The amino acid L-tyrosine is a precursor for several substances made in the body:

The amino acid L-tyrosine is a precursor for several substances made in the body:

  • neurotransmitters such as dopamine and norepinephrine1
  • melanins, the pigments largely responsible for skin and hair color2,3,4
  • thyroid hormones, such as thyroxine5

N-acetyl-L-tyrosine, which is converted in the body to L-tyrosine, is 20 times as soluble in water as L-tyrosine itself. For this reason, it serves as an efficient supplement for raising tyrosine levels in the body, since undissolved substances are not absorbed from the digestive tract. Our product also contains vitamin B-6 — a required cofactor for neurotransmitter synthesis.

What we can’t tell you

In the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration have adopted censorship as a method for intensifying their control over the supplement industry and its customers. Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments, even if they are, in fact, effective.

Accordingly, we will limit our discussion of N-Acetyl-L-Tyrosine to a brief summary of relevant research, and let you draw your own conclusions about what medical conditions it may be effective in treating.

Most of the medical research relating to tyrosine supplementation has been conducted using L-tyrosine itself, not acetyl-L-tyrosine. It is logical to assume, however, that the conclusions reached will apply to acetyl-L-tyrosine as well, since the latter is converted to L-tyrosine in the body. The following discussion therefore draws from studies of L-tyrosine.

Mood and depression

Chronic mild stress can cause neurotransmitter deficiencies, leading to depression or sullen moods.6,7 Tyrosine supplementation elevates neurotransmitter levels, cures certain kinds of depression,8 alleviates others,9 and can improve mood.10

Hair and skin color

Although, in theory, tyrosine supplementation should promote melanin production in human skin, no clinical studies have been performed to test this concept directly.11 On the other hand, the closely related amino acid L-phenylalanine has been shown to restore skin pigment in cases of vitiligo — a localized loss of skin pigment.12 In the body phenylalanine is converted to L-tyrosine, which suggests that L-tyrosine supplementation would have produced similar results.

Tyrosine has been tested In cats as an oral supplement in combination with phenylalanine and found to be an effective hair darkening agent.11

Melanin production in the human body can also be stimulated by certain antioxidant supplements. For example, either of the following two antioxidant regimens have been found to increase melanin in skin without UV exposure:13

  • 13 mg of beta-carotene, 2 mg of lycopene, 5 mg of vitamin E and 30 mg of vitamin C
  • 3 mg of beta-carotene, 3 mg of lycopene, 5 mg of vitamin E and 30 mg of vitamin C.

Such combinations of antioxidants may therefore be considered candidate regimens for enhancing the effects of tyrosine supplements on skin and hair pigmentation. Another supplement with a reported ability to darken the skin is piperine.14

Blood pressure

Stressful conditions often raise blood pressure. Such rises have been experimentally suppressed by L-tyrosine supplementation.10 On the other hand, chronic high blood pressure does not appear to respond to this treatment.15

Parkinson’s Disease

Acetyl-L-tyrosine is sometimes used by Parkinson’s patients to boost concentrations of the neurotransmitter dopamine in the brain, while avoiding the side effects of taking such dopamine precursors as L-dopa. A small clinical trial in the 1980s compared the use of L-tyrosine to L-dopa, and the researchers concluded that “For some patients, 3 years of L-tyrosine treatment was followed by better clinical results and many fewer side effects than with L-dopa or dopamine agonists.”16 This approach has not been followed up with further clinical studies.


Are N-Acetyl-L-Tyrosine supplements useful for the conditions and purposes mentioned above? We aren’t allowed to tell you, so you should take a look at some of the references cited here, and then decide for yourself.

ALC’s essential role in fat metabolism

Acetyl-L-carnitine (ALC) is a biochemical substance made by all organisms except bacteria. Every cell of every plant, animal, yeast, mold, mushroom, and protozoan makes acetyl-L-carnitine molecules and uses them in the extraction of energy from fats. In the body, ALC and L-carnitine are interconvertible.

ALC’s essential role in fat metabolism

Cells are constantly breaking down fat molecules and making new ones. This is how cells

  • maintain and repair their internal and external membranes;
  • adjust the structure of these membranes in response to changing conditions;
  • take advantage of the energy contained in dietary fats.

A fat molecule typically consists of three fatty acids bonded to a glycerol bridge. The process of breaking down fats starts with enzymes that pull the fatty acids off of their glycerol bridges. The free fatty acids are then sent to subcellular organelles called ‘mitochondria’ for further processing.

Mitochondria, however, are bounded by a protective barrier — a double membrane that prevents inappropriate molecules from entering and disrupting the specialized processes that take place inside. Even appropriate molecules may require assistance in passing through this barrier. In particular, many of our dietary fatty acids (the longer-chain ones) are unable to enter a mitochondrion in their free form.

To enable long-chain fatty acids to pass through this barrier, cells ‘tag’ them with a carrier substance called ‘L-carnitine’ — an enzyme attaches a molecule of L-carnitine to each fatty acid. A transporter protein in the inner membrane will now recognize the carnitine-fatty-acid construct and allow it to pass through the membrane into the interior of the mitochondrion.

Once a fatty acid molecule is inside the mitochondrion, its L-carnitine tag is stripped off and the fatty acid is taken up by a processing complex that breaks it into small pieces, exposes the pieces to oxygen atoms, and siphons off the energy released during the resulting chemical reactions, storing it for future use.

What happens to the L-carnitine tags? Some of them are directly transported back out through the mitochondrial membranes into the cell-at-large; these are now ready to transport more fatty acid molecules into the mitochondria. Others of the L-carnitine molecules are converted to acetyl-L-carnitine which is efficiently ferried out of the mitochondria by membrane proteins. Thus, acetic acid molecules use L-carnitine to ‘hitch a ride’ out of the mitochondria so that they can be used in the many ‘acetylation’ processes that take place in cells. Once outside the mitochondria, acetyl-L-carnitine can be deacetylated back to L-carnitine for reuse as a fatty acid transporter.

What we can’t tell you

In the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration have adopted censorship as a method for intensifying their control over the supplement industry and its customers. Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments, even if they are, in fact, effective.

Accordingly, we will limit our discussion of Acetyl-L-Carnitine to a brief summary of relevant research, and let you draw your own conclusions about what medical conditions it may be effective in treating.

ALC as a treatment for aging: the theory behind it38

‘Aging’ is a catch-all term that covers many different medical ailments — weakening bones, muscles, and skin; stiffening blood vessels and connective tissue; failing memory, cognition, and sensory organs; loss of cancer suppression; etc. Thousands of medical names have been given to different variations of these ailments — names such as ‘osteoporosis, arthritis, Alzheimer’s, atherosclerosis, pancreatic cancer, macular degeneration, etc. But these age-related ailments share some fundamental causes, such as:

  • structural damage by free radicals inside and outside of cells
  • protein damage from cross-linking sugars
  • growing numbers of incorrectly regulated genes
  • skewed proportions of molecules in biological membranes
  • biochemical feedback loops that stray from stable patterns.

These (and several other fundamental causes of aging) take place throughout the body, and they affect all the structures inside and outside the cells. Among the structures they affect are the mitochondria — the subcellular organelles that extract energy from fats and carbohydrates. As mitochondria extract energy from these substances, they store the energy in the form of ATP molecules, which are distributed to all parts of all cells in the body.

As cells age, their mitochondria age. The mitochondrial membranes develop skewed proportions of the various molecules they are made of — particularly the lipid molecules which are made from fatty acids. This disrupts the functions of complex nanomachinery which resides in the membranes. Some of these nanomachines transport molecules into and out of the mitochondria; others perform the actual extraction of energy from broken-down fats and carbohydrates, and channel this energy into the production of molecules of ATP.

Thus, a skewed membrane composition causes disrupted nanomachine function, which leads to a defective transport of raw materials and to a decline in ATP production. As the transport system fails and the wrong kinds of molecules are allowed into the mitochondria, the composition of the membranes becomes even more skewed. The energy-extracting nanomachines are forced into non-optimal positions in the membranes and they become less efficient; an increasing percentage of the energy they produce is wasted instead of being stored; and the mitochondria, and the cells they belong to, become starved for energy. The wasted energy is simply dissipated as heat instead of being used for maintaining biological structures and for enabling damaged cells to be replaced.

The current view is that ALC supplementation increases the amount of L-carnitine available for tagging fatty acids in cells. This, in turn, alters the distribution of fatty acids transported into mitochondria. A better fatty acid mix restores the proper proportions of lipid molecules in the mitochondrial membranes. With an improved membrane environment, the nanomachines embedded in the membranes perform better. As a result, the efficiency of energy production in mitochondria is enhanced, enabling more of the energy extracted from food to be stored as ATP instead of being wasted as heat. The subject is too complex to describe here in more detail than this, but the ‘bottom line’ is that ALC rejuvenates mitochondria, and the boost in useful energy that results from this enables cells to behave more youthfully, too.

Potential uses of ALC

Since ALC plays a central role in the production of energy in cells of all kinds, an increase in ALC availability would be expected to ameliorate many different kinds of ailments that involve cellular energy deficiency or impaired fat metabolism. Athletic individuals could reasonably expect that ALC consumption would lead to accelerated fat metabolism and increased endurance during exercise.

But ALC also has effects that seem to be independent of its involvement in energy production. For example, ALC enhances the production of the neurotransmitter acetylcholine, it stimulates the synthesis of protein, and it affects the fluidity of biological membranes. The mechanisms are poorly understood, but we can nevertheless exploit them to alter the performance of our bodies and minds.

Medical conditions which have responded well to ALC supplements include:

  • Alzheimer’s, Parkinson’s, and other neurodegenerative diseases2,3
  • Hepatic neuropathy and encephalopathy4,5
  • macular degeneration6
  • HIV-related lipodystrophy7
  • increased fat metabolism and endurance during exercise8
  • diabetes and diabetic neuropathy1,9,10
  • Peripheral neuropathy due to HIV or cancer chemotherapy1,11
  • high blood pressure41
  • recovery from heart attacks42
  • recovery from strokes12
  • age-related memory decline13,14
  • low libido and erectile dysfunction15
  • MS-related fatigue16
  • noise-induced hearing loss17,18
  • Peyronie’s disease19
  • Rett syndrome cardiac failure20
  • Nerve injury21
  • Peripheral neuropathy1,21
  • fibromyalgia22
  • eye-lens stiffening23
  • depression24

Several of these ALC applications have been receiving much attention recently. Let’s look briefly at these.

Alzheimer’s and Parkinson’s

The first clinical study of ALC for treating Alzheimer’s Disease was reported in 1983.25 Wouldn’t you think that by now, a quarter of a century later, the medical world would have settled the question of whether or not this substance should be a standard weapon against this disease? Well, it hasn’t, for reasons that are controversial. Cynics claim that the medical profession downplays all dietary supplements because physicians are being bribed by the makers of prescription drugs. Others claim that mainstream medicine shies away from supplements because they give inconsistent results in human clinical trials — and that these trials of supplements are conducted sloppily, on low budgets, in contrast to prescription drugs, which are tested in high-budget trials.

Be that as it may, many studies of ALC in cell culture, lab animals, and in humans have demonstrated unequivocal anti-Alzheimer’s effects. As summarized in one medical review, “improvements were noted in spatial learning tasks, timed tasks of attention, discrimination-learning tasks, and tasks of personal recognition.”2

Several mechanisms have been suggested through which ALC produces its anti-Alzheimer’s effects. These include anti-oxidant action,26 prevention of apoptosis (cell-death by caused by signalling molecules)26, and prevention of toxicity due to amyloid proteins.27

ALC has received attention from Parkinson’s researchers, too.28,29 The beneficial action of ALC in Parkinson’s Disease has been shown both in animal models30 and in humans.3 The mechanisms suggested by researchers to explain the anti-Parkson’s effects are vague and involve preventing oxidative damage.28

Brain rejuvenation and nerve repair

ALC enhances the effects of the Nerve Growth Factor — a substance made in the nervous system that stimulates nerve growth. Tissue culture and lab animal experiments show that ALC causes heightened production of the receptor with which nerve cells detect and respond to Nerve Growth Factor. This results in faster repair of damaged nerve cells31 and the replacement of brain neurons that have been lost through trauma or aging.32

Blood pressure and heart protection

Two potential cardiovascular benefits of ALC supplementation were recently shown in clinical studies. First, a significant lowering of blood pressure was seen in patients with coronary artery disease who were given combination of ALC with alpha-lipoic acid for 8 weeks.41 And second, it was found that heart attacks will cause less damage to the heart if the subjects (lab animals, in these studies) have been treated with ALC a few hours prior to the attacks.42


It is often stated by promoters of acetyl-L-carnitine that, for use as a supplement, this form of carnitine is superior to L-carnitine itself because it has a higher bioavailability. However, the absolute oral bioavailability of acetyl-L-carnitine has not been determined in humans. It may well be higher than that of L-carnitine (which varies dramatically and inversely with dosage33). Regardless of what the percentage bioavailability of ALC turns out to be, it does what we want it to do: it raises blood concentrations of ALC, making more of it available to cells throughout the body. In fact, 2 g/day of an oral ALC supplement will increase blood levels to 143% of the pre-dose value.34

Furthermore, ALC readily crosses the blood-brain-barrier.35,36 Its measurable effects on energy production and on neurotransmitter production in nerve cells have inspired numerous studies of its ability to reverse the mental symptoms of aging and neurodegenerative diseases.37

Dosages and co-supplements

Oral dosages of 1-3 g/day have been used in clinical trials for the medical conditions for which ALC has been studied. In Alzheimer’s studies, for example, a typical dosage would be 500 mg taken three times per day.36 Much higher doses have been studied informally as an anti-aging treatment, with no apparent ill effects.39

Since acetyl-L-carnitine enhances mitochondrial energy production, and since destructive free radicals are always a by-product of this process, it is important to scavenge these free radicals before they can damage the mitochondria and other cellular structures. The standard way to accomplish this scavenging is to use a second supplement — the antioxidant alpha-lipoic acid.40 A reasonable dosage would be 100 mg of alpha-lipoic acid three times per day.

Anyone who is considering the use of ALC for treating or preventing Alzheimer’s, Parkinson’s, or other neurodegenerative disease, should also consider the simultaneous use of a curcumin-containing product like LifeLink’s Primeric™. The mechanism of action of curcumin is unrelated to that of ALC, which means that the combination may benefit from synergism.


Are Acetyl-L-Carnitine supplements useful for the conditions and purposes mentioned above? We aren’t allowed to tell you, so you should take a look at some of the references cited here, and then decide for yourself.

NAC’s remarkable biological benefits

N-acetylcysteine (NAC) is a substance which is converted in the body to the amino acid L-cysteine. For reasons that are poorly understood, L-cysteine itself is neurotoxic when taken as a supplement; this toxicity is avoided by using NAC instead.1

L-cysteine, like the other standard amino acids, is a building block for the production of countless proteins needed by the body: enzymes, structural proteins, signalling molecules and their receptors, and a number of small polypeptide molecules with specialized functions. One such polypeptide is the tripeptide called ‘glutathione’ (GSH), a very important antioxidant that protects cells from being damaged or killed by certain metabolic byproducts.2

While NAC supplementation undoubtedly provides the body with all the benefits that derive from L-cysteine, the principal reason it is used as a supplement is to raise glutathione levels.


A good review of NAC and its medical applications is the one by Thorne Research3. Since NAC is a precursor for the body’s production of glutathione, Wikipedia’s article on glutathione2 is relevant for understanding why NAC has such a broad range of actions. The review by Arakawa and Ito4, of NAC’s value in preventing or treating neurodegenerative diseases, also makes good reading. A technically written review of what is known about NAC’s mechanisms of action is found in the article by Zafarullah, et al.5

What we can’t tell you

In the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration have adopted censorship as a method for intensifying their control over the supplement industry and its customers. Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments, even if they are, in fact, effective.

Accordingly, we will limit our discussion of N-acetylcysteine to a brief summary of relevant research, and let you draw your own conclusions about what medical conditions it may be effective in treating.

NAC’s remarkable biological benefits

NAC is one of the most studied of all supplements. Interest in it began during the 1960s when it was found to be useful as a ‘mucolytic’ agent — i.e., it lowers the viscosity of mucus in the respiratory tract, assisting people with cystic fibrosis and other pulmonary ailments.6 In the early 1990s medical researchers took a strong interest in it as an anti-HIV treatment,7 and it has been in the spotlight ever since.

The list of medical applications of NAC is a very long one, as can be seen from the outline that follows.

Pulmonary and respiratory ailments:

  • acute respiratory distress syndrome (ARDS)8
  • asthma9
  • bronchitis10
  • emphysema
  • Chronic Obstructive Pulmonary Disease (COPD)11,12,10,13,14,15
  • ideopulmonary fibrosis16,17,18,19
  • cystic fibrosis6,20

Accelerated aging:

  • diabetes-related or Alzheimer’s-related tissue aging21
  • mitochondrial aging22

Neurodegenerative diseases:4,23

  • Amyotrophic Lateral Sclerosis (ALS)24
  • multiple sclerosis25
  • Alzheimer’s26,27,28,29
  • diabetic neuropathy30
  • diabetic retinopathy31
  • amlyoid-related brain cell loss
  • adrenoleukodystrophy32

Other neurological conditions:

  • bipolar disorder33
  • depression33
  • autism33
  • attention deficit hyperactivity disorder33
  • memory loss27
  • hearing loss34
  • chronic fatigue syndrome35
  • pain36
  • brain damage from stroke37
  • myclonus epilepsy38

Muscle-degenerative conditions:

  • Duchenne muscular dystrophy39
  • age-related muscle loss40


  • oxidation-related cancer41
  • anti-angiogenesis therapy42
  • prostate cancer43
  • tobacco-related lung cancer44
  • chemotherapy damage to lungs45

Cardiovascular ailments:

  • atherosclerosis46
  • high homocysteine levels47
  • artery damage from tobacco smoke48
  • blood clots49
  • impaired heart function after heart attack50
  • sclerodermic Raynaud’s phenomenon51
  • kidney-related cardiovascular disease52


Immune system problems:

  • immune suppression58
  • Sjögren’s syndrome59
  • systemic inflammation


  • malaria60
  • HIV7
  • influenza61
  • hepatitis C62,63
  • ulcers due to Helicobacter pylori64
  • bacterial infections with systemic inflammation65
  • sepsis66,67


  • acetaminophen (Tylenol®) overdoses68
  • mushroom poisoning69
  • zinc-related neurotoxicity70

Other applications:

  • diabetes71,21
  • cysteine/glutathione deficiency72
  • muscle fatigue73,74
  • non-alcholic fatty liver disease75,76,77
  • sickle cell disease78

These are far too many applications to discuss in detail, so let us just look at one of them, as an example of the medical power of this supplement: the prevention of vascular damage caused by dietary AGEs — chemicals created in food by cooking.

NAC interferes with cardiovascular damage

Whenever food is cooked, some of the sugars in the food are converted into substances called ‘AGEs’ (Advanced Glycation Endproducts).79 These are inflammatory chemicals that, when consumed, cause damage to the walls of arteries and veins, as well as accelerated aging in other tissues in the body. The body actually produces its own AGEs, but usually in smaller amounts than are found in the diet. Diabetics, however, often have higher levels of sugar in their blood, and so AGEs are produced in larger amounts in these people. The total AGE burden is therefore much higher in diabetics.

In an important 2004 paper, researchers at Mount Sinai School of Medicine showed that diabetics experience substantially less damage to arteries when their consumption of AGEs is reduced.21 The research also showed that NAC interferes with a key process through which AGEs produce inflammation and tissue damage. Interestingly, this research project was motivated by the idea that atherosclerosis can be prevented by reducing dietary AGEs, not the idea that NAC can be used to counteract the effects of high AGE consumption. Yet NAC did, in fact, prevent AGEs from damaging vascular cells.

This is just one example of NAC’s far-ranging effects on harmful processes taking place in the body. NAC is an inexpensive supplement that is safe and easy to obtain — so it would be foolish not to take advantage of it.


Are N-acetylcysteine supplements useful for the conditions and purposes mentioned above? We aren’t allowed to tell you, so you should take a look at some of the references cited here, and then decide for yourself.

Imagine If Everything You Knew about Aging Was Wrong!

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The Mysterious Virus That Could Cause Obesity

Randy is 62 years old and stands tall at six foot one. He grew up on a farm in Glasford, Illinois, in the 1950s. Randy was raised with the strong discipline of a farming family. From the time he was five, he would get out of bed at dawn, and before breakfast he’d put on his boots and jeans to milk cows, lift hay, and clean the chicken coops. Day in and out, no matter the weather or how he felt, Randy did his physically demanding chores. Only when his work was complete would he come into the kitchen for breakfast.

Tending to the chickens was hard work—it involved getting into the pen, clearing birds out of their dirty cages, and shooing them into a holding enclosure. This process was always a little scary because the animals could be quite aggressive after being cooped up all night. On one of these occasions, when Randy was 11, a particularly large and perturbed rooster swung its claw and gave him a good spurring on his leg. Randy felt the piercing of his skin and squealed in pain. He said it felt like being gored by a thick fishhook. The rooster left a long gash, and blood streamed down Randy’s leg to his ankle. He ran back to the house to clean the wound, as chickens are filthy after a night in their cages.

Excerpted from The Secret Life of Fat: The Science Behind the Body’s Least Understood Organ and What It Means for You by Sylvia Tara.W. W. Norton & Company

Some days later, Randy noticed a change in his appetite. He was constantly hungry. He felt drawn to food and thought about it all the time. He started eating in between meals and overeating when he finally sat down to dinner. Randy had always been a skinny kid, but in the course of the next year, he gained about 10 pounds. His parents thought it might be puberty, though it seemed a little early. His pudginess was also unusual given that everyone else in the family was thin. Randy was no stranger to discipline. He forced himself to eat less, switched to lower-calorie foods and exercised more. But by the time he was a teenager, he was bouncing between 30 and 40 pounds overweight. He says, “I gained all of this weight even though these were some of my most active years on the farm.”

Randy’s family supported his efforts to control his weight. They made lower-calorie foods, gave him time to exercise, and didn’t pressure him to eat things he didn’t want. However, he continued to struggle with his weight through college. Randy kept thinking back to the moment everything changed. He had been the skinniest kid among his friends. And then he got cut by that chicken.

The Curious Case of Indian Chickens

In Mumbai, India, Nikhil Dhurandhar followed his father Vinod’s footsteps in treating obesity. But Nikhil ran into the same obstacle that had bedeviled obesity doctors everywhere. “The problem was that I was not able to produce something for patients that could have meaningful weight loss that was sustainable for a long time,” he says. “Patients kept coming back.”

Fate intervened in Dhurandhar’s life one day was when he was meeting his father and a family friend, S. M. Ajinkya, a veterinary pathologist, for tea. Ajinkya described an epidemic then blazing through the Indian poultry industry killing thousands of chickens. He had identified the virus and named it using, in part, his own initials—SMAM-1. Upon necropsy, Ajinkya explained, the chickens were found to have shrunken thymuses, enlarged kidneys and livers, and fat deposited in the abdomen. Dhurandhar thought this was unusual because typically viruses cause weight loss, not gain. Ajinkya was about to go on, but Dhurandhar stopped him: “You just said something that doesn’t sound right to me. You said that the chickens had a lot of fat in their abdomen. Is it possible that the virus was making them fat?”

Ajinkya answered honestly, “I don’t know,” and urged Dhurandhar to study the question. That fateful conversation set Dhurandhar on a path to investigate as part of his PhD project whether a virus could cause fat.

Dhurandhar pushed ahead and arranged an experiment using 20 healthy chickens. He infected half of them with SMAM-1 and left the other half uninfected. During the experiment, both groups of chickens consumed the same amount of food. By the end of the experiment, only the chickens infected with the SMAM-1 virus had become fat. However, even though the infected chickens were fatter, they had lower cholesterol and triglyceride levels in their blood than the uninfected birds. “It was quite paradoxical,” Dhurandhar remembers, “because if you have a fatter chicken, you would expect them to have greater cholesterol and circulating triglycerides, but instead those levels went in the wrong direction.”

To confirm the results, he set up a repeat experiment, this time using 100 chickens. Again, only the chickens with the SMAM-1 virus in their blood became fat. Dhurandhar was intrigued. A virus, it seemed, was causing obesity. Dhurandhar thought of a way to test this. He arranged three groups of chickens in separate cages: one group that was not infected, a second group that was infected with the virus, and a third group that caged infected and uninfected chickens together. Within three weeks, the uninfected chickens that shared a cage with infected ones had caught the virus and gained a significant amount of body fat compared to the isolated uninfected birds.

Fat, it seemed, could indeed be contagious.

Now, Dhurandhar is a man of science. He is rational and calm. But even he had to admit that the idea was startling. Does this mean that sneezing on somebody can transmit obesity? This now seemed possible in animals, but what about humans? Injecting the virus into people would be unethical, but Dhurandhar did have a way to test patients to see if they had contracted the virus in the past.

Dhurandhar says, “At that time I had my obesity clinic, and I was doing blood tests for patients for their treatment. I thought I might just as well take a little bit of blood and test for antibodies to SMAM-1. Antibodies would indicate whether the patient was infected in the past with SMAM-1. The conventional wisdom is that an adenovirus for chickens does not infect humans, but I decided to check anyway. It turned out that 20 percent of the people we tested were positive for antibodies for SMAM-1. And those 20 percent were heavier, had greater body mass index and lower cholesterol and lower triglycerides compared to the antibody-negative individuals, just as the chickens had.” Dhurandhar observed that people who had been infected with SMAM-1 were on average 33 pounds heavier than those who weren’t infected.

The Pounds Keep Coming

While Nikhil Dhurandhar was in India pursuing his curiosity about fat, Randy was looking for solutions of his own. After a brief stint as a teacher he moved back to the family land in 1977 because he loved farming.

Randy married and had four children. At family dinners and holiday gatherings, he ate alongside everyone else, but tried eating less than the others. Still, his weight ballooned; by his late 30s he had topped 300 pounds. He remembers feeling hungry all the time, though even when he abstained it didn’t help him lose weight. “I could have several good weeks of eating stringently, much less than others around me, but if I went off my diet for just one meal—boom, the weight would come back.”

The effort to control his eating, even when it was successful, made Randy miserable: “I can’t tell you what it is like to be hungry all the time. It is an ongoing stress. Try it. Most people who give advice don’t have to feel it.”

In the fall of 1989, Randy applied for a commercial driver’s license. The application required a medical exam. After his urine test, the nurse asked Randy if he felt all right. “Normal for the day,” he replied. But the nurse told Randy he would have to give a blood sample because she thought the lab had spilled glucose solution into his urine sample. The blood work showed that Randy’s glucose level was near 500 mg/dL (a normal reading is 100). The lab hadn’t made a mistake with the urine sample after all; Randy’s numbers were just off the charts. Alarmed, the nurse notified Randy’s doctor, who then tested him for fasting blood sugar levels. The results showed that Randy had insulin resistance and severe diabetes.

At 40 years old and 350 pounds, Randy was in trouble. If he didn’t fix this problem soon, he would start to develop serious complications of diabetes, including cardiovascular disease and nerve damage.

Having tried and failed multiple diets, Randy and his doctor decided the best hope was a hospital program for severe diabetics. The staff tested Randy’s blood frequently to determine the optimal dosage and timing of insulin injections to regulate his blood sugar. Randy learned about the Diabetic Exchange diet, which allots patients a specific number of servings of meat, carbohydrates, vegetables, and fat. He cut out all refined carbohydrates, including bread. He says, “I haven’t had a slice of bread or piece of pizza in years.”

But would even this program be enough? Randy had always had a difficult time controlling his weight, though not for lack of trying. He had been fighting fat since his childhood by controlling portions, exercising, and avoiding social eating. But his discipline was no match for his own fat. Randy had to get his weight under control permanently. The hospital environment was helpful. However, despite strictly adhering to the diet, he only dropped a few pounds.

The Virus in Americans

After taking on a postdoctoral fellowship at the University of Wisconsin, Madison under Dr. Richard Atkinson, Dhurandhar was excited to finally be at liberty to pursue what he loved. He had an intense curiosity about viruses and was eager to get started finding answers. However, when he tried to get samples of the SMAM-1 virus that he had worked with in India, the U.S. Department of Agriculture refused to grant him an import license. He was deeply disappointed.

Unable to get SMAM-1, Dhurandhar approached a company that sells viruses for research. Their catalog listed some fifty human adenoviruses. He says, “I was going to order the human adenovirus, but there was no the adenovirus—there were 50 different human adenoviruses! So I was stuck again. I wondered how do I go about this? Should we start number one, number two, number three, number 50, 49, 48? So [with] a little bit of guesswork and mostly luck, we decided to work with number 36. We liked number 36 because it was antigenically unique—meaning it did not cross react with other viruses in the group, and antibodies to other viruses would not neutralize it.”

That was a serendipitous choice. It turned out that Ad-36 had similar qualities to SMAM-1 in chickens. Atkinson thought Ad-36 might very well be a mutated form of SMAM-1. When Dhurandhar infected chickens with Ad-36, their fat increased and their cholesterol and triglycerides decreased, just as had happened with SMAM-1. Dhurandhar wanted to make sure he was not getting a false positive, so he injected another group of chickens with a virus called CELO to ensure that other viruses were not also producing fat in chickens. Additionally, he maintained a group of chickens who had not been injected with anything. When he compared the three groups, only the Ad-36 group became fatter. Dhurandhar then tried the experiments in mice and marmosets. In every case, Ad-36 made animals fatter. Marmosets gained about three times as much weight as the uninfected animals, their body fat increasing by almost 60 percent!

Now came the big question: would Ad-36 have any effect on humans? Dhurandhar and Atkinson tested over 500 human subjects to see if they had antibodies to the Ad-36 virus, indicating they had been infected with it at some point in their lives. His team found that 30 percent of subjects who were obese tested positive for Ad-36, but only 11 percent of nonobese individuals did—a 3 to 1 ratio. In addition, nonobese individuals who tested positive for Ad-36 were significantly heavier than those who had never been exposed to the virus. Once again, the virus was correlated with fat.

Next, Dhurandhar devised an even more stringent experiment. He tested pairs of twins for presence of Ad-36. He explains, “It turned out exactly the way we hypothesized—the Ad-36 positive co-twins were significantly fatter compared to their Ad-36 negative counterparts.”

Of course, it’s unethical to infect human subjects with viruses for research, so the study can’t be perfectly confirmed. But, Dhurandhar says, “This is the closest you can come to showing the role of the virus in humans, short of infecting them.”

A New Way to Manage Fat—Stop the Blame

Randy’s physician had been treating him for years and knew that his patient’s struggle was difficult and ongoing. The physician referred Randy to an endocrinologist—Richard Atkinson at the University of Wisconsin—who was having some success with difficult obesity cases.

Randy went to see Atkinson, knowing that if he didn’t get his fat under control, it was going to kill him. The first thing Randy noticed about Atkinson was that he was kind. He didn’t make Randy feel guilty about his weight. “Other places put the blame on you,” Randy says. “They go back into your past, what did you do to get here. It is very judgmental. Atkinson did none of that. He said okay we are here now, how do we fix it? He was very future oriented.”

Atkinson had designed a long-term program to treat obesity. He explained to his patients that obesity is a chronic disease and they would be in treatment “forever.” In the first three months of the program, patients would meet several days per week and attend a lecture explaining obesity and the underpinnings of fat. After that, visits decreased to one every one to two weeks, then one every one to two months. Those who started regaining weight were asked to resume more frequent visits. Subjects had to commit to the full program in order to enroll.

Atkinson also introduced Randy to his new postdoctoral assistant, a young scientist from India, Dr. Nikhil Dhurandhar. Dhurandhar examined Randy and studied his blood samples. Randy tested positive for antibodies to Ad-36, meaning he had likely been infected with the virus at some point in the past. Randy remembered being scratched by that rooster as a child, and that afterward his appetite exploded and he started gaining weight quickly. His troubles with food and rapid fat accumulation—he understood it all now. If he was like the chickens, the marmosets, the twins, and the other humans in the study, then his infection with Ad-36 was helping his body to accumulate fat. He says, “What Atkinson and Dhurandhar did for me changed my life. They made everything make sense. It was very liberating and very empowering.”

How Does a Virus Lead To Fat?

How would a virus like Ad-36 cause fat? Atkinson explains, “There are three ways that we think Ad-36 makes people fatter:
(1) It increases the uptake of glucose from the blood and converts it to fat; (2) it increases the creation of fat molecules through fatty acid synthase, an enzyme that creates fat; and (3) it enables the creation of more fat cells to hold all the fat by committing stem cells, which can turn into either bone or fat, into fat. So the fat cells that exist are getting bigger, and the body is creating more of them.”

The researchers acknowledge that the rooster scratch may have been the start of Randy’s infection. But they are cautious—the transmissibility of Ad-36 from chickens to humans has never directly been studied.

Though Dhurandhar and Atkinson have conducted several strong studies showing the contribution of Ad-36 to fatness, skepticism remains. Atkinson says, “I remember giving a talk at a conference where I presented 15 different studies in which Ad-36 either caused or was correlated to fatness. At the end of it, a good friend said to me, ‘I just don’t believe it.’ He didn’t give a reason; he just didn’t believe it. People are really stuck on eating and exercise as the only contributors to fatness. But there is more to it.”

Dhurandhar adds, “There’s a difference between science and faith. What you believe belongs in faith and not in science. In science you have to go by data. I have faced people who are skeptical, but when I ask them why, they can’t pinpoint a specific reason. Science is not about belief, it is about fact. There is a saying—‘In God we trust, all others bring data.’”

Reprinted with permission from The Secret Life of Fat by Sylvia Tara. Copyright 2016 by W. W. Norton & Company.

Why the Blood-Brain Barrier Is So Critical (and How to Maintain It)

blood_brain_barrierYou all know about intestinal permeability, or “leaky gut.” The job of the gut lining is to be selectively permeable, allowing helpful things passage into the body and preventing harmful things from getting in. Nutrients get through, toxins and pathogens do not. Leaky gut describes the failure of this vetting process. But what about “leaky brain”?

A similarly dynamic barrier lies between the brain and the rest of the body: the blood-brain barrier. Since the brain is the seat of all the conscious machinations and subconscious processes that comprise human existence, anything attempting entry receives severe scrutiny. We want to admit glucose, amino acids, fat-soluble nutrients, and ketones. We want to reject toxins, pathogens, and errant immune cells. Think of the blood-brain barrier like the cordon of guards keeping the drunken rabble from spilling over into the VIP room in a nightclub.

The blood-brain barrier (or BBB) can get leaky, just like the gut lining. This is bad.

A compromised BBB has been implicated in many neurodegenerative diseases, like Alzheimer’s, Parkinson’s, and vascular dementia.

More generally, the BBB regulates passage of inflammatory cytokines into the brain, prevents fluctuations in serum composition from affecting brain levels, and protects against environmental toxins and infectious pathogens from reaching the brain. A leaky BBB means the floodgates are open for all manner of unpleasantries to enter the brain.

Some pathogens even wield chemical weaponry that blasts open the blood-brain barrier, giving them—and anything else in the vicinity—access to the brain. To prepare for that, you must support the integrity of your blood-brain barrier.


Optimize your B vitamin intake

In adults with normal B vitamin levels, mild cognitive impairment, high homocysteine levels, and a leaky BBB, taking vitamins B12, B6, and B9 (folate) restored the integrity of the blood-brain barrier.

Review this post and make sure you’re getting the B vitamins you need. Primal folks tend to overlook them.

Nourish your gut

A leaky gut accompanies, and maybe causes, a leaky brain. Funny how that works, eh?

It’s a rodent study, but it’s quite illustrative: a fecal transplant from healthy mice with pristine BBB integrity to unhealthy mice with leaky BBB and pathogen-filled guts restored the integrity of the blood-brain barrier.

DIY fecal transplants are an extreme intervention. Until that becomes more feasible, simply eating more prebiotic fiber, experimenting with resistant starch, taking a quality probiotic, and eating fermented foods on a regular basis will get you most of the way there.

Eat plenty of magnesium

Okay, Sisson. Enough already with the magnesium. We get it! But magnesium can attenuate BBB permeability, even if you inject an agent explicitly designed to induce leaky blood-brain barriers.

This is yet another reason to eat enough magnesium-rich foods (like spinach, almonds, blackstrap molasses, winter squash), drink magnesium-rich mineral water (I love Gerolsteiner, but you can also just go down to the local Euro food market and check the labels for high-Mg waters), or take a good magnesium supplement (anything ending in “-ate” like magnesium glycinate or citrate).

Don’t eat a 40% cocoa butter diet

Rodents given a 40% saturated fat (from cocoa butter) diet experienced elevated BBB permeability.

Except wait: The remaining 60% of calories was split up between white sugar, wheat starch, casein, and dextrin (PDF). So this isn’t the type of 40% SFA diet you folks are eating.

Except wait again: Adding in either aged garlic extract, alpha lipoic acid (ALA), niacin, or nicotinamide completely abolished the increase in permeability.

It looks like a refined diet high in saturated fat and sugar/starch and absent any phytonutrient-rich plant foods like garlic or antioxidant supplements like ALA will cause elevated BBB permeability (in rodents). I’m not sure I’d recommend a 40% SFA diet either way, however. Balance is probably better.

Use phytonutrient-rich plants and spices

Recall the study from the last section where some garlic extract was enough to eliminate the bad BBB effects of a refined lab diet. That’s because aged garlic extract is particularly rich in phytonutrients with strong antioxidant effects. What about other fruits, vegetables, and spices with different phytonutrients—do those also help BBB function?

Curcumin (from turmeric) certainly helps. Astragalus root, used in many ancient medical traditions, can help. Sulforaphane, from cruciferous veggies like broccoli, Brussels sprouts, and cabbage, shows promise.

Drink coffee and/or tea

As phytonutrient-rich plants, they technically belong in the previous section, but coffee and tea are so special that they deserve their own space. Both are sources of caffeine, a noted protector of BBB integrity.

Supplements can help

Supplement forms of the aforementioned nutrients are worth a look. Also:

Alpha-GPC (a type of choline that readily crosses the blood-brain barrier) has been shown to reduce BBB permeability in hypertensive rats.

Inositol (which you can get from foods like egg yolks but not in very large amounts) improves BBB integrity. Another option is to consume phytate-containing foods; if you’ve got the right gut bacteria, you can convert phytate into inositol.

Berberine, noted anti-diabetic compound, reduces BBB permeability and increases resistance to brain damage following head trauma.

Control your blood pressure

Both acute and chronic hypertension increase BBB permeability. This means you’ll have to control your sleep and stress. You’ll need to reduce insulin resistance. Eat dark chocolate (the horror). Figure out if you’re salt-sensitive (you may even have to increase salt intake if it’s too low). Get enough magnesium (yes, again) and potassium.


Sleep really is everything. You can’t avoid it, and if you skimp on it, things fall apart. The blood-brain barrier is no exception: sleep restriction impairs BBB function and increases permeability.

If you can’t stick to the bedtime you know is ideal, a little (0.25-0.5mg) melatonin can help set your circadian rhythm. Plus, supplementary melatonin may also preserve BBB integrity.

Don’t drink too much alcohol

Alcohol is a tough one. While I just wrote a big post explaining the merits of wine consumption, ethanol is undoubtedly a poison in high doses, and I derived real benefits when I gave it up for a few months. One way alcohol exerts its negative effects is by inducing BBB dysfunction. This allows both the pleasant effects of alcohol (low-dose ethanol migrating across the BBB and directly interacting with neurons, triggering endorphins and interacting with GABA receptors) and the negative effects (high-dose ethanol migrating across the BBB to damage the neurons, leaving the door open long enough for immune cells to sneak in and cause all sorts of trouble).

Stimulate your vagal nerve

After a traumatic brain injury or stroke, the resultant increase in BBB permeability floods the brain with inflammatory cytokines, causes swelling and neuronal death, and worsens the prognosis. Stimulating the vagal nerve after such an injury decreases the BBB permeability and improves the prognosis.

One treatment for epilepsy is to wear vagal nerve stimulators which send light electronic pulses to the nerve, akin to a pacemaker for the brain. Easier options include humming, cold water exposure (even just splashing the face can help), singing, chanting, meditating, deep breathing, coughing, moving your bowels (or summoning the same abdominal pressure required for said movement; girding your core for a heavy squat or deadlift should also work along the same lines), and many more.

Perhaps an entire post on the vagal nerve is in order. It’s an interesting area that impacts more than just the BBB.

Stop eating so often

Ghrelin is the hunger hormone. When you haven’t eaten in a while, ghrelin tells you that it’s time to eat. It also increases blood-brain barrier stability after (again) a traumatic brain injury.

So, never eat? No. But make sure to feel actual hunger. It’s the best spice, and it confers a whole host of other benefits, including better blood-brain barrier function. Heck, try intermittent fasting for the ultimate boost to ghrelin.

You might notice that a lot of the studies I cite involve traumatic brain injuries to rodents. Dropping a weight on a rat’s head or triggering a stroke in a mouse are two of the most reliable ways to induce BBB permeability. Brain injuries are also quite common in humans, and the BBB permeability that results is a major therapeutic target, but we can’t study it so easily in people. While acute and chronic BBB permeability are different beasts, and mice are not men, they operate along the same rough pathway.

That’s about it for today, folks. I hope you feel encouraged and able to fortify your blood-brain barrier. Don’t wait for cognitive decline to set in. Get started now.

How do you improve the integrity of your blood-brain barrier? Have you even considered it prior to today?


Aging Now a Disease? Humanity Should Treat It Like One, Scientist Says

Scientists are starting to reconsider our major preconception about aging. Is it really a natural phenomenon or a disease that could be treated?

It may be helpful to remember that under this question are a lot of factors. For instance, is aging really just a natural process that we should recognize? Why then are we so focused on creating technologies that will reverse its effects?

Philosophers have regarded aging as one of the reasons why we are afraid of death, and it has led to quite a lot of lessons about “cherishing life” and “making every moment count.”

However, the biomedical community seems to be on the verge of rethinking their stance on the matter.

Cambridge University’s Aubrey de Grey has pondered the question for a while. A trained computer scientist and a self-taught biologist and gerontologist, de Grey has been trying to reframe our mentality about aging.

In an article by Scientist, De Grey said it may be time to consider aging as a pathologic process, as in one like cancer and diabetes that can be “treated.”

It is important to remember that “aging” is the term we use to describe the changes our bodies undergo over time. The early changes are good as we develop stronger muscles and better reflexes. However, our problems begin when we start getting thinner hair and weaker resistances. Not to mention, the human body has different parts that develop at different paces.

Any wrong move in the pacing of the growth of our body results to diseases. For instance, while lipids are a natural part of our diet, too much of it will make our blood vessels harden and narrow, leading to heart attacks.

De Grey said we can (and we should) view aging as something that could be prevented. A team of scientists also share this belief.

In their paper published in Frontiers in Genetics, scientists Sven Bulterijs, Raphaella Hull, Victor Bjork, and Avi Roy believe that a lot of diseases that affect us over time are caused by aging.

Diseases such as the Hutchinson-Gilford Progeria syndrome, Werner syndrome, and Dyskeratosis Congenita are considered diseases that affect teenagers and young adults. However, they are considered normal and unworthy of attention when they are seen in older people.

Interestingly, common bodily afflictions that come with aging such as hypertension, atherosclerosis, dementia, and sarcopenia are all considered “diseases.” What makes aging different?

And while some consider the debate as something purely semantic, as in the way in which we define certain terms, there are “benefits” for such a label.

For instance, labeling aging as a disease will better help physicians make more medical efforts to remove and treat conditions associated with aging that we normally ignore. Calling something a disease will merit some form of commitment to medical intervention.

Source: natureworldnews