The Mysterious Virus That Could Cause Obesity

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

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

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

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

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

The Curious Case of Indian Chickens

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

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

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

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

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

Fat, it seemed, could indeed be contagious.

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

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

The Pounds Keep Coming

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

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

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

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

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

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

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

The Virus in Americans

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

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

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

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

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

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

A New Way to Manage Fat—Stop the Blame

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

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

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

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

How Does a Virus Lead To Fat?

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

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

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

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

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

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

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

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

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

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

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

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

How?

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

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?

Source:  www.marksdailyapple.com

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

Selenium is a trace element a Swedish chemist, Baron Jöns Jacob Berzelius, discovered almost 200 years ago. Today, modern scientists recognize it as “an essential mineral of pivotal importance for human health,” with anti-inflammatory, antiviral and anti-cancer potential.1

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:

“Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants”3

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

Cancer

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

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

HIV/AIDS

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.)

mercola.com

 

How bugs in your gut can make you fat (or thin)

This is the second part in our series on the microbial populations we harbour and their effects from brain to bowel.


By far the majority of our companion microbes,
weighing an impressive 1.5 kilograms and containing more than 1,000 species, reside in our gut, mostly in the large intestine.

As soon as a baby is born – and perhaps even before – microbes move in. Many are seeded from bacteria in the mother’s birth canal if it’s a vaginal birth or from her skin if it’s a caesarean birth.

An infant’s milky diet fosters a unique set of gut microbes. The infant microbiome gradually changes until, by the time a toddler is three years old, it has morphed into a more diverse ecosystem that is indistinguishable from an adult’s.

Gut communities differ from one person to the next, and are heavily influenced by the food we eat. They are also rapid responders to dietary change, re-configuring for a new diet in just a day or two.

Gut microbes do more than just scavenge from the food we eat. They also harvest energy and synthesise essential nutrients, such as certain B vitamins and folate, for us. Indeed, pregnancy sways a mother’s gut ecosystem towards one that harvests more calories per bite.

Mice raised to be germ-free are skinnier than their germy counterparts, even when they eat more; with no microbes at all, they can’t extract as many calories from their food.

There’s now compelling evidence that tinkering with microbes living in the depths of our bowels could be contributing to our expanding waistlines. Scientists are still figuring out what microbiota changes are most detrimental and how such changes cause weight gain.

Some of the earliest evidence that gut bugs affect weight gain came from farm animals. Since the 1940s, farmers have fattened livestock by feeding them low doses of antibiotics – enough to affect their gut microbiota but not enough to be therapeutic.

Humans, it turns out, aren’t immune to this effect. Taking repeated courses of antibiotics during infancy increases the risk of becoming overweight, at least in childhood, which is a good predictor of obesity in adulthood. The first six months of life are particularly critical. And boys seem to be more susceptible than girls, though why is a mystery.

many strains of so-called ‘good bacteria’ that are available in commercial probiotic concoctions don’t stick around to become long-term members of the gut community

And why infancy is such a crucial time isn’t fully understood either. One suggestion is that it coincides with the time our body decides how many fat-storing adipose cells to lay down to accommodate calories.

It’s not just antibiotics that can make a baby’s microbiota fattening. Birth by caesarean section and being fed formula instead of breast milk also seem to tip the scales towards greater childhood weight gain.

In many cases, antibiotics, caesarean delivery and baby formula can’t be avoided. And an untreated infection or undernourishment can be far more harmful than a potential increase in the risk of being chubbier as a toddler.

Another thing to remember is that even with microbiota disruptions as a child, it’s not a foregone conclusion you’ll end up obese, says Laura Cox, a biologist at the Brigham & Women’s Hospital and Harvard Medical School in Boston in the US who has studied the antibiotic-obesity connection: “The risk of being overweight from microbiota disruption [in early life] is not as big as other risk factors, such as certain genetic factors or eating certain diets or never exercising.”

The situation in adults is murkier.

Scientists are still getting a handle on how disruptive antibiotics – and other chemicals and food additives we encounter daily – might be. Our gut communities tend to bounce back after a dose of antibiotics, but Western gut microbiota are generally less diverse – and perhaps less resilient to disruption – than those of people living more traditional lives. And there’s enormous individual variation.

Mice demonstrate the power of gut microbes to influence weight gain between individuals. In 2006, a research group from Washington University in St Louis took poo from obese mice and transplanted it into the gut of skinny, germ-free mice, which promptly became obese.

It didn’t matter whether the original obese mice were fat from too much healthy chow or from eating a high-fat ‘Western’ diet. Excess calories seemed to be the key factor turning their microbiota into an obesity-causing (or ‘obesogenic’) community.

Lactobacillus species are often found in commercial probiotics. But whether they do much for your metabolism is still contentious. Credit: Dr Kari Lounatmaa/ Getty Images

Lactobacillus species are often found in commercial probiotics. But whether they do much for your metabolism is still contentious.
Credit: Dr Kari Lounatmaa/ Getty Images

A single case report from 2015 suggests the same applies to human-to-human poo transplants. A woman who received poo from her overweight daughter to treat severe diarrhoea became obese in the months following the procedure.

So, what makes a microbial ecosystem obesogenic?

According to Cox, there doesn’t seem to be any ‘bad’ microbes that take over in an obese gut community. But along with an overall loss of diversity in the ecosystem, a handful of microbes consistently become less common.

Other studies have focused not just on who’s there, but what they collectively do.

A hallmark of an obesogenic microbiota is a change in the types and amounts of short chain fatty acids microbes pump out after fermenting dietary fibre (and to a lesser extent, protein).

Short chain fatty acids provide up to 10% of calories absorbed when consuming a Western-style diet – and probably more in extremely high-fibre, plant-based diets. But they also act as signalling molecules, dialling up satiety messages in our brain, slowing food movement through our gut and boosting fat cell production.

How do we keep good microbes happy? Unfortunately, cultivating protective microbes with dietary supplements called prebiotics has seen mixed results. When mice are fed a low-fibre diet, their microbial ecosystem becomes less diverse. Simply re-adding fibre to their diet doesn’t fix the problem – once an organism is lost, it may be lost for good. And over generations, the problem is compounded – mothers can’t seed their offspring with gut bacteria they no longer have.

Similarly, in obese women given the fermentable fibre inulin – to boost short chain fatty acid production – weight loss was only modest. And the best responders already harboured particular clusters of beneficial bacteria that could blossom with the added nutrient.

Probiotics – consuming live bacteria to replenishing the gut with microbes that have been lost or are limited in number – has been touted as a possible solution. But scientists are yet to identify microbes that reliably work to reduce weight gain, and many strains of so-called ‘good bacteria’ that are available in commercial probiotic concoctions don’t stick around to become long-term members of the gut community.

The more drastic approach of replacing the entire ecosystem with a poo transplant hasn’t fared much better. In 2012, researchers in the Netherlands transplanted poo from lean donors to people showing early signs of developing type 2 diabetes, a metabolic disorder that frequently accompanies obesity.

Although metabolism improved in the immediate aftermath of the transplant, microbes and metabolism reverted to an unhealthy state within six months.

The lesson seems to be that the best way to foster a healthy, diverse gut community is to feed it right from the get-go – with foods high in fibre, low in fat and not overloaded with calories.

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.