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?

(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

The Significance of Selenium


This mineral is also a powerful antioxidant, which plays itself out in many ways in regard to your health. You need only a little, though, to help keep your immune system and other functions humming along in proper order.

As much as your body requires selenium, taking the proper amount is crucial, because too much (such as 400 micrograms [mcg] daily) is associated with an increased risk of diabetes.2

However, unless you’re taking a supplement, it’s not likely you’ll overdose on selenium through the foods you eat. In fact, most people have trouble getting what they need, and as many as 1 billion people worldwide have a selenium deficiency.

Your chance of having a selenium deficiency is higher if you smoke cigarettes, take birth control pills, drink alcohol or have a condition that keeps you from absorbing the nutrients you need through the foods you eat.

Free Radicals: The ‘Bad Guys’ You Don’t Want Lurking in Your Body

As previously mentioned, one of the most important aspects of selenium is that it functions as a free-radical-zapping antioxidant. What does that mean, exactly?

When you take the word apart, “anti” is something you’re against and the word or phrase that follows it is the “bad guy.” In this case, what you’re against is oxidation because it can cause oxidative stress, which in turn can lead to tissue and organ damage. According to News-Medical:


While “free radicals” may be another murky term, in short, free radicals and other assorted reactive oxygen species (ROS) are caused by either normal, internal metabolic processes or via outside influences such as nicotine and X-rays, or exposure to harmful chemicals like those used to kill mosquitoes, germs in your bathroom or weeds around your patio. One study explains:

“Free radicals, reactive oxygen species (ROS) and reactive nitrogen species are generated by our body by various endogenous systems, exposure to different physiochemical conditions or pathological states. A balance between free radicals and antioxidants is necessary for proper physiological function.

If free radicals overwhelm the body’s ability to regulate them, a condition known as oxidative stress ensues. Free radicals thus adversely alter lipids, proteins and DNA and trigger a number of human diseases. Hence application of external source of antioxidants can assist in coping (with) oxidative stress.”4

It may be helpful to remember that free radicals can cause cell damage, and antioxidants fight free radicals.

Thyroid Function and the Role of Selenium

Your thyroid contains more selenium per gram of tissue than any other organ. One study explains:

“In 1957, studies investigating the requirements of nutrients in rodent diets revealed selenium (along with vitamin E) to be essential for prevention of liver necrosis. This led to the realization that selenium deficiency was responsible for a number of disorders observed previously …

(Selenium is) a contributing factor to Keshan disease in humans. Although toxicity at higher levels is still a serious problem, the importance of selenium as an essential micronutrient is now recognized.”5

Another study states that the value of selenium supplementation for people with autoimmune thyroid problems is becoming more understood and deficiency even appears to have an impact on the development of thyroid problems, possibly due to selenium’s ability to regulate the production of ROS and their metabolites.

In patients with Hashimoto’s disease, selenium supplementation “decreases anti-thyroid antibody levels and improves the ultrasound structure of the thyroid gland.”6 Further, studies for pregnant women regarding selenium say that supplementation significantly lowers the risk of postpartum thyroiditis.7

Selenium Strengths: Proper Amounts Cut Your Risk of Serious Disease

According to one meta-analysis:

“Selenium may play a beneficial role in multi-factorial illnesses with genetic and environmental linkages … Tissues particularly sensitive to changes in selenium supply include red blood cells, kidney and muscle.

The meta-analysis identified that for animal species selenium-enriched foods were more effective than selenomethionine at increasing (glutathione peroxidase) activity.”8

Immune Function

One of the most important functions of selenium is its ability to help your body fight disease. It raises your white blood cell count so you’re more able to resist infections.

An example is a study showing that selenium may help prevent a skin infection prevalent in people with lymphedema (swelling of the tissues in your arms and/or legs, usually as a result of chemotherapy or injury), and mycoplasma pneumonia, aka “walking” pneumonia.9


In 2012, researchers reported that in areas of the world where selenium levels are naturally low, supplementing with selenium may be cancer protective.10 Study author and professor John Hesketh of Newcastle University, U.K., explained:

“The difficulty with selenium is that it’s a very narrow window between levels that are sub-optimal and those that would be considered toxic.

What our study shows is a possible link between higher levels of selenium and a decreased risk of colorectal cancer and suggests that increasing selenium intake may reduce the risk of this disease.”11

Heart Benefits

While it should be noted that some researchers say taking selenium supplements doesn’t appear to influence heart disease one way or the other or protect against heart attack, the University of Maryland Medical Center reported:

“Scientists know that low levels of selenium can contribute to heart failure, and being deficient in selenium seems to make atherosclerosis worse. Atherosclerosis, or hardening of the arteries, happens when plaque builds up in arteries, which can lead to heart attack and stroke.”12

Another study found that patients who took selenium supplements on a regular basis are “far less likely” to have another heart attack.13


Asthma sufferers tend to have higher incidences of low selenium levels in their blood. Scientists found that diets containing high amounts of antioxidants are associated with lowered asthma prevalence in epidemiologic studies, as a report on accumulated data revealed:

“Accumulated data indicate that asthma is associated with reduced circulatory selenium (Se) … In the Se-supplemented group there were significant increases in serum Se

… Further, there was a significant clinical improvement in the Se-supplemented group, as compared with the placebo group.”14

Among 24 subjects with asthma, those who took supplements for 14 weeks had fewer symptoms than those taking a placebo, one study found. However, scientists agree that more studies are needed.15

Male infertility

Proteins found in sperm and involved in their formation are impacted by selenium and other antioxidants.

An interesting dichotomy, however, is that while studies show male infertility may be improved by the selenium in a man’s system, levels that are too high can inhibit the sperm’s ability to swim, according to the University of Maryland Medical Center.16 Another study concluded:

“Selenium-enriched probiotics or inorganic selenium supplementation gave better results than probiotics supplementation and may be used to improve animal and human male fertility compromised by hyperlipidemia or obesity.”17


Most of the African continent is selenium deficient. Simultaneously, AIDS is the most common cause of death. News-Medical, examining diseases impacted by selenium, reported:

“Taken as a whole, the geographical evidence, therefore, strongly suggests that selenium is protective against HIV infection.

Such a relationship is not limited to this virus. A frequently fatal illness of the heart, known as Keshan disease, is widespread in the population of the low selenium belt that crosses China from northeast to southwest. Keshan disease occurs only in individuals who are both selenium deficient and infected by the coxsackievirus”18

While the highest death rates from AIDS affect several of the southwestern-most portions of the continent, such as Botswana, Uganda and Kenya, “the prevalence rate for HIV infection still hovers at an unusually low 0.5 percent among women attending antenatal clinics” in Dakar, the capital city of Senegal.

The difference, scientists say, is that Senegal is located on the far western coast of Africa, where the soil is enriched with trace elements of selenium, contrasting the eastern portion, where the soil is devoid of the selenium that might help make a difference in this regard.

A similar situation is taking place in Finland where, to combat heart disease, legislation was passed in 1984 ordering sodium selenite to be added to all fertilizers throughout the country. Perhaps as a result, the country’s HIV rates are half that of other Scandinavian countries.

Selenium From Food: Seafood, Mushrooms and Meat

The best selenium sources from food include salmon (although only wild-caught Alaskan salmon is recommended due to widespread pollution in other fish), free-range organic turkey, lamb and grass-fed organic beef. You can also find high amounts of selenium in Brazil nuts, sunflower seeds, onions and garlic and certain mushrooms.19 SFGate says:

“Mushrooms are one of the top vegetable sources for selenium. One cup of cooked shiitakes or white button mushrooms provides 19 micrograms of selenium, or 35 percent of the RDA. A more typical serving of ¼ cup provides less than 10 percent of the daily value.

A cup of cooked Lima or pinto beans averages 9 to 11 micrograms of the mineral, or about 15 to 20 percent of the RDA. Frozen cooked spinach, which is packed more tightly per cup than fresh cooked, provides 10 micrograms of selenium, or 18 percent of the RDA.”

It’s not just how much selenium is in your food, though, that determines how much you’re getting. It’s also about how much selenium is in the soil your food is grown in. Related factors include how much selenium was in the grass eaten by the cattle producing your grass-fed beef.

(Grass-fed beef, by the way, contains a healthy ratio between omega-6 and omega-3 fats. Naturally, you also want it to be free of hormones and antibiotics.)




By far the majority of our companion microbes,














The situation in adults is murkier.





Credit: Dr Kari Lounatmaa/ Getty Images


So, what makes a microbial ecosystem obesogenic?











Microbes & you: A partnership millions of years old

It doesn't matter how much you wash, you're crawling with microbes – inside and out. Eye of Science / Getty Images

It doesn’t matter how much you wash, you’re crawling with microbes – inside and out.
Credit: Eye of Science / Getty Images

We are not alone. Our bodies are teeming metropolises of microscopic life – and the microbes that call us home influence everything from bowel to brain.

Over the past decade, technological advances in the lab have allowed us to take a census of our microbial entourage – known as the microbiota – like never before. Instead of seeing only the small fraction of microbes from our skin or poo that blossom on a petri dish, we can now blend, extract and read the genetic essence – the DNA – of all microbes, called the microbiome, to get a better idea of who’s there.

The picture that has emerged is one of staggering complexity. From nostrils to armpits, wisdom teeth to bowels, lungs to vaginas, unique communities of bacteria, fungi, viruses and parasites have got us covered.

“Every single surface of our body is colonised with microbes,” says Laura Cox, a biologist at the Brigham & Women’s Hospital and Harvard Medical School in Boston in the US.

Bacteria alone are as numerous as the cells of our own body. The genes they harbour dwarf our own genetic endowment more than a hundred times over. Together, we work in concert in what some consider a ‘super-organism’ – with our existence as reliant on theirs as theirs is on us.

Gut microbes synthesise vitamins, while those on our skin earn their keep by eating dead cells and transforming oils into natural moisturiser. And microbes everywhere play a role in keeping harmful pathogens at bay.

Families of gut microbes diverged from a common ancestor some 15 million years ago.

On the other side of the ledger, a mother’s milk contains some nutrients useless to her baby, but essential for the early microbial colonisers of her baby’s gut.

The assemblages of species inhabiting each bodily niche represent complex ecosystems that have evolved with us over millennia. The microbes lurking on the doorknob of the public toilet might give us the heebie-jeebies. But those that take up residence on or in us aren’t usually picked up from the environment. They are passed down from generation to generation, and have been for millions of years.

Families of gut microbes living in both us and other apes diverged from a common ancestor some 15 million years ago.

And bacterial strains from Africa and America diverged 1.7 million years ago, around the time early humans made their first forays out of Africa. If you wanted to, you could trace the history of human migrations around the globe using our microbiome.

Our microbes continue to evolve with us, and in response to our modern lifestyles. People living in industrialised societies have less diverse microbial communities than people in places such as Malawi.

Microbiome composition ebbs and flows depending on the food we supply and the various chemicals and drugs we send their way. Not surprisingly, the fluctuations in our microbial residents have clear implications for our health – from immune responses to how we think and act.

Tomorrow, we’ll explore how gut microbes tinker with our metabolism.

Resolving the ‘Hispanic paradox’

Study co-authored by a UCSB researcher reveals Latinos age slower, neutralizing higher health risks of obesity and diabetes

University of California – Santa Barbara

A new paper co-authored by a UC Santa Barbara researcher reveals that Latinos age at a slower rate than other ethnic groups. The findings, published in the current issue of Genome Biology, may one day help scientists understand how to slow the aging process for everyone.


According to the Centers for Disease Control and Prevention, Latinos in the United States live an average of three years longer than Caucasians, with a life expectancy of 82 versus 79. At any age, healthy Latino adults face a 30 percent lower risk of death than other racial groups, according to a 2013 study in the American Journal of Public Health.

The UCLA team used several biomarkers, including an “epigenetic clock” developed by Horvath in 2013, to track an epigenetic shift in the genome that’s linked to aging. Epigenetics is the study of changes to the DNA molecule that influence which genes are active but don’t alter the DNA sequence.

“Our findings show that ethnic disparities in health risk are not just due to socioeconomic differences, which we adjust for in the analyses,” explained co-author Michael Gurven, a UCSB professor of anthropology. “The epigenetic analyses show biological differences in aging-related processes — but in a novel way — in how the genome is maintained and expressed through methylation, rather than conventional differences in genetic alleles.”

Horvath and his colleagues analyzed 18 sets of data on DNA samples from nearly 6,000 people. The participants represented seven ethnicities: two African groups, African-Americans, Caucasians, East Asians, Latinos and an indigenous people called the Tsimane, who are genetically related to Latinos. The Tsimane live in Bolivia.

When the scientists examined the DNA from blood — which reveals the health of a person’s immune system — they were struck by differences linked to ethnicity. In particular, the scientists noticed that, after accounting for differences in cell composition, the blood of Latinos and the Tsimane aged more slowly than that of other groups.

According to Horvath, the UCLA research points to an epigenetic explanation for Latinos’ longer life spans. For example, the biological clock measured Latino women’s age as 2.4 years younger than non-Latino women of the same age after menopause.

“We suspect that Latinos’ slower aging rate helps neutralize their higher health risks, particularly those related to obesity and inflammation,” said Horvath, who is also a professor of biostatistics at the UCLA Fielding School of Public Health. “Our findings strongly suggest that genetic or environmental factors linked to ethnicity may influence how quickly a person ages and how long they live.” Gurven added “Epigenetic aging measures are fascinating because they subsume many environmental and psychosocial factors we know matter in life. One hypothesis to explain the Hispanic paradox emphasizes the strong family ties and social support found in many Hispanic families. Such a social support network may leave its biological signature in the epigenome.”

The Tsimane aged even more slowly than Latinos. The biological clock calculated the age of their blood as two years younger than Latinos and four years younger than Caucasians. This possibly reflects the group’s minimal signs of heart disease, diabetes, hypertension, or obesity, the researchers said.

“Despite frequent infections, the Tsimane people show very little evidence of the chronic diseases that commonly afflict modern society,” Gurven said. “Our findings provide an interesting molecular explanation for their robust health.”

In another finding, the researchers learned that men’s blood and brain tissue ages faster than women’s from the same ethnic groups. The discovery could explain why women have a higher life expectancy than men.



Is Coffee Good or Bad for you?

“Dr. Hyman, I’m so confused about coffee,” writes this week’s house call. “One day I read that it’s so bad for me and the next it’s good for me. Why all the conflicting information?”

Let’s face it: Americans love their coffee, which is the number one source of antioxidants in our diet – which actually makes me kind of sad!

In a recent animal study, researchers saw improvements in non-alcoholic fatty liver disease (NAFLD) and cholesterol when mice consumed coffee and fat together. (More on that combo in a minute.) They also found coffee can help reduce gut permeability or leaky gut.

Among its other benefits, studies show coffee decreases your risk for type 2 diabetes, lowers cancer risk and improves mood and memory. Coffee can also boost metabolism and sports performance.

On the other hand, coffee can become highly addictive, altering stress hormones while making you feel simultaneously wired and tired.

So I understand the confusion. It feels like one day we see studies that support coffee and the next day we see 10 reasons why coffee is bad. So let’s uncover the truth about this aromatic beverage that most of us love.

When to Avoid Coffee

Before jumping to conclusions, remember those blurred lines aren’t entirely about coffee itself. It also depends on the person drinking the coffee. The way you respond to coffee is often determined by genetics that affect caffeine metabolism. For one person, a cup could have them bouncing off the walls, while another person can have a triple espresso at dinner and fall fast asleep easily.

In other words, everyone is different and we all experience coffee’s effects differently. One patient complained about fatigue, restlessness and heart palpitations. Obviously, in that situation, I recommended avoiding coffee.

Likewise, if you suffer from adrenal fatigue, coffee could easily become dangerous. Some individuals might also be sensitive to coffee beans, meaning their bodies can’t tolerate them and they create unpleasant symptoms.

Constituents in coffee can also interfere with normal drug metabolism and liver detoxification, making it difficult for your liver to regulate the normal detoxification process.

Sometimes, too, I find patients substitute coffee for real food. Never ignore your hunger and eat regularly to prevent low blood sugar levels. Keep protein on hand and snack on a handful of nuts or seeds like almonds, pecans, walnuts or pumpkin seeds.

I had one patient who drank 12 cups of coffee a day yet constantly fell asleep at his desk. This person could barely function and couldn’t understand why he felt so exhausted.  The truth is he wasn’t sleeping well at night due to all the caffeine but he was too exhausted to realize it.  He wasn’t getting the proper rest his body desperately needed at the right time.

So we tapered him off coffee, and he began to sleep soundly at night, rather than nodding off  at his desk during the day.

If you fall into those categories, coffee probably isn’t for you.

Regardless, I recommend treating coffee like any other potential toxic trigger and eliminate it for at least three weeks, especially if you’re addicted and can’t seem to function without coffee or if you drink multiple cups a day.

If you need coffee every day to feel motivated or even function, you have a coffee addiction. If you have withdrawal symptoms and headaches from stopping coffee or feel like you can’t live without it, you are biologically addicted to it.  There’s also a big chance your stress hormones are out of whack and need resetting.

How to Quit Coffee   

The best way to wean off coffee is switching from drinking multiple cups to just one cup and eventually half a cup. You might also switch to green tea or herbal teas and warm lemon water.

As with any detox plan, drink adequate amounts of water and get plenty of rest during this time. I also suggest regular exercise to stabilize energy levels. Should you get irritable or have difficulty sleeping, supplement with 200 to 500 mg of magnesium citrate before bed.

My favorite detoxification rituals include a sauna, meditation and yoga. I provide powerful techniques to relax and combat stress on my website.

If you can handle it, remove coffee from your diet for three weeks and add it back in slowly. Be attentive to how you feel once you reintroduce coffee. Pay attention to your energy levels, symptoms (like anxiety or jittery feelings) or changes in digestion.

In other words, monitor how you personally respond to coffee. You are your own best doctor here.

It’s perfectly fine if you realize coffee just does not work for you. Other health-friendly beverages include green tea or non-coffee-based lattes using reishi powder and other powerful herbs.

If you find you can occasionally tolerate coffee, avoid adding milk and sugar. These two culprits do more damage than the actual coffee.

Alternately, add fat to your coffee. Once people taste the creamy, frothy goodness of fat blended with coffee, they don’t miss milk at all. You’ve probably heard of Bulletproof® Coffee, which blends MCT oil and a bit of  grass-fed butter or ghee with high-quality, organic coffee.  If you are a vegan, try adding 1 tablespoon of cashew butter for the creamy texture.

This delicious beverage keeps me satiated for hours, cuts cravings and keeps my brain extremely sharp. You can also drink this before exercise for steady energy levels without coffee’s crash.

Here is a version of my friend Dave Asprey’s Bulletproof Coffee:

In a blender, add:

  • 2 cups of hot coffee (regular or decaf), ideally fresh brewed with organic beans
  • 2 tablespoons of grass-fed butter or ghee
  • 2 tablespoons of organic coconut oil or 2 Tablespoons of MCT oil
  • ½ teaspoon of organic cinnamon (optional) or 1 teaspoon of organic cocoa powder for a mocha

Blend until creamy. For best results, I suggest using a metal mesh filter in your drip coffee maker or a French press.

Note: Always be very careful when pureeing hot liquids in a blender. The heat from the liquid can cause the pressure in the blender to build up under the lid, and when the blender is turned on, the top can blow off and your hot soup will go everywhere. Keep the lid vented by removing the small window insert from the middle of the blender lid; hold a towel over the open window to prevent splattering. Always start on the lowest speed possible.

The bottom line is that much no one-size-fits-all approach exists for diet and lifestyle, and that includes your coffee intake.

One person may be able to enjoy raw, cruciferous vegetables while another needs to avoid them because of digestive issues. This same thing applies to coffee. For some people it works; others, not so much.

If you’re a coffee drinker, have you ever felt like you’ve over-relied on this popular beverage? If you temporarily gave it up, how did it affect you? Comment below or on my Facebook page. And be sure to submit your questions to

Wishing you health and happiness,


Now Even the US Attorney General Is Slandering Supplements!

Like the flawed Frontline documentary, like New York state’s attorney general, US Attorney General Loretta Lynch is spreading gross misinformation about dietary supplements. Action Alert!

Last week, Attorney General Lynch released a video for National Consumer Protection Week about supplements. Excuse us, but since when is the US attorney general an expert on this subject? Since she obviously isn’t, she must be relying on distortions and untruths she has been fed by other agencies of the government such as the FDA and Centers for Disease Control.

For instance, Ms. Lynch warns consumers against “ingesting substances whose safety and efficacy are not guaranteed” by FDA study. As we pointed out in our response to PBS, pharmaceutical drugs are also not studied by the FDA. The agency relies on industry studies to determine if new drugs can come to market. No independent review is done to check the industry’s results, which has led to all kinds of manipulation and sometimes disastrous outcomes (see the examples of Vioxx and Avandia). And after approval is granted, the actual medicine itself is never tested, even though it may be manufactured in Chinese plants or other faraway locales.

FDA approval is certainly no guarantor of safety. Consider that pharmaceutical drugs, when properly prescribed, cause an estimated 1.9 million hospitalizations and 128,000 deaths each year. And that’s just in hospitals—deaths outside hospitals would add considerably to this total if they were recorded. In stark contrast, dietary supplements caused zero deaths in 2013, the last year reported.

Ms. Lynch also charges that supplements “endanger public health” by containing harmful ingredients. The supplement industry—like all industries—has some bad actors. But supplements that contain unsafe ingredients are already “adulterated” which means that the FDA has a responsibility to remove them and prosecute the makers. Nor does Ms. Lynch mention that supplement companies must follow stringent guidelines known as current good manufacturing practices (cGMPs) intended to ensure the safety and quality of dietary supplements. In other words, supplements are federally regulated.

Finally, Ms. Lynch says that many supplements “falsely claim to cure illness and disease.” As a student of the law, Ms. Lynch must be aware that the FTC and FDA regulate what can be said on supplement labels. By law, supplements cannot make disease claims—only drugs can. Any supplement that does make such claims is therefore breaking the law. We don’t agree with this law, but if it isn’t being followed why doesn’t the government simply enforce the law. In past years, FDA memos have indicated that sometimes the agency does not enforce the law on purpose, in the hopes that an ensuing scandal will lead to even more federal control over supplements. The cost of this would in turn drive their cost sky high and largely eliminate them as competition for drugs.

No, Ms. Lynch, supplements are regulated, are safe, and are effective. Just the opposite of what you suggested. You are not a doctor or scientist. But as the top law enforcement official of the country, you can at least get your law right.

Action Alert! Write to Attorney General Loretta Lynch and urge her to correct the misinformation she spread to consumers about dietary supplements. Please send your message immediately.


Doctors Have Known For 10 Years They’re Killing You

This is one of the most-damning studies that has ever been brought to my attention.

The “standard”, if you have ever had a cardiac “event” or coronary artery disease, is to immediately place you on a statin (for the rest of your life) and, in most cases (exception: if you have ulcer issues) low-dose aspirin as a low-level anticoagulant.

Here’s the problem: It doesn’t work because it’s not targeting where the actual issue resides.

This has now been known since 2004, when this study published; the study itself was initiated in 1999.  304 patients with a history of coronary artery disease were tested and baselined.  Only those with normal glucose levels were accepted into the study; clinical diabetes was an exclusionary factor.  202 of the 304 were excluded at baseline for this reason, leaving the study authors with 102 patients.

The results ought to wake you up; they’re here in this table.

CAD Study

The CVE+ entries are for those who had a second cardiac event during the three years of the study, the CVE- entries are for those who did not.  ALL of the CVE+ entries had elevated (by double on average) insulin levels despite both groups having normal blood glucose.

Further, those who had a second event had no material difference in cholesterol levels compared to those who did not.  In other words “management” of cholesterol levels was not protective.  Finally, there was a material difference in statin use — in the negative sense, in that a greater percentage of those who had an event were taking a statin (and a nitrate!) than those who didn’t, and even worse, aspirin wasn’t protective either.

One cautionary note: All of these results are associative, as they must be in such a study.  Even though the divergence in insulin levels was ridiculous between the two groups that does not prove causation.

But remember — while associations can provide strong evidence of a connection they are just as valuable, if not more-so, in disproving said connections.  In this case it appears that both statins and aspirin are worthless when it comes to preventing a second CAD event.

Further, since all of the participants had normal glucose levels there is no intervention that targets “diabetes management” which helps in this case.  Indeed the study showed that “management” of diabetes symptoms (specifically, blood glucose levels) that allows high insulin to persist may actually potentiate — that is, cause — the second heart attack and CAD event.

There is no medicine for the condition of high insulin — that is, “insulin resistance.”  We can and do treat the symptom that it (eventually) produces, that is, high blood glucose, but the cause of the high glucose remains unaddressed.

There is, however, a means to improve your insulin sensitivity — that is, to move yourself either from that second column to the first one or at least get closer to itGet all of the vegetable oils and carbohydrates (that is, grains and starches including breads, cereals and similar), with the exception of green vegetables and modest amounts of fruit, out of your diet.

Again — this study has been out since 2004.  Why hasn’t your doctor — and especially, if you have one, your cardiologist — told you?

Further, if you’ve got evidence of CAD in your medical history why hasn’t your insulin sensitivity (NOT just cholesterol and glucose tolerance) been tested and monitored?  Is it because there is no pill for it and that the actual means of improvement available to us require admitting that the so-called “standard recommendations” for what to eat, especially for those with heart disease, are exactly backward?


The World Health Organization Red Meat Brouhaha

The World Health Organization (WHO) just announced that red meat is “probably carcinogenic to humans.”

Yep–Right up there with glyphosate, cigarettes, alcohol and asbestos.

——–> insert facepalm <——–

This announcement is absurdly misguided and largely based upon the notoriously two least reliable forms of science we have:

1) Observational studies driven by…

2) Food questionnaires

(By the way, what did YOU have for lunch on Thursday of last week/month year?)

This is all fully based on the idea of “guilt by weak association” and any rational person knows that association is NOT causation.

UGH–Back to the nutritional Dark Ages we go…

The WHO seems to be mostly citing evidence from research based on observational studies and food questionnaires published in the Archives of Internal Medicine in 2012, which included an analysis of “two prospective cohort studies.”[1] Similar in its failures to the ill-conceived and embarrassingly poor 2011 World Cancer Research Fund “Meta-analysis”[2]—also entirely based upon observational studies and questionnaires— ZERO distinction was made between feedlot meat and 100% grass-fed meat (a potentially huge distinction), and no real effort was made to distinguish the effect of the red meat from whatever else people happened to be eating. What did they include as “red meat?”   McDonald’s hamburgers, pizza, hot dogs, tacos, bologna, nitrate-laced bacon and feedlot meat (GMO-fed and God knows what else). Although they did graciously concede that red meat is “only slightly less hazardous than preserved meats.” And red meat consumption was not separated in any way from whatever else anyone was eating or doing to their health (alcohol intake, sugar consumption, grains, etc. or other lifestyle factors). And since 97% of all meat production is commercial feedlot-based, grass-fed meat likely didn’t even factor into these results at all.

Suspiciously, too, the Archives of Internal Medicine study used what is called relative risk to show their results. “Relative risk” is frequently used to make things look far worse than they are—rather than what is called absolute risk, which really tells it like it is (but might make your results look less dramatic and, well, boring and meaningless).

It is a significant fact that cancer has been consistently reported to be extremely rare to even non-existent in red meat-eating, hunter-gatherer societies.[3],[4] What in particular has characterized the difference between even Neolithic hunter-gatherer diets and the modern-day Western diet causing us so much trouble now? Data from 229 hunter-gatherer societies included in the Revised Ethnographic Atlas indicate that hunter-gatherer diets differ from typical Western ones in basically two aspects: first, a strong reliance on animal foods (45-65% of energy or E%) and second, the consumption of low-GI [glycemic index] plant foods such as fibrous vegetables, some fruits, nuts and seeds.[5] But we also need to take the quality of the foods they had available to them into account and the very, very different nutrient/fatty acid profile between feedlot meat and 100% naturally grass-fed meat/wild game. Grain fed meats are predominated by potentially inflammatory omega-6 content (while being nearly devoid of healthy omega-3’s), versus 100% grass-fed and finished meat (and wild game) which supplies a high percentage of highly anti-inflammatory omega-3 fatty acids (EPA/DHA). Omega-3’s have additionally shown some significant anti-cancer benefits.[6] [7] [8]

Quality counts for a LOT and we all need to start taking that seriously. Deadly seriously.

In spite of the WHO declaration, other research has shown no meaningful link between diets higher in dietary animal fat and increased cancer risk.[9],[10] With respect to colon cancer, alone, there are many, many more (and better designed) studies finding little to no significant association with red meat and cancer than those that do, some even showing an actual lowered risk![11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25]

With respect to Paleo—at least the form of Paleo I personally recommend and the form adopted by The Paleo Way, bases its meat consumption overall on two very distinct recommendations:

  • Red meat should only come from 100% pasture fed and finished animals. NO feedlot and/or commercial processed meat!
  • I recommend meat/protein in general to be consumed in strict moderation—no more than about 1 gram per kg of ideal body weight (i.e., approximating the weight of a person’s lean tissue mass)

Excessive protein from any source is potentially bad by virtue of 1) its up-regulation of proliferative mTOR pathways 2) its increase of IGF-1, which increases non-specific cellular proliferation and 3) the excess presence of glutamine and 4) protein in excess of what we need in order to meet our basic requirements is readily (up to 40% or so) converted to sugar and used the same way. –And SUGAR (not red meat) is cancer’s #1 most essential metabolic fuel.

With respect to the benefits of exclusively grass-fed meat (over feedlot meat), a particular form of fat that has been more recently lauded for its anti-cancer benefits is one exclusively found in the fat of animals fed on nothing but natural pasture.[26] [27] [28] [29] [30]    In fact, CLA may be one of the most broadly beneficial and potent cancer-fighting substances in our diet. It is somewhat uniquely able to (in very small amounts) block all three stages of cancer: 1) initiation 2) growth/promotion and 3) metastasis. Most “anticancer nutrients” are typically helpful in only one of these areas. To date, beneficial effects of natural CLA from animal fat have been found in cancers of the breast, prostate, colon and skin. In animal studies, as little as one half of one percent CLA in the diet of experimental animals reduced tumor burden by more than 50 percent.[31]   As if this wasn’t exciting enough, there is more direct evidence that CLA may reduce cancer risk in humans. In a Finnish study, women who had the highest levels of CLA in their diet had a 60 percent lower risk of breast cancer than those having the lowest levels. Switching from grain-fed to exclusively grass-fed meat literally places women in this lowest risk category!

Additionally, French researchers measured CLA levels in the breast tissues of 360 women and found that the women with the most CLA had the lowest risk of cancer. In fact, the women with the most CLA had a staggering 74% lower risk of breast cancer than the women with the least CLA. [32]   In yet another study, human breast cancer cells were incubated in milk fat high in CLA or in an isolated form of CLA without any milk fat. The high CLA milk fat decreased cancer growth by 90 percent but the isolated CLA decreased it by only 60 percent. When the cells were incubated in the omega-6 fat, linoleic acid, found most abundantly in grain and grain-fed animals, cancer cell growth increased by 25 percent![33] Other women with the most CLA in their diets were also shown to have a 60% reduction overall in the incidence of breast cancer.[34]

Other studies have additionally shown breast cancer and even colon cancer preventative benefits.[35] [36] [37] [38] In keeping with this, CLA additionally exerts potent anti-inflammatory effects.[39] The inherent stability of CLA also seems to maintain itself even when meat is cooked.[40],[41] One study pointed out the following, Of the vast number of naturally occurring substances that have been demonstrated to have anticarcinogenic activity in experimental models, all but a handful of them are of plant origin. Conjugated linoleic acid is unique because it is present in food from animal sources, and its anticancer efficacy is expressed at concentrations close to human consumption levels.”[42]   CLA is highly abundant, too, in wild game. The implication here is that naturally occurring CLA in animal fat has always played an important role in our diets and may possibly even be a contributing factor to the near-zero incidence of cancer found in hunter-gatherer populations.[43] For all you Aussies out there, one study reported unusually high levels of CLA in (of all things) kangaroo meat![44]

ONLY CLA from the fat of wild game and fully pastured animals has the real anticancer health benefits you want.[45] Even though synthetic CLA is sold in capsules in health food stores, it lacks the beneficial form found exclusively in grass-fed meats and may even have potentially adverse effects. But I digress…

According to a research collaboration between Clemson University and the USDA in 2009, in addition to cancer-fighting CLA, fully pastured meat contains the following additional, potentially anti-cancer benefits[46]:

  • Higher in beta-carotene
  • Higher in vitamin E (alpha-tocopherol)
  • Higher in the B-vitamins thiamin and riboflavin and B12
  • Higher in the minerals calcium, magnesium, and potassium
  • Higher in total omega-3’s[47] [48] [49]
  • A healthier ratio of (inflammatory) omega-6 to anti-inflammatory omega-3 fatty acids (1.65 vs. 4.84)
  • Higher in trans-vaccenic acid (TVA–which can be transformed into CLA)

Also, lamb/sheep fed exclusively on pasture vs. grain contains twice as much lutein (closely related to beta-carotene but more easily absorbed), which has shown possible preventative benefits with respect to both colon and breast cancer (while additionally reducing the risk of macular degeneration).[50]

So…in a nutshell, this WHO declaration will not change the recommendations I have been making all along. 100% grass-fed and finished meat (not just red meat, by the way) consumed in moderate amounts along with quality, organic fibrous plant-based foods has been and will continue to be among my foundational recommendations for optimal health.

~ Nora Gedgaudas, CNS, CNT, BCHN


“Red meat is NOT bad for you. Now blue-green meat, THAT’S bad for you!”

                           —Tommy Smothers


Global Research Shows Dairy Products and Calcium Supplements Do Not Make Bones Stronger

The dairy industry has finally been given one big swift kick where they need it most, in the scientific credibility department where top officials have been falsely linking dairy and bone strength for decades. The study, published by the British Medical Journal, found that people don’t get stronger bones by eating dairy products or taking calcium supplements.

pg_10_mrsa_gettyDairy products, specifically milk is one of the beverages still aggressively pushed on children as a health promoting food, especially relating to strong bones.

What interesting about cow’s milk is that the more people drink, the more likely they are to die or experience a bone fracture and other diseases. The risks are especially pronounced for women.

Taking into account studies from around the world, the systematic review and meta-analysis found that those who took calcium were just as likely to suffer from fractures as those who did not.

Dr Ian Reid from the University of Auckland in New Zealand stated that the focus on treating bone diseases, such as osteoporosis, needs to be elsewhere.

“I think we’ve actually misdirected a whole lot of effort into the use of calcium supplements, in particular in North America, where use has been higher for last 30 years,” he said.





The research investigated putative mechanism by which calcium intake affects bone health namely by increasing bone mineral density (BMD). BMD is a surrogate endpoint for fracture risk that allows biological effects to be explored in randomised controlled trials of modest size.

Following old information

The results from the new study flies in the face of long-held beliefs that calcium makes for stronger, better bones.

For years, US guidelines have advised men and women to take anywhere from 1,000 to 1,200 mg of calcium per day to help prevent fractures and improve bone density.

Reid said this likely lasted for so long due to an overreliance on studies from the 1970s and 1980s.

Now, there are more sophisticated bone density studies, and none have shown the need for anything more than 500mg of calcium per day for bone density health.

Going a step further, the study said too much calcium may cause build ups in the arteries or in the kidneys, which can cause ailments such as heart disease or kidney stones respectively.



Methodology of the study

The researchers looked at two studies, finding in one that increasing calcium intake from supplements increases bone density by 1% to 2%, something they said is unlikely to create a meaningful reduction in the risk of fracture.

“This is not a cumulative benefit,” Reid said. “It’s only 1% at any year. It’s a one off small gain. When you look at the fracture data in the large high quality studies carried out in the last 10 to 15 years, we found there is no total benefit to total number of fractures. There may even be an increase. I think we should really be deleting calcium as a significant tissue in management of osteoporosis.”

In another study, researchers found that dietary calcium is not associated with risk of fracture, with no clinical evidence finding that increase in consumption helps prevent fractures.

Professor Karl Michaelsson from Uppsala University in Sweden wrote in an accompanying commentary with the study that the although recommendations point to those over 50 taking calcium, most will not benefit by increasing their intakes.


Supplement Quality Key

While some dairy may be useful to help the elderly keep weight on their body as they get older, many low-quality calcium supplements appear to be ineffective for bone health.

Most supplements on the supplement market today contain calcium carbonate which is an inferior form of calcium and manufacturers attach a simple chelating agent like citric acid to make it more absorbable, however the end product is inferior to other calcium supplements such as calcium orotate, which is the only known form of calcium which can effectively penetrate the membranes of cells.

Many of these supplements are increasing the risk of kidney stones and abdominal problems and whose risks are greater than the benefits.

“They’ve been so entrenched and supported by industry for so long that it’s taking a while to turn around,” Reid said.

Effective Supplementation

If you want to supplement for calcium intake you must seek a reputable and balanced calcium/magnesium formula. Researchers examined 21 formulations of calcium carbonate (both natural [i.e., oyster shell] and refined). Four out of seven natural products and four out of 14 refined products, including brand products, had measurable lead content. A research team in California found essentially the same contamination in calcium supplements.

Acid rebound. Calcium carbonate may cause acid rebound: the stomach overcompensates for the high dose of calcium carbonate, which is alkaline, by churning out more acid. For that reason, people with a history of stomach ulcers are advised that they may not tolerate it and may have to switch to calcium citrate.

Constipation. Calcium supplements can have a mild binding effect but by themselves don’t usually cause serious constipation. But if you’re taking another supplement or medication that binds the stool, the addition of calcium supplements could cause a problem.

Too much calcium. Although it doesn’t happen often, some people have taken so much calcium that it causes hypercalcemia, an above-normal level of calcium in the blood since most of the calcium carbonate is not absorbed. Hypercalcemia may cause nausea, vomiting, confusion, and other neurological symptoms.

The type of minerals in the formula determines the absorption levels: Opti-Cal/Mag with Vitamin K2 is a co-enzyme complex, heat-stabled molecules that must be associated with another enzyme for them to perform their function in the body. It is necessary in the utilization of vitamins and minerals for proper delivery to the cell nucleus. One study found that Opti-Cal/Mag complex is 8.79 times more absorbed into the blood than calcium carbonate and 2.97 times more than calcium gluconate.


1. Eat calcium rich foods
Eat foods high in calcium. The best food sources are non-pasteurized raw dairy sources such as raw milk/yogurt, as well as bony fish, such as sardines. Leafy green veg such as kale, broccoli and spinach are also rich in calcium. Dried herbs and dried fruits such as figs and currants are also good choices. Seeds such as sesame, chia and flax are also rich sources of calcium. Also, enjoy foods that contain sulfur such as garlic and onions.

2. Food selections/combinations are critical
Try not to eat whole grains and calcium-rich foods at the same time. Whole grains contain a substance that binds with calcium and prevents proper absorption. Some foods that contain compounds such as oxalic or phytic acids, such as sweet potatoes, beans, rhubarb, celery and beets, can also decrease the amount of calcium that’s absorbed when eaten at the same time as calcium-rich foods.

3. Avoid the causes of mineral excretion
Pass on phosphate-containing foods such as soft drinks. Phosphorus causes the body to excrete calcium. Limit or avoid high-protein animal foods. A diet high in protein causes calcium to be excreted from your body. Decrease caffeine consumption. People who smoke have significantly lower bone density, while drinking alcohol can also prevent your bones from absorbing the maximum nutrients from your food.

4. Get more Sunlight and Vitamin D
Vitamin D helps the body absorb calcium. Although some is found in oily fish, our main source comes from the effect of sunlight on your skin. It’s estimated that half of us have a deficiency because we don’t get outside enough or because we always use sunblock. It is especially important to maximize sun exposure between May and September to keep vitamin D levels topped up. Just 10 minutes of sunlight a day on bare arms and your face can cut your risk of bone fractures by a third. A half hour exposing your torso is equivalent to roughly 10,000 units of Vitamin D.

5. The right exercise
Another vital way to boost your bones is weight-bearing exercise –basically anything that has you upright and using your body weight. Good choices include squatting, rope skipping, aerobics, plyometrics, dancing or brisk walking. “Research shows that if you don’t exercise you end up weeing out all the calcium you take in instead of storing it in your bones,” warns Professor Dawn Skelton, an aging and health specialist at Glasgow Caledonian University. “Ideally we should aim for 150 minutes of moderate activity per week. “Put simply, the more hours we spend on our feet, the fewer bone breakages we should have in later life.”

6. Avoid Medications and Medical Therapies
Acid-blocking medications used for heartburn and other gastrointestinal conditions can block the absorption of calcium through the stomach walls. Stomach acids break down food during the digestive process, allowing the nutrients to become absorbed into your body. Medications designed to stop acid production or decrease the amount of acids present in your stomach can have a negative effect on calcium.

Cold sores increase risk of dementia

DementiaInfection with herpes simplex virus increases the risk of Alzheimer’s disease. Researchers at Umeå University, Sweden, claim this in two studies in the journal Alzheimer’s & Dementia.

“Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer’s disease. This also means that we have new opportunities to develop treatment forms to stop the disease,” says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study.

Alzheimer’s disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer’s disease. A majority of the population carries this virus. After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer’s disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain. There this can in turn start the process which results in Alzheimer’s disease.

Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies. In one study, which is based on the Betula project, a study on aging, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer’s disease. This study had 3,432 participants who were followed for 11.3 years on average. In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer’s disease were examined and as many matched people who had not developed dementia. The samples were taken on average 9.6 years before diagnosis. This study showed an approximately doubled risk of developing Alzheimer’s disease if the person was a carrier of the herpes virus.

“Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer’s disease,” says Hugo Lövheim.

Story Source:

The above story is based on materials provided by Umeå universitet. Note: Materials may be edited for content and length.

Journal References:

  1. Hugo Lövheim, Jonathan Gilthorpe, Anders Johansson, Sture Eriksson, Göran Hallmans, Fredrik Elgh. Herpes simplex infection and the risk of Alzheimer’s disease—A nested case-control study. Alzheimer’s & Dementia, 2014; DOI: 10.1016/j.jalz.2014.07.157
  2. Hugo Lövheim, Jonathan Gilthorpe, Rolf Adolfsson, Lars-Göran Nilsson, Fredrik Elgh. Reactivated herpes simplex infection increases the risk of Alzheimer’s disease. Alzheimer’s & Dementia, 2014; DOI: 10.1016/j.jalz.2014.04.522


Britain Is the Fattest Country in Europe: Here’s the Real Reason Why

Britain’s “obesity epidemic” is mainly caused by the fact that its population are lazy slobs and not because they eat too much, a shock new study called The Fat Lie has found.

The only reason the study – produced by Christopher Snowdon of the Institute of Economic Affairs (IEA) – is shocking is because it contradicts one of the great received ideas of our politically correct times: that fatties are the hapless victims of the rapacious and bullying food and drink industry which pressures them into eating and drinking far too much fat and sugar.

What Snowdon’s research clearly shows that this claim is nonsense. Yes, it is indeed true that British people are getting porkier. Since 2002 the average body weight of English adults has increased by two kilograms, contributing to Britain’s unenviable status as the fattest country in Europe.

But what is rarely mentioned by health campaigners is that this rise in obesity over three decades has coincided with a steady fall in average sugar and fat consumption.

Fat consumption has fallen from 111 grammes per day in 1974 to 81 grammes per day in 2012.

Sugar consumption has fallen by 16 percent since 1992.

Total calorie consumption has fallen from 2534 calories per person per day in 1974 to 1990 in 2012 – a decrease of 21.5 per cent.

Yet obesity has gone on rising. Why? Because, as Snowdon explains, obesity is a simple function of repeatedly eating more calories than you burn off.  And people are taking much less physical exercise than they used to. Britons are walking less (from 255 miles per year in 1976 to 179 miles in 2010) and cycling less (from 51 miles per year in 1976 to 42 miles in 2010). At work, 63 per cent never climb stairs; while 40 per cent never walk. Outside work, 63 per cent report spending less than ten minutes a day walking, while 53 per cent claim to do no sports or exercise at all.

This is worth keeping in mind next time you read some shrill lobby group – such as Action on Sugar – demanding that the government does more to rein in the food and drink industry or pushes for a ban on supersize portions in fast food outlets or higher taxes on fizzy drinks.

The reason these lobbyists get away with such drivel is because they find a ready audience among the panic junkies at places like Mumsnet and in much of the mainstream media which thrives on public health scare stories.

And the reason they find a ready audience in government is because there are few things a minister on the make enjoys more than being seen to clamp down on some greedy industry or other.

With most departmental budgets being cut, ministers can no longer make a name for themselves by spending their way into public favour. But what they can do – because notionally it’s “cost-free”, though of course it’s not really – is introduce more regulations in the name of public health and safety. It has happened to the tobacco industry. Now it is happening to the food and drink industry.

This is why reports like Christopher Snowdon’s are so unusual and refreshing. They’re one of our few remaining toeholds on reality in a world which finds it more convenient to fall for the cultural Marxist lie that nobody is responsible for their own problems and that it’s the government’s job to sort them out.

Will a Nicotine Patch Make You Smarter?


Nicotine? Yes, nicotine.
























Source:  Scientific American

Hormones help in sex







Hormones that control desire








After foreplay, comes…





At the peak



During recovery






Nutrition for better sex










Anti-aging drug breakthrough

Drugs that combat aging may be available within five years, following landmark work led by an Australian researcher.

The work, published in the March 8 issue of Science, finally proves that a single anti-ageing enzyme in the body can be targeted, with the potential to prevent age-related diseases and extend lifespans.


“Ultimately, these drugs would treat one disease, but unlike drugs of today, they would prevent 20 others,” says the lead author of the paper, Professor David Sinclair, from UNSW Medicine, who is based at Harvard University. “In effect, they would slow aging.”

The target enzyme, SIRT1, is switched on naturally by calorie restriction and exercise, but it can also be enhanced through activators. The most common naturally-occurring activator is resveratrol, which is found in small quantities in red wine, but synthetic activators with much stronger activity are already being developed.

Although research surrounding resveratrol has been going for a decade, until now the basic science had been contested. Despite this, there have already been promising results in some trials with implications for cancer, cardiovascular disease and cardiac failure, type 2 diabetes, Alzheimer’s and Parkinson’s diseases, fatty liver disease, cataracts, osteoporosis, muscle wasting, sleep disorders and inflammatory diseases such as psoriasis, arthritis and colitis (inflammatory bowel disease).

“In the history of pharmaceuticals, there has never been a drug that tweaks an enzyme to make it run faster,” says Professor Sinclair, a geneticist with the Department of Pharmacology at UNSW.

The technology was sold to pharmaceutical giant GlaxoSmithKline in 2008[i]. Four thousand synthetic activators, which are 100 times as potent as a single glass of red wine, have been developed – the best three are in human trials.

“Our drugs can mimic the benefits of diet and exercise, but there is no impact on weight,” says Professor Sinclair, who suggests the first therapeutic to be marketed will be for diabetes.


The drugs can be administered orally, or topically. So far, there have been no drugs developed targeting ageing skin, but one major skin care range has developed a crème with resveratrol in it.

While any drug would be strictly prescribed for certain conditions, Professor Sinclair suggests that one day, they could be taken orally as a preventative. This would be in much the same way as statin drugs are commonly prescribed to prevent, instead of simply treating, cardiovascular disease.


“Now we are looking at whether there are benefits for those who are already healthy. Things there are also looking promising,” says Professor Sinclair, who also heads the Lowy Cancer Research Centre’s Laboratory for Ageing Research at UNSW.

“We’re finding that aging isn’t the irreversible affliction that we thought it was,” he says. “Some of us could live to 150, but we won’t get there without more research.”

Media contact: Susi Hamilton, UNSW Media Office, +61 422 934 024,

[i] Professor Sinclair formed a started up company Sirtris to develop the anti-ageing technology. This was subsequently sold to GlaxoSmithKline (GSK). Professor Sinclair is now a scientific advisor to GSK. Several other authors on the paper work for GSK or an affiliated company.

Insulin Doubles Death Rate in Type 2 Diabetics: Study


Enough with Insulin! by Jeff Fillmore

It seems so intuitive: People with diabetes should inject insulin. In the case of people with type 1 diabetes, in which the pancreas doesn’t produce insulin, that’s probably true. However, modern doctors routinely give insulin to people with type 2 diabetes simply because it reduces blood sugar levels.

The reality, though, is that type 2 diabetics who take insulin injections die at more than double the rate of those given non-insulin treatment!

The Study

The study,  Mortality and Other Important Diabetes-Related Outcomes With Insulin vs Other Antihyperglycemic Therapies in Type 2 Diabetes, investigated 84,622 primary care patients with type 2 diabetes from 2000 to 2010 and compared the results of these treatments:

  • Metformin monotherapy
  • Sulfonylurea monotherapy
  • Insulin monotherapy
  • Metformin plus Sulfonylurea combination therapy
  • Insulin plus Metformin combination therapy

These groups were compared for risks of certain severe adverse events: cardiac, cancer, and mortality. A primary outcome was defined as any one of these events occurring, but each such event was counted only once and only if it was the first adverse result. Any one of these events happening at any time, plus microvascular complications, counted as a secondary outcome. The results were dramatic.

Those on Metformin therapy had the lowest death rates, so that group was used as the reference.

In terms of primary outcome – that is, consideration of first adverse events only:

  • Sulfonylurea therapy resulted in patients being 1.4 times more likely to suffer one of these outcomes.
  • A combination of Metformin and Insulin resulted in 1.3 times greater risk.
  • Insulin therapy alone resulted in 1.8 times greater risk.
  • Those considered to be at greater risk because of glycosylated hemoglobin had as much as 2.2 times greater risk with Insulin therapy alone.

When considering any of these events happening, whether they were the first event or a subsequent one, the results were even more dramatic:

  • Insulin monotherapy resulted in:
    • 2.0 times more myocardial infarctions.
    • 1.7 time more major adverse cardiac events
    • 1.4 time more strokes
    • 3.5 times more renal complications
    • 2.1 time more neuropathy
    • 1.2 times more eye complications
    • 1.4 times more cancer
    • 2.2 times more deaths

Medical Hubris

Modern medicine’s hubris allows it to make claims that simply are not supported. Based on those unsupported claims, thousands—and in the case of diabetes, millions—of people are placed on drugs and regimens that have never been demonstrated to have any beneficial effect. The result is that the general public becomes a mass of guinea pigs for medical experimentation—experimentation that isn’t even documented and analyzed!

The use of insulin in type 2 diabetics is only one example, but it’s been clearly demonstrated again and again with disasters like Vioxx.

Redirection to Markers

The method by which these treatments are justified is a little redirection away from what really counts. What matters is whether lives are improved and lengthened. But drugs are rarely tested on that basis. The excuse generally given is that it would take too long. But if that were a valid explanation, then surely we’d see the regulating agencies keeping careful and formal oversight over the experiences of all new drugs for the first few years of use. That, though, simply doesn’t happen.

Instead of looking at the outcomes that matter, substitutes are used. They’re called markers, which are intermediate results that are assumed to be indicative of benefit. In the case of insulin, the marker is blood sugar level. Insulin is required to transport glucose (blood sugar) into cells so that they can produce energy. Thus, insulin reduces blood sugar levels. If artificial pharmaceutical insulin brings blood sugar to more “normal” levels, then the treatment is considered successful.

Invalid Markers

As this study has demonstrated, markers are simply not a valid way to determine effectiveness of a treatment. In type 2 diabetes, the problem isn’t a lack of ability to produce insulin; neither is it high blood glucose. The problem is the cells’ ability to utilize insulin to transport glucose from blood into cells.

The problem is that cells’ ability to use insulin has deteriorated. So, how can it be beneficial to give more insulin when cells are unable to utilize what’s already there? Clearly, that’s counterproductive.

Yet, that’s precisely what doctors do! They give insulin to replace insulin, when a lack of insulin isn’t the problem! It should come as no surprise that the real concerns of anyone being treated for diabetes are not answered by insulin treatment.

As this study has demonstrated, forcing insulin into the body actually results in worse outcomes. How many decades has this treatment been in vogue? All that time it’s been justified because it reduces blood sugar. But the effects that count—quality of life and longevity—haven’t been considered.

There’s one lesson to be learned here: Health isn’t found in pharmaceutical drugs, not even old tried-and-true drugs.



5 Amazing Properties of Sunlight You’ve Never Heard About




Below are detailed five noteworthy properties of sunlight exposure:



One of them, titled “Association of plasma vitamin D levels with adiposity in Hispanic and African Americans,” and which was published in the journal Anticancer Research in 2005, found that vitamin D levels were inversely associated with adiposity in Hispanics and African-Americans, including abdominal obesity.[iii] The point? Exposure to UVB radiation, which is most abundant two hours on either side of solar noon and responsible for producing vitamin D, may be an essential strategy in burning fat, the natural way.

3) Sunlight via Solar Cycles May Directly Regulate Human Lifespan: Published in 2010 in the journal Medical Hypotheses and titled, “The effect of solar cycles on human lifespan in the 50 United states: variation in light affects the human genome,” researchers review the possibility that solar cycles directly affect the human genome.  According to the researchers:

In the current study we report that those persons conceived and likely born during the peaks (MAX approximately 3 years) of approximately 11-year solar cycles lived an average 1.7 years less than those conceived and likely born during non-peaks (MIN approximately 8 years). Increased energy at solar MAX, albeit relatively a small 0.1% increase from MIN, apparently modifies the human genome/epigenome and engenders changes that predispose to various diseases, thereby shortening lifespan. It is likely that same energy increases beneficial variety in the genome which may enhance adaptability in a changing environment.

Sunlight exposure, therefore, may directly affect the length of our life, and may even accelerate genetic changes that may confer a survival advantage.[iv]

4) Daytime Sunlight Exposure Improves Evening Alertness: A 2012 study published in the journal Behavioral Neuroscience titled, “Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion,” found that subjects felt significantly more alert at the beginning of the evening after being exposed to 6 hours of mainly daylight exposure, whereas they became sleepier at the end of the evening after artificial light exposure.[v]

5) Sunlight May Convert To Metabolic Energy: If a novel hypothesis published in 2008 in the Journal of Alternative and Complementary Medicine is correct,[vi] a longstanding assumption that animals are incapable of utilizing light energy directly is now called into question.  In other words, our skin may contain the equivalent of melanin “solar-panels,” and it may be possible to “ingest” energy, as plants do, directly from the Sun.

Melanin has a diverse set of roles in various organisms. From the ink of the octopus, to the melanin-based protective colorings of bacteria and fungi, melanin offers protection against a variety of threats: from predators and similar biochemical threats (host defenses against invading organisms), UV light, and other chemical stresses (i.e. heavy metals and oxidizing agents). Commonly overlooked, however, is melanin’s ability to convert gamma and ultraviolet radiation into metabolic energy within living systems.

Single-celled fungi, for instance, have been observed thriving within the collapsed nuclear reactor at Chernobyl, Ukraine, using gamma radiation as a source of energy. Albino fungi, without melanin, were studied to be incapable of using gamma radiation in this way, proving that gamma rays initiate a yet-unknown process of energy production within exposed melanin.

Vertebrate animals may also convert light directly into metabolic energy through the help of melanin. In a review  titled, “Melanin directly converts light for vertebrate metabolic use: heuristic thoughts on birds, Icarus and dark human skin,” Geoffrey Goodman and Dani Bercovich offer a thought-provoking reflection on the topic, the abstract of which is well worth reading in its entirety:

Pigments serve many visually obvious animal functions (e.g. hair, skin, eyes, feathers, scales). One is ‘melanin’, unusual in an absorption across the UV-visual spectrum which is controversial. Any polymer or macro-structure of melanin monomers is ‘melanin’. Its roles derive from complex structural and physical-chemical properties e.g. semiconductor, stable radical, conductor, free radical scavenger, charge-transfer.

Clinicians and researchers are well acquainted with melanin in skin and ocular pathologies and now increasingly are with internal, melanized, pathology-associated sites not obviously subject to light radiation (e.g. brain, cochlea). At both types of sites some findings puzzle: positive and negative neuromelanin effects in Parkinsons; unexpected melanocyte action in the cochlea, in deafness; melanin reduces DNA damage, but can promote melanoma; in melanotic cells, mitochondrial number was 83% less, respiration down 30%, but development similar to normal amelanotic cells.

A little known, avian anatomical conundrum may help resolve melanin paradoxes. One of many unique adaptations to flight, the pecten, strange intra-ocular organ with unresolved function(s), is much enlarged and heavily melanized in birds fighting gravity, hypoxia, thirst and hunger during long-distance, frequently sub-zero, non-stop migration. The pecten may help cope with energy and nutrient needs under extreme conditions, by a marginal but critical, melanin-initiated conversion of light to metabolic energy, coupled to local metabolite recycling.

Similarly in Central Africa, reduction in body hair and melanin increase may also have lead to ‘photomelanometabolism’ which, though small scale/ unit body area, in total may have enabled a sharply increased development of the energy-hungry cortex and enhanced human survival generally. Animal inability to utilize light energy directly has been traditionally assumed. Melanin and the pecten may have unexpected lessons also for human physiology and medicine.



  • [ii] Association Between Visceral Obesity and Sarcopenia and Vitamin D Deficiency in Older Koreans: The Ansan Geriatric Study. J Am Geriatr Soc. 2012 Feb 8. Epub 2012 Feb 8. PMID: 22316299
  • [iii] Association of plasma vitamin D levels with adiposity in Hispanic and African Americans. Anticancer Res. 2005 Mar-Apr;25(2A):971-9. PMID: 19549738
  • [iv] Walter E Lowell, George E Davis. The effect of solar cycles on human lifespan in the 50 United states: variation in light affects the human genome. Med Hypotheses. 2010 Jul;75(1):17-25. Epub 2010 May 7. PMID: 20452128
  • [v] Mirjam Münch, Friedrich Linhart, Apiparn Borisuit, Susanne M Jaeggi, Jean-Louis Scartezzini. Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion. Behav Neurosci. 2012 Feb ;126(1):196-203. Epub 2011 Dec 26. PMID: 22201280
  • [vi] Geoffrey Goodman, Dani Bercovich. Melanin directly converts light for vertebrate metabolic use: heuristic thoughts on birds, Icarus and dark human skin. J Altern Complement Med. 2008 Jan-Feb;14(1):17-25. PMID: 18479839

Treat ACNE outbreaks without a prescription


Metazene – Niacinamide Gel

Acne vulgaris — or common acne — isn’t just a cosmetic issue: it’s a serious medical problem often leading to permanent skin damage and scarring, and emotional distress with a lifelong psychological impact. Contrary to popular belief attributing it to hygiene, stress, or diet, acne is actually caused by a bacterium, Propionibacterium acnes, feeding on skin oils. When the body dispatches immune cells to deal with the infection the result is irritation, swelling, and, sometimes, nodules or cysts. While acne primarily affects teenagers — and virtually all of them report having acne at some point — it plagues many adults well into their thirties or even forties!

Whether it be short- or long-term, acne can lead to substantial, permanent skin damage with few viable treatment options beyond cosmetic surgery — including dermabrasion, collagen injections, and grafts. As many as forty percent of acne sufferers seek medical treatment at least once. Traditional treatments include benzoyl peroxide creams, oral antibiotics (clindamycin, erythromycin, and tetracycline), and isotretinoin or retinoic-acid products (Accutane™, Roaccutane ™, and Retin-A™).

Benzoyl peroxide is hard on the skin and can cause irritation. Oral antibiotics are troublesome because of bacterial resistance, digestive upset, discolored teeth or skin, sun sensitivity, and interference with other medications. Isotretinoin compounds cause severe health problems, ranging from skin disorders, sun sensitivity, and nausea to vision irregularities, serious birth defects, depression, and even suicide. Side effects and poor results cause many acne sufferers to abandon traditional approaches. There is, however, a safe and effective alternative treatment: Lifelink’s Metazene, a Vitamin B-3 derivative.

Vitamin B-3, or niacinamide, is a potent topical anti-inflammatory. In clinical trials for acne, niacinamide gels proved superior to antibiotics without their side effects, which is why they are used worldwide. When a niacinamide gel is prescribed by a physician in the United States, however, federal law requires that it be made only by a specialized compounding pharmacy, often at considerable expense. Lifelink’s Metazene is the only niacinamide gel available in the United States that is made to pharmaceutical standards and sold over the counter without a prescription. Because Metazene is not compounded one tube at a time, it costs a fraction of what physicians and pharmacies charge.

Some people report amazing results using only Metazene. Others find it dramatically improves the results of traditional acne treatments, often with the added benefit of reducing the dosages for prescription drugs. We cannot, of course, guarantee that Metazene will work for you. What we can guarantee is that unless you try it, you will never know.

1 in 6 Americans infected with herpes











Source: Reuters

For information on using dietary BHT as a treatment for Herpes see:

Download the latest eBook on BHT here


Aging is Just Diabetes, Only Slower

zarkovAging, diabetes, toast, and roast beef all have something in common: crosslinking.

To a chemist, this means that sugars – from carbohydrates, starches, and natural sources – have reacted with cellular components like amino acids, fats, proteins, and DNA.

To a chef, it means that the Maillard reaction (See article in this issue) has browned a roast or caramelized onions.

To a doctor, it means that your arteries, organs, and cells have been hardened or damaged, causing cardiovascular disease, neurological disorders, vision loss, kidney problems, and chronic inflammation.

To you, it means premature aging, diabetes, and lowered quality of life.

Joined at the Hip

The basis of crosslinking is what chemists call intermolecular bonding. This means that molecules bond to other molecules. (Bonding inside the same molecule is called cyclization.)

Crosslinking is very useful: leather is tanned (crosslinked) skin, paint is cured (crosslinked) polymer films, plastics are polymerized (crosslinked) oils, and tires are made from vulcanized (crosslinked) rubber. Many of the natural products that we enjoy – fibers, wool, fur, and feathers, to name just a few – depend upon crosslinking.

Nearly anything can crosslink, which creates both opportunities and problems for the body.

A Double-Edged Sword

Crosslinking is a lot like Janus, the two-faced Roman god of doorways. With it we age, but without it we can’t live at all. Consider collagen, a critical protein in connective tissue, tendons, ligaments, cartilage, skin, bone, and even the cornea of the eye.

Crosslinked collagen is hard, which creates a host of problems: skin deterioration (wrinkles, sagging, stiffness), connective tissue rigidity (often misdiagnosed as arthritis), bone problems, organ stiffening (heart problems, bladder incontinence, lung issues), etc. But collagen is an example of the two faces of crosslinking; while unwanted bonds destroy collagen, they are also crucial for connective tissue strength. Without this web of interlocking we’d fall apart.

Our hair and fingernails are a type of crosslinked protein called keratin. (Hair straightener and depilatories rely on breaking crosslinks.)

Any solution to the crosslinking problem must target the unwanted type causing damage, while leaving the remainder alone. This is not always so easy to do, and considering how crosslinking originates will explain why.

Literally Tied Up in Knots

Consider a strand of protein as a flexible piece of rope. Imagine two adjacent strands of rope (protein) fixed only at the ends, such that each has total freedom to bend and move, independent of the other.

As more and more horizontal pieces of twine are tied from one rope to the other, the flexibility of movement declines until the two have become somewhat rigid. As the joining twine contracts, as it often does in crosslinked molecules, the ropes pull together simplifying adding new crosslinks.

This is exactly what happens in the body, as proteins and other molecules bind together. This changes their shapes, and thus their biological properties, preventing normal functioning.

Chemists call changes like these ‘denaturing’, since the original properties of the molecule have been altered. This isn’t always bad; cooking a steak denatures the proteins, making them far more digestible, and much tastier, too.

The idea that crosslinking causes aging is hardly a new one; back in 1941, Dr. Johan Bjorksten, a Wisconsin chemist, first proposed that undesirable bonding gradually damages proteins, fats, DNA, vitamins, etc.

These damaged molecules bind together into sticky tangles; over time, these blobs grow and wrap around other molecules, growing and posing more and more of a problem.

Leather, Hectographs, & Aging

Bjorksten came to his discovery because of his background in leather chemistry and his work on hectograph films, which were used to duplicate pages prior to the invention of the photocopier.

This wet process, which dates back to the late 19th century, uses a gelatin film to transfer ink to paper, much like a printing press. It was good for about fifty copies of the same sheet. (Remember this the next time you use fast, inexpensive, and dry copier technology.)

The problem plaguing Bjorksten was how to stop the gelatin films from hardening with age and use. He quickly identified the culprit as protein crosslinking, and noticed that the hard gelatin films were remarkably similar to damaged skin. He concluded that the same chemical processes must be at work in both cases and that inhibiting crosslinking would prevent any human diseases and disorders, and thus extend life.

Cracking Bonds With Enzymes

Bjorksten began taking vitamin E, the only anti-crosslinking agent available to him, and began searching for a means to crack the strong bonds with proteins.

The first approach used soil bacteria a rich source of raw material for pharmaceuticals fed crosslinked protein, exclusively. (Many antibiotics, like the potent streptomycin, originated with bacteria from dirt.)

The bacteria that survived would, of necessity, produce enzymes capable of breaking protein bonds. Bjorksten felt that these enzymes could then be used in humans.

The Real World Intrudes

Facing him were two big problems: science and funding. Every single enzyme he found that could break protein crosslinks was so toxic it couldn’t be used in lab animals, let alone humans. Beyond science, however, the debate over extending human lifespan was as contentious as today’s debates over stem cell research, and this made funding his work controversial.

Bjorksten also contributed to the controversy, including a proposal that the United States Department of Defense fund development of a “rapid-aging spray” to be used against enemy soldiers during wartime. The military’s reaction was, needless to say, not enthusiastic.

Running out of money and deciding the search for enzymes was hopeless, at least in any time frame that would benefit him – both of Bjorksten’s parents died from Alzheimer’s Disease, which exhibits a great deal of crosslinking – he abandoned breakers for other approaches.

Cracking Bonds With Chelation

Moving into chelation agents like Ethylenediaminetetracetic acid (EDTA), Bjorksten reasoned that if these compounds can break bonds with metals that they would prevent, or even break down, the protein tangles in the body.

There is evidence that copper and iron catalyze reactions between sugars and proteins, particularly in cataracts and Alzheimer’s disease, Johan Bjorksten and that eliminating excess metalions may slow crosslinking. This is, of course, a topic so big it needs to be covered in its own article.

A Theory Now Accepted as Fact

Bjorksten’s work on the ‘crosslinking theory of aging’ provides an explanation for aging and diabetes making perfect sense; the body’s proteins do harden over time. One example is the leathery skin of cowboys and habitual beach goers. His theory is accepted today as a crucial component in aging and disease, especially diabetes.

Origins of the Ties That Bind

Crosslinking is caused by such diverse factors as: inter-molecular bonding (metabolic by-products), ultraviolet light (sun, tanning salons), ozone (pollution), acetaldehyde (alcohol, cigarette smoke, pollution), ketones (diabetics, high-protein/low-carb diets), metal ions (lead, cadmium, mercury, copper, iron, aluminum), x-rays, and free radicals (normal metabolism, rancid or overheated oils and fats).

It wasn’t until 1965, however, that one of the leading culprits in crosslinking and aging was identified: sugar bonding to protein via the “maillard reaction”. (See the article in this issue.) This is why diabetics age prematurely and why otherwise healthy people need to protect themselves from even typical blood-sugar levels.

Other types of crosslinking, such as between proteins, lipids (fats) or involving metals like copper and iron, are very important as well. So are the sulfur-sulfur (disulfide) bonds made between the sulfur bearing amino acids in proteins. Sugar, however, seems to be the leading cause of damage and aging, even in non-diabetics.

Increases in blood-sugar happen after consuming starches and carbohydrates – these are broken down into simple sugars – as well as fruits and vegetables which also contain sugars and carbohydrates.

The problem is that sugar is a biochemical straight jacket: before it can be broken down and metabolized it locks up molecules needed for routine cellular function and creates toxic compounds.

Marrying Sugar to Protein

The overall process is very simple, but sounds a little complicated because of terminology. All you really need to know is in the next two paragraphs.

It all begins when sugar oxidizes, giving it a reactive carbon-oxygen (carbonyl) group that binds to proteins in a process called glycation. These glycated, or sugared, proteins eventually form stable, long-lived, and highly damaging Advanced Glycation End-products (AGE). This is the key phrase to remember, because the crosslinking theory of aging is basically all about AGEs.

Similar results occur when fats and proteins bond together. Reactions between proteins, sugars, and fats explain why sautÃ©ed food is tastier than steamed, and why sauces are made from browned bones (reacted proteins, fats, and sugars), roasted vegetables (caramelized carbohydrates and natural sugars), and butter (fat). (See the article on the “Maillard Reaction”.)

How Sweet It Isn’t

Arteries and the fine capillaries in the retina and kidney are particularly vulnerable to sugar protein reactions because, unlike other cells, they cannot break down some forms of sugar like sorbitol. These then attack the proteins in the blood-vessel walls, leading to damage and AGEs.

Artery-clogging plaque is nothing more than globs of crosslinked AGEs made from a variety of material sugars, proteins, lipids and fats like cholesterol, metals, fibrin, etc.

You’re Showing Your AGE

Over time, AGEs crosslink the inside of your body like a browned roast, causing diseases like cardiovascular hardening and heart attacks, retinal deterioration, cataracts, glaucoma, peripheral nerve damage, kidney failure, osteoarthritis, stroke, scleroderma, and atherosclerosis.

Once a long-lived protein, such as those in the eye s lens or the collagen in skin and joint cartilage, is damaged it usually remains so. This is why levels of the AGE product pentosidine in the joint cartilage of an eighty-year old have been measured as being over thirty times those of a twenty-year old.

Implicated in many diseases, AGEs are known to activate a variety of inflammatory cytokines, or messenger molecules, including tumor necrosis factor alpha (TNF-a) and interleukin, even in otherwise healthy people.

Stop Doing That Right Now!

A variety of prescription drugs and nutritional supplements with anti-crosslinking effects are readily available. (See “Which of the Crosslinking Inhibitors and Breakers Are Right For You” in this blog.)

Nearly a thousand such compounds are known, but many of them, as Bjorksten discovered a long time ago, are completely unsuitable for use in the body.

Crosslinking inhibitors – available as both prescription and supplements – typically interfere with the binding of the carbonyl groups (just a carbon-oxygen bond) on sugars to amino acids and other molecules. Some inhibitors are sacrificial, binding to an active site on the sugar before it can disrupt an amino acid in a protein.

The aptly-named crosslinking breakers crack the bond between the sugar and the protein, undoing some of the damage and allowing repair. This is more difficult, and many of the breakers target bonds – like those giving cartilage its strength – that must remain untouched.

Breaking Sugar’s Hammerlock

Supplement-based compounds are known to break existing AGE bonds without serious side effects. Prescription drug breakers are still relatively new, however, and have limited safety histories. Until their long-term, and even short term, effects are well known and understood, supplements are generally a safe, effective, and very affordable alternative.


Toast, roasts, and caramelized onions can be delicious, but you certainly don’t want the same reactions occurring in your body. So, if you have diabetes or just want to put the brakes on your age-related deterioration, you’ll definitely want to add crosslinking inhibitors and breakers to your supplement list. Before your body gets tied up in knots!

For a more information on Aging & Diabetes see:

Imagine If Everything You Knew about Aging Was Wrong!

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