” compounds that cause cancer, but this is only part of the truth. Free radicals and reactive oxygen species (ROS) are produced by chemical reactions in our mitochondria, and are even produced by our own immune system.
These molecules can cause damage called oxidative stress, but these molecules are not universally bad. They exist as feedback loops or signaling molecules so our body knows what is going on.

What Happens if There is Too Much Oxidative Stress?

If there is too much oxidative stress in an area, then our cells and organelles (organelles are basically the organs of our cells) know there is something wrong, and they will often self destruct.
This can be a crucial healing process as long as it happens in limited amounts. For example, the death of unhealthy cells like cancer can be a good thing because our body can recycle and repurpose the nutrients that the cell is made of.
However, if we constrict blood flow, nutrients, or oxygen to a certain area of the body for an extended period of time, then the damage can be too great to repair. If unchecked, then this can cause oxidative damage to run rampant, and can even cause cell death which is called necrosis. Read our 
Full Article on Reactive Oxygen Species (ROS)here.

It’s All About Balance

A little bit of oxidative stress can create a little inflammation which tells our body where to send resources so our body can heal a damaged area. Like I said before though, unchecked oxidative stress can cause cell damage and even cell destruction.
ATP is one of the primary resources needed to rebuild an area in our body if there is damage so as a general rule of thumb, we want to lower our oxidative stress, and raise our levels of ATP.

Tons of Antioxidants is Not The Answer

Studies show that if we just flood our bodies with mega-doses of antioxidants all the time, then it can actually impair our body’s ability to heal because it confuses our body’s signaling mechanisms that tell it where and how to heal.
A little stress, oxidative or otherwise, is a good thing! It is unchecked, chronic stress that causes problems especially if our body never gets a break. There are a lot of supplements that we can use to lower oxidative stress and raise ATP all at the same time.

How Do I Raise ATP for Healing and Energy?

There are a few ways that ATP can be produced. The most common way is the Kreb’s Cycle (aka The Citric Acid Cycle). There are other ways like beta oxidation and oxidative phosphorylation, but for the sake of this article, we are going to keep it simple so you dodged that bullet.
There are certain molecules called redox signaling molecules. Redox simply means “reduction and oxidation”. These molecules can donate an electron or take an electron away from another molecule to facilitate a chemical reaction.
These molecules have many purposes, but many of these molecules help to facilitate the Kreb’s Cycle that produces ATP. Co-enzyme Q10 (aka CoQ10) for example, is one of these molecules that can help our mitochondria produce more ATP. As such, it has numerous benefits for our brain, and heart.

Endogenous Antioxidants: The Super Supplements Your Body Makes!

Many of these compounds like CoQ10 are produced naturally by our own bodies, but as we get older and incur stress or damage to our bodies, we are less able to produce these compounds.
Alpha lipoic acid (ALA; not to be confused with the omega-3) is another antioxidant produced by our body that facilitates ATP production, and reduces oxidative stress. However, ALA has some additional benefits like removing heavy metals.
ALA also activates a compound called PGC-1a that not only protects our DNA from the effects of aging (by protecting our telomeres), but it also stimulates mitochondrial biogenesis.
This means that it signals our cells to make more mitochondria! This in combination with CoQ10 can be a powerful one-two punch to boost your energy at a cellular. Creatine is another very common and safe supplement used by body builders because it increases ATP.

What About Nutrition?

Besides simply eating calories, there are certain micronutrients that can increase you ATP levels by optimizing our bodies enzymatic processes and nutrient transport.
Most of the B vitamins help facilitate the Kreb’s Cycle in our mitochondria especially vitamin B1, B2, and B3 (also known as thiamine, riboflavin, and niacin respectively). Many common meats, algaes, and sea veggies contain these crucial B vitamins.

The Magnesium Factor

Optimal magnesium levels are associated with our mitochondria working well, and this mineral aids in nutrient transport that also helps our body produce ATP
Many nuts and seeds like pumpkin seeds ad almonds contain magnesium as well as leafy greens like spinach and chard are great sources of magnesium.

Glutathione: “The Master Antioxidant”

Reducing stress and oxidative stress with antioxidants like glutathione, vitamin C, and vitamin E can also indirectly increase ATP production. Our body creates glutathione using sulfur and selenium, and it uses vitamin C and E in the creation process.
These nutrients and more can be found in all crucifers like broccoli, kale, cauliflower, brussel sprouts, radishes, turnips, arugula, bok choy, and more. Our body also gets sulfur for glutathione from alliums like garlic, onion, green onion, and shallots.

What Supplements Are Best?

There are many more things that raise ATP like NADH, Cordyceps, fermented ginseng, and more. Below, you will find our favorite combinations of the most well-researched supplements for raising ATP safely and effectively. I also love CoQ10 because there is so much data behind it.
Creatine and exogenous ketones are also a great way to create more ATP without burdening your body with more sugars. These are both alternative energy substrates for ATP especially in the muscles in the case of creatine, and especially in the brain and nervous system for ketones.
Products that reduce oxidative stress can also help optimize our body’s ATP production.
Read our Full Article on Reactive Oxygen Species (ROS) to learn more about antioxidants.

BDNF: Fertilizer for the Brain [Research Mirror]


BDNF: Brain Derived Neurotrophic Factor

Neurotrophins are a group of compounds that regulate brain growth, development, and repair. One of the most well-researched of these neurotrophins are BDNF (Brain Derived Neurotrophic Factor) which many scientists call “fertilizer for the brain”.
BDNF regulates the growth, protection, maintenance, and repair of neurons in our brain. It even has an anti-depressant effects according to new research. In this article, we are going to show you how to raise your BDNF naturally!

3D Map of BDNF

A Healthy Life Means a Healthy Brain

There are many natural ways to raise BDNF that sound like they came straight out of a personal development book! What amazes me is how many simple things that make us feel alive can also gives us a tangible physiological boost.
It is a no-brainer that doing things that bring us joy, and enhance our brain function are some amazing habits to integrate into our life. Below are just a few examples of what has been shown to boost BDNF.
For example:

  • Getting out in the sun

  • Doing yoga

  • Doing  mental tasks like puzzles

  • Doing physically demanding tasks 

  • Doing anything new and/or challenging for you.

  • Spending time with loved ones

  • Curcumin (from turmeric)

  • Resveratrol (from red grapes or Japanese knotweed)

  • Proanthocyanidins (from blueberries)

  • Intermittent fasting (even with as little as 12 hours of fasting)

  • Avoiding high fructose corn syrup, sugar, and processed foods

  • Eating a diet high in omega-3’s

  • Getting at least 7 hours of sleep each night

  • Reducing stress levels

Common Sense Makes Sense

We know intuitively that we feel better when we are around loved ones, and when we get out and get some fresh air. Now we know that many of these activities that “feel good” actually provide tangible biological benefits.
Any time when we are learning something new, or doing something challenging, we are giving our brains a reason to adapt and grow. As such, our brain responds by enhancing its own ability to grow.

Use It Or Lose It

“Use it or lose it” may actually be more true, then we once thought. By simply pushing the limits of what our mind can do, we are giving our brains a reason to become more complex.
According to Dr. Datis Kharrazian, author of “Why isn’t My Brain Working?”, says that the best way to raise BDNF is simply to get your heart rate up with high intensity exercise even for just 30-60 seconds a few times a day.
There was a 5 week study that showed that moderate exercise reduced cognitive decline in aging rats (CITE). Lower levels of BDNF have been associated with dementia, depression, and a shorter life-span. This is important stuff!

Putting Our Mouth Where Our Mind Is…

In addition to exercise, we see that sleep, stress reduction, and cutting out junk food are all great ways to raise BDNF. We all know these are great things to do, but now we have a great reason to do them!
If living a long and healthy life was not a good enough reason to start doing all of these things, we now find that 1 in 3 Americans have a genetic defect that can lower their BDNF! 
This means they are more susceptible Alzheimer’s and age-related cognitive decline. If you think that you may have this gene, then these lifestyle changes may help you save your own brain!

What About Supplements?

There are many supplements that have been shown to raise levels of BDNF in our brains. Many of these supplements simply reduce oxidative stress in our brains like curcumin and reseveratrol.
Some like PQQ (pyrroloquinoline quinone) are found endogenously in the body, but they can also be taken as supplements. Others are synthetic compounds like the nootropic called Noopept. We recommend starting with diet and lifestyle first before resorting to supplements.
Read our Full Article on Nootropics to learn more about our take on smart drugs.

Antioxidant Helpers

In addition to raising BDNF, there are some other great ways that you can increase your cognitive abilities. Lowering oxidative stress and free radicals with antioxidants like curcumin and resveratrol that can raise BDNF at the same time is one option.
Read our Full Article on Reactive Oxygen Species to learn what antioxidants we use to help our brains.

Synaptic Plasticity

Another great way to boost brain function is consume the nutrients for synaptogenesis like choline, uridine, and omega-3’s like DHA. This starts the Kennedy Cycle which is connected to more neurons, and more synaptic plasticty.
Read our Full Article on Synaptogenesis here to learn how you can enhance your brain plasticity.

Boosting The Energy Output

Raising levels of ATP (adenosine triphosphate) production is also a critical step because it gives each neuron the fuel it needs to function. There is no point in having a cool car if it doesn’t have any fuel, right? Our brain is the same way.
Read our Full Article on ATP to learn more about how to increase your energy output at the cellular level.

Borrelia Burgdorferi, Collagen, Collagen’s Role in the Nervous System [Research Notes]

Borrelia scavenging for collagen in blood vessels

Citing new research from the Moriarity Lab at the University of Toronto, microbiology professor Holly Ahern says it appears as though the Borrelia bacteria enters the blood, crawls along blood vessels, finds a place to breach and then exits the bloodstream. The bacteria then binds to collagen rich (gelatinous) tissues that predominate in the nervous system linings, the heart linings, and the joints.

“Once established in these locations, the bacteria switches from being motile(moving) to stationary cells that build a biofilm,” says Ahern. “Once the biofilm is established it is extremely hard to kill the bacteria within — not only because there are many bacteria in thick layers but because a proportion of the cells are genetically hardwired to shut down metabolism and exist as dormant persister cells, which are ‘tolerant’ to antibiotics.”


Collagen in the brain, CNS, and PNS

In the central nervous system, collagen is present only in the meninges and vasculature. On the contrary, the peripheral nervous system contains substantial amounts of collagen which effect the function of the nerve (Mei Liu 1988).
The central nervous system, brain, and spinal cord are completely enclosed by connective tissue membranes, the meninges. There are three meninges: dura mater, arachnoid, and pia mater. The dura mater is the strongest, thickest, and outermost membrane. It is chiefly made up of thick collagen fibers. The arachnoid is thin, netlike structure. The pia mater is a thin connective tissue net closely adherent to the surface of the brain and spinal cord. The arachnoid has no blood vessels. In contrast, the pia mater contains a large number of vessels. Both meninges, together called the leptomeninges, consist of interlacing collagenous bundles surrounded by fine elastic networks (Shellswell et al. 1979). The main cellular elements are fibroblasts and macrophages.
Although the brain parenchyma contains no collagen, the presence of glycosaminoglycans in the central nervous system has been documented by histochemical and biochemical methods (Robinson and Green 1962; Singh and Bachhwat 1965; Castej6n 1970; Margolis et al. 1976; Branford White and Hud- son 1977; Vitello et al. 1978; Kiang et al. 1978; Margolis and Margolis 1979; Bertolotto and Margassi 1984). Their physiological role has not been uncovered. It is suggested that proteoglycans take part in the regulation of the ionic environment and fluid volume in the brain as well as in the storage and releaseof some neurotransmitters or enzymes of their metabolism. Glycosaminoglycans in the brain are produced by the glial cells (Glimelius et al. 1978; Dorfman and Ho 1970; Norling et al. 1978). This is

Kucharz E.J. (1992) Collagen in the Nervous System. In: The Collagens: Biochemistry and Pathophysiology. Springer, Berlin, Heidelberg

Choline: Super Brain Nutrient [Research Mirror]

Research Roundup:

Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel.

Health outcomes associated with choline involve memory, heart disease, and inflammation, which also explain the consideration of choline as a plausible intervention in traumatic brain injury (TBI)…
It is hypothesized that CDP-choline may exert neuroprotective effects in an injured brain through its ability to improve phosphatidylcholine synthesis (Adibhatla and Hatcher, 2002). In addition to its neuroprotective capability, CDP-choline potentiates neurorecovery, which has led to its evaluation as treatment for both stroke and TBI in animal models and in human clinical trials (Cohadon et al., 1982; Levin, 1991; Warach et al., 2000). The positive effects seen in models of ischemia and hypoxia may be explained by increased Bcl-2 expression, decreased apoptosis, and reduced expression of pro-caspase. Inhibiting caspase activity may decrease apoptotic activity and calcium-mediated cell death. Supporting these ideas, in vitro studies have also revealed that choline deficiency induces apoptosis in the liver by mechanisms independent of protein 53, which likely involve abnormal mitochondrial membrane phosphatidylcholine, leakage of oxygen radicals, and activation of caspases (Albright and Zeisel, 1997; Albright et al., 1996, 1998, 1999a, 199b, 2003; Chen et al., 2010). In humans, a choline-deficient diet also causes DNA damage and apoptosis (da Costa et al., 2006).


CDP-choline is generally considered safe; the side effect most noted in clinical trials has been mild diarrhea, with leg edema, back pain with headache, tinnitus, insomnia, vision problems, and dizziness reported much less frequently (Adibhatla and Hatcher, 2002; Clark et al., 1997; Levin, 1991). There were no adverse events reported even with doses as high as 4,000 mg/day (Calatayud Maldonado et al., 1991). It is notable that in a study by Clark and colleagues (2001), a dose of 2,000 mg/day by enteral administration did not induce severe adverse events at a rate any higher than placebo in the 899 patients.

Revisiting choline alphoscerate profile: a new, perspective, role in dementia?

Pier Luigi ScapicchioPages 444-449 | Received 19 Sep 2012, Accepted 09 Jan 2013, Accepted author version posted online: 07 Feb 2013, Published online: 19 Feb 2013

In four trials, alpha-GPC was given orally at the dose of 1200 mg/day (466 patients treated for 6 months and 39 for 3 months). In the remaining studies, alpha-GPC was administered intramuscularly at the dose of 1000 mg/day for 3 months. These trials showed that alpha-GPC improved the patients’ clinical condition with particular reference to memory and attention impairment [10]

The role of citicoline in cognitive impairment: pharmacological characteristics, possible advantages, and doubts for an old drug with new perspectives.

Gareri P, Castagna A, Cotroneo AM, Putignano S, De Sarro G, Bruni AC.

Administered by both oral and intravenous routes, citicoline is converted into two major circulating metabolites, cytidine and choline. It is metabolized in the gut wall and liver. Pharmacokinetic studies suggested that it is well absorbed and highly bioavailable with oral dosing. A number of studies have clearly shown the possible role of citicoline in cognitive impairment of diverse etiology. It can also modulate the activity/expression of some protein kinases involved in neuronal death and increases SIRT1 expression in the central nervous system. The VITA study and the IDEALE study suggested that both parenteral and oral citicoline are effective and safe. Other studies have clearly demonstrated citicoline’s effects on several cognitive domains.

Pivotal role of choline metabolites in remyelination.

Skripuletz T, Manzel A, Gropengießer K, Schäfer N, Gudi V, Singh V, Salinas Tejedor L, Jörg S, Hammer A, Voss E, Vulinovic F, Degen D, Wolf R, Lee DH, Pul R, Moharregh-Khiabani D, Baumgärtner W, Gold R, Linker RA, Stangel M.

The objective of this study was to determine potential regenerative effects of the substance cytidine-5′-diphospho (CDP)-choline in two different murine animal models of multiple sclerosis. The effects of exogenously applied CDP-choline were tested in murine myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. In addition, the cuprizone-induced mouse model of de- and remyelination was used to specifically test the hypothesis that CDP-choline directly increases remyelination. We found that CDP-choline ameliorated the disease course of experimental autoimmune encephalomyelitis and exerted beneficial effects on myelin, oligodendrocytes and axons. After cuprizone-induced demyelination, CDP-choline effectively enhanced myelin regeneration and reversed motor coordination deficits. The increased remyelination arose from an increase in the numbers of proliferating oligodendrocyte precursor cells and oligodendrocytes. Further in vitro studies suggest that this process is regulated by protein kinase C. We thus identified a new mechanism to enhance central nervous system remyelination via the choline pathway. Due to its regenerative action combined with an excellent safety profile, CDP-choline could become a promising substance for patients with multiple sclerosis as an add-on therapy.

Changes in brain striatum dopamine and acetylcholine receptors induced by chronic CDP-choline treatment of aging mice.

R. Giménez, J. Raïch, and J. Aguilar

1. Spiroperidol binding (dopamine D2 receptors) and quinuclidinyl benzilate binding (muscarinic receptors) in striata of 19-month old mice was analyzed for animals that had received chronic administration of cytidine 5′-diphosphocholine (CDP-choline) incorporated into the chow consumed (100 or 500 mg kg-1 added per day) for the 7 months before they were killed. 2. Treated animals displayed an increase in the dopamine receptor densities of 11% for those receiving 100 mg kg-1 and 18% for those receiving 500 mg kg-1 as compared to the control aged animals that had received no CDP-choline. Control animals showed, from 2 months to 19 months of life, a 28% decrease in the receptor density. No change in the affinity of the receptors for spiroperidol was found in the treated or untreated animals. 3. Muscarinic acetylcholine receptor densities were also partially recovered by the same treatment in aged animals that showed a 14% decrease of these receptors in this case. The muscarinic receptor density increased 6% for the animals that received 100 mg kg-1 and 17% for the animals that received 500 mg kg-1 without any change in the affinity of the receptor for quinuclidinyl benzilate. 4. Aged animals displayed a slight increase in brain membrane fluidity as indicated by a decrease in the polarization value of the non-polar fluorophore 1,6-diphenyl-1,3,5-hexatriene. Interestingly, in the treated animals a greater increase in membrane fluidity was determined and found to be very similar for the two doses.

Our Article About Choline:

The Effects if Choline on Cholesterol and The Liver:

Citicoline or cognizin is known in the scientific realm as CDP-choline (cytidine 5’ diphosphocholine). In the nutritional world, it is usually just called choline, but choline comes in many forms other than just CDP-choline. 
Our bodies produce choline in the form of CDP-choline so it is considered a conditionally essential nutrient. However, if we restrict choline in our diets then the first thing to occur is the onset of nonalcoholic fatty liver disease (NAFLD). 
NAFLD will eventually lead to cirrhosis (scarring of the liver), steatosis, and eventually liver cancer. In addition to having many benefits for our brains and neurotransmitters, choline also helps our liver direct where fat and cholesterol where to go and how to be utilized. 
Without it, all of the fat and cholesterol builds up in our liver.

My Favorite Dietary Sources of Choline:

  • Grass-fed beef liver (356 mg/3 oz serving)

  • Pastured, organic eggs (147 mg/1 large egg ) 

  • Grass-fed beef (97 mg/3 oz serving)

  • Scallop (94 mg/3 oz serving)

  • Wild-caught salmon (75 mg/3 oz serving)

  • Organic chicken (73 mg/3 oz serving)

  • Wild-caught Atlantic cod (71 mg/3 oz serving)

  • Shrimp (69 mg/3 oz serving)

  • Organic broccoli (63 mg/1 cup serving size)

  • Organic brussel sprouts (63 mg/1 cup serving size)

*NOTE: a 3 oz serving size is about the size of a deck of cards
(Nutritional data comes from an article by the Linus Pauling Institute at Oregon State; click HERE for full article)

Choline and The Brain:

Choline is also an important component of the phospholipids that make up our neurons. Many people take sunflower lecithin or rice bran to get these phospholipids in the form of phosphatidylserine, and phosphatidylcholine. 
Choline is also an essential component of acetylcholine which is a neurotransmitter that is responsible for focus, learning, and memory. It is one of the most important neurotransmitters for learning, and it is up there with dopamine that drives motivation, and learning.

It is possible to get Citicoline, phosphatiadylserine, phosphatidylcholine, betaine, choline bitartrate, and alpha- GPC (glycerophosphocholine). Citicoline (CDP-choline) is my favorite.

CDP-Choline is Our Favorite for Brain Health

Interestingly enough, when we take the specific form of choline called CDP-choline, we see that not only do new neurons begin to grow, but also that these new neurons have more acetylcholine and dopamine receptors. 
Most of the time when we see more receptors, as in the case of stimulants like amphetamines, it takes more of a neurotransmitter like dopamine to create the same effect. However, with CDP-choline supplementation, we see the exact opposite. 
We see an increased sensitivity to these neurotransmitters which improves our ability to learn and solve problems significantly. 

What Happens to the Supplemental Choline in My Brain?

Approximately 18% of the CDP-choline is converted into acetylcholine following ingestion, and the rest is stored in our neurons as phosphatidylcholine for later use. 
It is, in my opinion, one of the best all-around brain supplements. The nucleoside uridine is also produced in the conversion process of CDP-choline in the brain. 
This nucleoside is involved in the creation of the mRNA (messenger ribonucleic acid) that tells our brain to make more neurons. 
In fact, uridine is often the rate limiting factor for these neurogenesis, and synaptogenesis reactions.

The Brain Trifecta!

This is why as a stand-alone brain supplement, CDP-choline is definitely one of the best because it converts into so many other beneficial nutrients. 

That being said, CDP-Choline is even more effective for synaptogenesis when combined with DHA (docosahexaenoic acid), and uridine monophosphate. 

Learn more from our Full Article on Synaptogenesis, and
Learn more about DHA’s Effect on the Brain here.

What Kind of Choline is Right for Me to Take?

Here we see choline becoming acetylcholine which is a neurotransmitter that helps with focus memory and learning.

We discussed before that our bodies produce choline so there is no recommended daily intake or RDI, however, we will become ill if we do not consume a certain amount. 
The Linus Pauling Institute recommends between 400-500mg per day for most adults.
There are other supplemental forms of choline like choline bitartrate and Alpha-GPC. Choline bitartrate is the cheapest form of choline. It is also the least bioavailable, and thusly less of it converts into acetylcholine.

Natural Nootropics

Alpha-GPC ( aka alpha-glycerophophorylcholine) is typically favored in the nootropic world because it has the highest conversion into acetylcholine
This makes it great for those who take nootropics like the Racetams. 
Read our 
Full Article on Nootropics here
It also upregulates human growth hormone (HGH) which makes it a great supplemental addition for athletes. However, it can also increase risk factors for prostate cancer since it alters hormone function. 
CDP-choline is our favorite as a standalone supplement and a general brain health supplement. CDP-choline has been shown to increase neurogenesis even on its own, but when combined with DHA and uridine, this becomes a nutritional powerhouse for the brain. 
CDP-choline (or Citicoline) not only produces uridine in the brain as it converts to acetylcholine, but it also increases the number of cell receptors for dopamine and acetylcholine which both help with learning, and motivation.

DHA and Our Brains [Research Mirror]


The Importance of Omega-3’s:

DHA is one of the most important omega-3 fatty acids in our diet. First off, what is an omega-3 fatty acid? There are two essential fatty acids (EFA’s) which are alpha linoleic acid (an omega-3 fatty acid), and linoleic acid (an omega-6 fatty acid). 
They are called “essential” because our bodies cannot produce them so we must acquire them from food sources. When it comes to omega-3’s, there are three main players:

  • ALA (alpha linoleic acid)

  • EPA (eicosapentaenoic acid)

  • DHA (docosahexaenoic acid)

ALA must be acquired from food sources because we can’t create it. The other two Omega-3’s are often also considered to be essential by many experts, but they are “conditionally essential” because ALA can be converted into EPA and DHA. 
The problem is that our bodies’ ability to convert ALA into EPA is typically only about 10% (depending on what study you look at), and our ability to convert  EPA into DHA is only about 1% of that initial 10%!

Love Your Liver

Additionally, this conversion occurs in the liver, and only works if your liver is functioning optimally.
Since we live in a world that we humans have filled with pollution, most people’s livers are dealing with a total crisis of contamination, so this conversion is likely even less!

DHA and Your Brain

As you will read, these fatty acids are very important for brain health, but because we technically can convert ALA into DHA and EPA, there is no officially set recommended daily intake.
In this article, we will talk about what these fatty acids do, how much to take, and some easy ways that we can supply these nutrients.

What About Vegan Sources?

ALA can be found in many vegetarian and vegan sources like flax, hemp, and chia seeds while EPA and DHA (the important conditionally essential fatty acids) are primarily found in animal foods like fatty fish and eggs. 
If you are a vegan, then I highly recommend supplementing EPA and DHA. Luckily, there is one vegan source of EPA and DHA that is cold-pressed from algae. You can find our favorite vegan omega-3 supplement (including EPA and DHA) by clicking on the image below. 

Why is DHA so special? 

First of all, it is the rarest in foods, and it is the final stage of the conversion process that Omega-3’s undergo in our bodies. If we can get an optimal amount from diet and/or supplementation, then it takes the pressure off our liver to convert other omega-3’s into DHA. 
Much of the research on Omega-3’s show DHA specifically to have the most beneficial effects on memory, and brain health. In the Chicago study (1), a strong neuroprotective effect was observed with DHA that was not seen to the same degree with EPA. 
Several studies have also shown that people with Alzheimer’s have severely low levels of DHA in key areas of the brain related to memory formation like the hippocampus (2)(3).

In another study at Rotterdam (4), it was discovered that eating even one meal per week that included fatty fish like salmon could reduce the incidence of cognitive decline and dementia by up to 60%! 
DHA also helps improve cognitive abilities in aging rats who do not have a neurodegenerative disease (5). Other studies show DHA improving cognitive abilities, and learning in healthy young rats as well (6) which means that you do not have to be sick to get better from using DHA! 
Many of these health benefits come from the antioxidant, and anti-inflammatory effects of DHA shown in the image below. However, many of the brain benefits, as you will soon see, come from the fact that it is a crucial structural component of the brain itself.

The next crucial piece of this omega-3 puzzle lies in fetal brain development and the first few years of our lives which are some of the most formative years for our brains and neurons. 
I have often stated the importance of healthy fats because our brains are about 60% fat. I also like to remind everyone that our brains consume about 25% of our total energy and nutrition even though our brains make up only a small part of our body mass. 
When we are in the womb, this energy consumption goes up to 70%! Almost all of our energy resources go to building our brain and nervous system when we are a fetus, and DHA is a crucial part of this building process.

Our Brain and Our Eyes

DHA makes up about 30% of our brain matter and approximately 50% of the retinal structure in our eyes. Adding DHA to your diet not only increases cognitive function, but it also increased visual acuity in developing humans and animals (7). 
As if this were not enough of a reason to make sure you are getting enough DHA in your diet, another study found that babies born with neurological problems had low levels of DHA, and other important fatty acids, and had elevated levels of trans fats in their brains (8).

Avoid Trans Fats and Get DHA

Humans are basically just grown up babies which is why we recommend avoiding trans fats and other inflammatory fats, and adding in anti-inflammatory fats like DHA and EPA into your diet. DHA reduces inflammation by reducing the expression of Nf-kB (Nuclear factor kappa-beta) among many other anti-inflammatory actions shown in the image below. 
Nf-kB is an inflammatory marker in our bodies that we can measure that can generally show us how much inflammation or oxidative stress is occurring in out bodies.

How Big of a Problem is This?

What’s pretty scary is that we in the United States have an imbalance of fats in our diets that is reaching epidemiological proportions. It is recommended that we eat a 1:1 ratio or at most a 1:2 ratio of omega-3 fatty acid to Omega-6 fatty acid. 
However, the average American eats between 1:16 and 1:36 ratio of Omega-3 to Omega-6. Many of us are eating too many fried foods that are cooked in rancid (oxidized) Omega-6 oils like vegetable oil, canola oil, cottonseed oil, soybean oil, and other common polyunsaturated fatty acids (PUFA’s).
In order for our bodies to properly metabolize these fats, we need a balance of them in pretty even ratios. 
Some oils like olive oil are naturally in a healthy balance of Omega-3 to Omega-6 while oils like vegetable oil are almost entirely Omega-6 fatty acids.

How Much is Enough?

The American Heart Association says that we should eat two or more servings (3.5 oz.) of fatty fish like salmon, sardines, tuna, etc. in order to support cardiovascular health, but a dietary survey of shows that most Americans eat half that amount or less. 
According to one dietary study (9), most Americans get a dose of combined EPA and DHA equalling 100-200mg per day while many experts recommend getting at least 650mg (combined EPA/DHA) per day.

This is our favorite salmon supplier: Vital Choice

Wild Alaskan Smoked Sockeye Salmon in a BPA-free can: 997 mg of Omega-3

Ventresca Tuna Bellies by Vital Choice: 3550mg total omega-3s per 1/2 can: 
EPA 840mg • DHA 2430mg

Vital Choice Meals with Wild-Caught Fish

What If You Are Deficient in Omega-3’s?

Bear in mind that this recommendation is if you are healthy, and not deficient in Omega-3’s! You may require far more under certain circumstances. 
In addition to supporting a healthy brain, Omega-3’s have also been shown to have beneficial effects on obesity, metabolic syndrome, and cardiovascular health (10).

A National Health Crisis

When we combine all of this data, we can clearly see that EPA and DHA are much more essential than we once thought, and that most people in the U.S. are not getting enough which is leading to a lot of complications. 
There was a study done at Harvard that was funded by the Center for Disease Control. It was estimated that approximately 96,000 deaths every year were caused by diseases related to omega-3 deficiency (mainly cardiovascular and neurodegenerative disease)!

Food First, Supplement Second

In our opinion getting these nutrients from your diet is the best option because there are other amazing nutrients found wrapped up in food sources of Omega-3’s that you will not get with a supplement. 
However, if you live on the go like most of us, or cannot eat fatty fish, and/or eggs for some reason, then we highly recommend getting a supplement just to cover all of your bases. Below are some of the suppliers we love for fish, and fish oil.

Vital Choice and JJ Virgin

We have taken great care to select only the highest quality fish products from pristine fisheries with very low contamination from toxins that are all too common in your average store bought fish. 
We also choose companies that fish sustainably in order protect our environment from further degradation. All of the fish oils we recommend are molecularly distilled to remove neurotoxins like mercury, and are held to international quality standards that are validated by third party laboratories.