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.

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

 

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?

Source: http://market-ticker.org/

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

Source:  http://www.primalbody-primalmind.com/who-red-meat-brouhaha/

Lecture on vitamin C by brilliant Suzanne Humphries