Friday, December 15, 2017

There May Be Just Enough Healthy Coral Left to Save the Great Barrier Reef

First, the meme that all that damage is caused by temperature change is rubbish and an exercise in misdirection.  The most probable cause is agricultural run off which has been heavy in nitrogen for the past several generations.  As well that run off will be in the surface waters most likely to affect reefs.

The switch out to organic agriculture will  allow these reefs to completely reverse and stage a total recovery.
In the meantime we have this nonsense to put up with in order to hide the true culprit..

There May Be Just Enough Healthy Coral Left to Save the Great Barrier Reef 

Australian scientists see a way back from the mass bleaching events brought on by climate change.
Jackie Flynn MogensenNov. 28, 2017 2:00 PM 

The Great Barrier Reef is called “great” for a reason. As the world’s largest reef system, it’s half the size of Texas, home to about 10 percent of the ocean’s fish species, and generates billions of tourism dollars annually. Plus, it’s damn beautiful.

The Great Barrier Reef in 2012

Mark Conlin / VW Pics via ZUMA Wire In recent years, however, the reef has lost half its coral in two consecutive mass bleaching events, caused by rising ocean temperatures as a result of (you guessed it) climate change.

Reefs are created by coral building polyps and photosynthetic algae, working together in a symbiotic relationship. When corals are stressed, the polyps can expel their colorful algae, dulling their brilliance and, in extreme cases, turning reefs bone white. That’s why big parts of the Great Barrier Reef now look like this:


Bleaching on the Great Barrier Reef

Shutterstock But, there is hope! According to a study published Tuesday in the open-access journal PLOS Biology, small clusters of the reef are ideally situated to re-populate the bleached areas with the organisms that make coral, and make it beautiful.

Of the 3,800 individual reefs that make up the Great Barrier Reef, scientists identified 100 that live in naturally cooler areas—and are therefore healthy—and that sit near ocean currents that can transport fertilized coral eggs to new locations across the reef.


A healthy coral reef in the Great Barrier Reef system

Peter J. Mumby “Finding these 100 reefs is a little like revealing the cardiovascular system of the Great Barrier Reef,” said author Peter Mumby, a professor at the University of Queensland, in a press release. “Although the 100 reefs only make up 3 percent of the entire GBR, they have the potential to supply larvae to almost half (45 percent) of the entire ecosystem in a single year.”

Although the findings are cause for celebration, the authors warn that the corals will only have a real chance at recovering through local protection and global efforts toward “serious mitigation of climate change.”

A Clue in the Bee Death Mystery

Disturbing the fungi balance could well be the actual vector, but it is certainly triggered by the application of a spectrum of pesticides.

The damage done is huge and ongoing.  Collapsing the insect biomass naturally collapses the song bird biomass as well..   Worse the toxins do enter the hydraulic system and this means it all crosses the skin barrier of all aquatic animals.  This surely has led to the collapse of the population of amphibians.

Add in the attack by Roundup on the biological world, including the human decline in fertility and the case for organic methodology is made.

A Clue in the Bee Death Mystery 

Insecticides are often blamed, but new signs point to another chemical. 

Tom PhilpottNov. 29, 2017 6:00 AM 

A rusty-patched bumble bee. Smithsonian's National Zoo/Flickr

Domesticated honeybees get all the buzz, but wild bumble bees are in decline too, both globally and here in the United States. What gives? It’s an important question, because while managed honeybees provide half of the pollination required by US crops, bumble and other wild bees deliver the other half.

Insecticides used in agriculture are one possible trigger—they exist to kill insects, after all, and bumble bees are insects. But a different kind of farm chemical, one designed to kill fungi that harm crops, has emerged as a possible culprit. A new study by a team of researchers led by Cornell University entomologist Scott McArt adds to the growing dossier of studies pinpointing fungicide as a potential bee killer (see here, here, and here).

In their paper, McArt and his team looked at two factors related to bumble bee decline. The first is that many bumble bee species appear to be confining themselves to ever smaller geographical regions—a phenomenon known as range contraction. The other is a microscopic parasite called Nosema bombi, which has turned up at high rates in bumble bee species known to be deteriorating.

Many bumble bee species appear to be confining themselves to ever smaller geographical regions. The team analyzed samples of bumble bees from eight species taken by previous researchers from 284 sites across the country between 2007 and 2009. For the areas surrounding each site, the McArt team crunched data for 24 environmental factors that might affect bee health: Everything from the level of nearby residential development to the portion of land devoted to forests to the amount of insecticides, herbicides, and fungicides applied by farmers.

Their goal was to see which of these factors was most closely associated with shrinking habitats and Nosema bombi infections. Total fungicide applications in a given area emerged as the best predictor of range contraction; and a single widely used fungicide, chlorothalonil, proved to be the clearest indicator of Nosema bombi prevalence.

The result wasn’t a total surprise. A 2015 study by University of Wisconsin and US Department of Agriculture researchers found that bumble bee hives exposed to small amounts of chlorothalonil—which is widely used in fruits, vegetables, and orchard crops—”produced fewer workers, lower total bee biomass, and had lighter mother queens than control colonies.”

Here’s a map of where chlorothalonil is used, from the US Geological Survey:

To make matters worse, the fungicides can exacerbate the effect of other types of chemicals. “While most fungicides are relatively nontoxic to bees, many are known to interact synergistically with insecticides, greatly increasing their toxicity to the bees,” McArt said in a press release accompanying the study.

Meanwhile, bumblebees continue to struggle. In its final days, the Obama administration declared the rusty-patched bumble bee, pictured above, as endangered—and its plight is so severe that the Trump administration opted to secure the designation, after hinting it would undo it.
Unlike murders, ecological collapses rarely have a single perpetrator. Rather, they’re caused by a host of culprits working together in ways that are hard to unpack. Add fungicides to the list of potential offenders in the ongoing pollinator crisis.

President Trump saves the elephants of Zimbabwe

Image: President Trump saves the elephants of Zimbabwe: Big game hunting trophy ban to remain in place

At least he is paying attention to this problem.  Also we get mike's take on the whole issue of hunting with which i fully concur.  I am not so sure that we want to let up yet on wild hogs but that is actually only the beginning.

Our long term problem is successful wild life management and the necessary harvest of surplus animals.   None of that is addressed by an idiot running around with a rifle, nor can it be addressed successfully by adding in a large range of carnivores.  Fencing has done the most in this regard but it is hardly perfect.

It will really take human mind augmentation allowing mind to mind communication or more correctly mind to mind no trespassing fences.   I do not think this is impossible at all.
President Trump saves the elephants of Zimbabwe: Big game hunting trophy ban to remain in place

(Natural News) Believe it or not, the murder of elephants with hunting rifles is routinely called “conservation” by government regulators. (Note carefully that human depopulation is also being promoted as a way to “save the planet” these days.) After government bureaucrats at the US Fish and Wildlife department announced a recent decision to allow big game “trophies” to be imported into the United States, President Trump reversed the decision and reinstated the elephant trophy ban, reports the UK Daily Mail.

“Put big game trophy decision on hold until such time as I review all conservation facts. Under study for years. Will update soon with Secretary Zinke. Thank you!” he tweeted.

This means that U.S. big game hunters will no longer be able to bring their “trophies” back to the United States, creating a strong disincentive for them to go hunt the elephants in the first place (big game hunters think it makes them “macho” to hang the heads of dead animals on their walls). Effectively, President Trump just saved many elephants of Zimbabwe.

Hunting elephants is one of the most insanely cruel and evil acts imaginable

Now, for my take on all this:

As you probably know, I’m a long-range target shooter, trained to hit targets at 1,000+ yards with precision and accuracy. Yet I would never think of deploying such skills against an innocent, intelligent conscious being such as an elephant.

Elephants are intelligent, aware and majestic creatures. They have excellent memories, they experience emotions, and they grieve for the loss of their loved ones. In many ways, elephants display the “humanity” that now seems to be lacking in most humans. We should look to elephants for inspiration, not for target practice.

To this day, I still cannot understand how a human being can think of hunting elephants or other big game as a form of entertainment. The depth of cruelty and evil in such acts is almost too intense to accurately describe in mere words. The murder of an elephant is, in many ways, much like the murder of an innocent child. Yet all across America, the ultra-wealthy line up to murder elephants and other large game so that they might acquire bragging rights for having killed an innocent being.

Note that only the ultra-wealthy can afford to hunt big game in Africa. This is not an activity that everyday firearms owners pursue. Hunting big game probably costs on the order of $100,000+ by the time you factor in the travel, hunting guides, local licenses and all the rest. Big game hunting, in essence, is the cruel “sport” of the heartless and wealthy… people with too much time and money on their hands and no sense of empathy for the animal kingdom.

As a firearms advocate, I often encounter people who enjoy hunting animals. It has never made any sense to me, and I often try to explain to these people, “Rifles are for defending liberty, not for killing innocent animals.” The Second Amendment, after all, was actually written to protect the rights of the people to shoot tyrants, not for hunting purposes.

Wild hogs, rattlesnakes and “nuisance” creatures

In Texas, where I’m based, there’s a lot of hunting of wild hogs, which are a genuine nuisance to farmers and ranchers across the South. These wild hogs tear up fields, effectively creating potholes that subsequently tear up tractors and other equipment. Because these wild hogs are such a nuisance, Texas and other states have declare “open season” on those hogs year-round. So farmers routinely shoot them, even when such efforts seem to do nothing to stem the tide of the hogs. (They reproduce rapidly and live off the wild onions in the dirt. These wild hogs are the ultimate survivalists…)

At one level, I can sort of understand other people shooting wild animals that become a strong nuisance to their own ranch operations, but I personally don’t hunt them on my ranch. I see them frequently, however. On certain days, I’ll encounter 40 – 50 of these wild hogs when walking my own animals, and just yesterday I spotted what surely must have been a 350 lb. male hog, journeying on his own. All wild hogs run from humans and seem to pose no actual risk to human beings (although they do have tusks, but I’ve never seen one attempt to attack me or any other human).

Technically, shooting one of these wild hogs is child’s play. It takes virtually no skill at all (and therefore proves nothing). So I wouldn’t even think of shooting one of these creatures as any sort of “challenge” in the first place. Anyone can easily approach these wild hogs to within 75 yards or closer, and if you can’t hit your target at 75 yards, you probably shouldn’t own a rifle in the first place.

(By the way, I do shoot rattlesnakes when I encounter them on my property. I do not shed any tears over shooting rattlesnakes, as they pose a very serious hazard to my goats, donkeys and dogs. They are also extremely dangerous to humans and can cause you to lose an entire foot or leg due to medical amputation. Importantly, when shooting rattlesnakes, you must accurately hit their head on the first shot to completely nullify them as a threat. Even half a rattlesnake can still bite you as long as their head is still functioning. Fortunately, when coiled in their striking position, rattlesnakes make a very still target that’s easy to shoot: Their rattles are going off, but they are motionless and coiled. One shot to the head instantly stops the rattle and causes the snake to collapse dead. If you’re a terrible shot and can’t accomplish this with a solid bullet, try a revolver with a .410 gauge shotgun shell in it, such as The Judge. Or just use a 20 ga. shotgun.)

Cruel to kill wild hogs for sport, but justifiable in extreme survival situations

As a prepper and practical person, I should disclose that if a total collapse event were to take place that thrust us all toward starvation due to a collapsed food supply, I might harvest a few wild hogs for meat (for myself as well as my dogs), but shooting a wild animal is never something I would pursue as “sport” or “entertainment.” Wild hogs have consciousness, too. They are intelligent, aware and capable of feeling pain. To put any animal through the pain and suffering of being shot is an unacceptable activity except in the most dire survival circumstances, in my view.

I say all this as an accomplished shooter. I recently tied for first place in a pistol competition shoot. My battle rifle skills are well polished, and my long-range rifle skills are better than probably 99 out of 100 rifle owners, since most rifle owners have no clue how to calculate long-range ballistics to put rounds on target at extreme distances. I’m saying all this because I want you to know that just because a person is proficient in firearms doesn’t mean they enjoy shooting innocent animals. Firearms proficiency and “hunting” are not synonymous. Many anti-gun people on the Left tend to dishonestly conflate these two concepts, falsely asserting that all firearms owners are simultaneously cruel to animals. That’s a blatant lie.

My mission is the protection of life and liberty. That’s why I advocate for natural medicine while also being a highly proficient firearms operator. In my view, firearms should be deployed to save lives, not to take innocent life. Even in a case where firearms must be deployed to defend liberty, such actions must always be pursued only as a last-ditch defense when all other options have been exhausted.

Firearms are tools that should be used to SAVE lives, not take lives

Firearms are tools that, in my view, should be used to save lives. That’s why you will never find a big game “trophy” in my house. Nor will I ever hunt animals for entertainment purposes, as such acts stand in total violation of my principles and ethics.

Hunting is not a necessary activity to acquire very high-end proficiency as a long-range shooter, by the way. Technically, the skill that most hunters lack is mathematics. You need good math skills to compensate for real-world conditions such as wind, inclination, moving speed of the target, the cosine of the wind angle, etc. That’s because all bullets follow the laws of physics, and the laws of physics are well described by mathematics. If you suck at math, you will also suck at long-range shooting. (There are a lot of hunters in America who are terrible at math and terrible at shooting. I would tell hunters that it is highly unethical for you to hunt animals when your firearms skills are so poor, as you’re more likely to wound the animal than actually kill it. If you’re going to hunt a living creature, at least have the decency to take its life as quickly and painlessly as possible.)

My hope is that I never have to take a life with a firearm. Should that unfortunate day come — due to collapse, self-defense or national defense — I will of course deploy all the tools in my possession in the defense of life and liberty, but I won’t celebrate it. I’ll probably shed tears of sadness.

Until then, I pray that we may all live in a world where innocent beings can be free to roam without being targeted for murder. And I pray that we can live in a world where the tyranny of the deranged, totalitarian Left is held at bay so that the Second Amendment need never be activated in national self-defense. I pray that my firearms need only shoot paper and steel targets, never flesh and bone. And I pray that the Left never attempt a nationwide confiscation of citizens’ firearms, for such a proclamation would likely unleash a torrent of bloodshed across our nation, probably ending in civil war or armed revolt.

– Mike Adams

The New Mind-Body Science of Depression

Members Download Article: NPTV5I11pp26-45

Charles Raison, MD, is the Mary Sue and Mike Shannon Chair for Healthy Minds, Children & Families and Professor in the School of Human Ecology and the School of Medicine and Public Health at the University of Wisconsin–Madison. He also serves as Director of Clinical and Translational Research for Usona Institute, as Interim Director of Research in Spiritual Health for Emory Univer¬sity Healthcare, and as the Founding Director of the Center for Compassion Studies in the College of Social and Behavioral Sciences at the University of Arizona.

Dr. Raison is internationally recognized for his studies examining novel mechanisms involved in the development and treatment of major depression and other stress-re-lated emotional and physical conditions, as well as for his work examining the physical and behavioral effects of compassion training. Dr. Raison received the Raymond Pearl Memorial Award from the Human Biology Association “in recognition of his contribu-tions to our understanding of evolutionary biocultural origins of mental health and illness”.

Dr. Raison’s book The New Mind–Body Science of Depression was published by W.W. Norton in 2017. In addition to his other activities, Dr. Raison serves as the mental health expert for

Dr. Dave: Dr. Charles Raison, welcome to Shrink Rap Radio. You and your co-author, Vladimir Maletic have written the 2017 book The New Mind-Body Science of Depression. I must say it’s a real tour de force on the topic of depression.

Raison: Thank you. It took us five years to do it.

Dr. Dave: What led to the writing of this book?

Raison: Well, it’s interesting. Vlad and I are colleagues. We’ve been colleagues and friends for years. We do a lot of medical education stuff, a lot of lecturing to mental health people. Vlad is a walking encyclopedia of neurobiologic and clinical knowledge. I have been in awe of him for years. Back, six, seven years ago, we began to talk about the fact that we should try to get some of this down. We were wandering around talking about it and people seemed really, really interested. So we decided to capture this program of education we’ve been doing for years and put it in print form. That’s what really launched the book.

Dr. Dave: I think it’s a really important book, but it seems like things are moving so fast in the field that it may not be a classic because the information will change.

Raison: I’ve already thought about how if and when the time came that we did a second edition, it’d be a major rewrite. From when we started the book to when we finished it, we had to go back and rewrite part of it. There’s been a lot of interesting discovery in the last four to five years.

Dr. Dave: Well, I have to say your book is very carefully argued, is evidence-based, and it presents a complex picture which makes for challenging reading.

Raison: Yeah, I know. It’s hard. Parts of it are very dense, you know. The book runs a gamut. We have some case studies in the back that are very approachable. We’ve got some sections about the neurobiology—there’s a lot in there. Very dense and detailed.

Dr. Dave: Well, I’m going to try to lead you through much of the book. Can you give us the highlights to start? Your focus is on major depressive disorder as opposed to what? There’s major and there’s?

Raison: There’s minor, there’s all sorts. The manual of psychiatry, the DSM, that codifies diagnoses. It has a number of new disorders. We focus on major depression because it’s the sort of standard depression. But one of the key arguments we make in the book is that it’s not—even though it has a code and we call it an illness, it’s not a discrete thing. In fact, we explicitly say that we prefer to use the word depression because we recognize that depression far exceeds the more limited bounds of major depression and that depression, in almost all of its forms, is very, very painful and can be very problematic for people.

I’ve come to prefer the word depression better. It’s not as clinical, not as exacting, but it gets closer to the fact that there is a phenomenon out there that is not one thing. It’s more like a cloud of symptoms, and something that is very common. You see something like it all around the world. You can see it in hunter-gatherers. It’s a thing. It’s not a thing that has hard boundaries, but it is a thing, and it really is depression.

Dr. Dave: I was really struck by what you just said, going back to hunters and gatherers, because you make the point that it’s not a symptom of western culture which many people might assume, but it goes all the way back.

Raison: Yes, as far as we know. We know it is in historical times. There’s a couple of ancient papyri from about 3,000 BC from Egypt that articulate something that we would clearly recognize as major depression. Mood disorders were beautifully described in the ancient world. Hippocrates did a good job. There were others. There’s a famous guy from Turkey … his name escapes me … who laid out mood disorders beautifully and recognized bipolar disorder as a type of mood disorder. Beautiful descriptions of depression in the renaissance. But more recently, there’s been some interesting work, part of which was done to test one of the theories that we talk about in the book, having to deal with why depression may have evolved.

A group of anthropologists out at the University of New Mexico went down to one group that may not be fully hunter-gatherers, but they’re pretty close, and did very, very rigorous depression screening there. It found a number of interesting things. One of them was that the biology of depression there looks like the biology of depression here, and second, that the symptoms looks the same. The people had very much the same symptoms and they had the symptoms from many of the same reasons. There’s a little cadre of reasons for why humans tend to get depressed. I think the best evidence suggest that those reasons are very ancient. Depression evolved probably as a response in one way or another for coping with those reasons.

Dr. Dave: I was also surprised to learn that individuals who have experienced more than one major depression show lasting cognitive decline. I wasn’t aware of that. That’s rather alarming.

Raison: Very alarming. I mean, for those of us that have struggled with depression.

Dr. Dave: As I have.

Raison: Yeah, I have too. If you’ve had a depression, if you think about it, you probably recognize that it impairs your thinking, it makes you feel sluggish, you have a hard time remembering things. Then there’s this indecisive thinking that comes up, but we don’t sometimes think of that as cognitive, but you have a hard time making decisions, things seem overwhelming that way. There’s older data that those symptoms take longer to clear up than mood symptoms do. They’re not always as responsive to antidepressants, they linger, and they are a major source of morbidity in the disorder.

Part of what nails people with depression is it screws up their ability to think and remember. It’s a huge problem, and it’s a problem that we’re becoming more aware of in the last few years. Certainly, it’s become of more interest since we started writing the book because it’s become a focus of the pharmaceutical industry. There are a couple new antidepressants that target a serotonin receptor that has been associated with improved cognition, you know, so all of a sudden, people are very interested in this idea, “Oh, man. Maybe we can specifically do something about it.” Not so clear if that’s true, but anyway, it’s a big deal.

Dr. Dave: One of the things that you take on is the DSM-5 which has some coverage of depression. What is it that they’ve got wrong there?

Raison: Well, what they’ve got a couple of things wrong, but they’ve got a couple of things right. What they have wrong is that it’s built upon an idea that is extremely admirable and it was the idea of one of my main mentors. I went to a school in a place called Washington University in St. Louis. That was really one of the two primary founding sites for what became the DSM. The chairman of the department Samuel Guze along with Eli Robins felt and provided some evidence that psychiatric conditions were really diseases. That if you look at their symptoms and if you follow their symptoms over time, that it would be like discovering a bacteria and saying, “Oh, hey, that’s what causes tuberculosis.”

So, they thought that something like major depression was a disease state and that it was a disease state that differs, say, from something like bipolar disorder or differed from something like schizophrenia. Why did it differ? Because it had different symptoms and tend to have different outcome over time. It’s not that that’s exactly wrong, but it’s pretty clear now that it’s really not true. That in fact, as we have come to understand the mechanisms for these disorders, both genetic and systems within the body. There’s a huge overlap between many of these disorders. For instance, the genetic risk factors for depression are largely shared with something like bipolar disorder and even with schizophrenia.

When you look at the mechanisms that underlie these disorders, there’s some evidence that there’s some differences between them. But what strikes me is the fac that so many of the changes were reminiscent of each other. We look at brain changes or immune changes. What is emerging now in psychiatry, is that in ways we never would have guessed 30, 40 years ago, these disorders we label as being separate have powerful genetic and biological overlaps. We don’t know how to cleave nature at the joints. What we don’t know how to do though is to take these emerging scientific data and say, “Oh, well, let’s come up with a whole bunch of new disorders.” If two people with depression have got the same symptoms and one of them has a problem with their immune system, with TNF (tumour necrosis factor alpha), that’s a immune molecule then they’ve got a TNF disorder, so hey, what we used to call it major depression, we can now call it TNF disease.

Another person has got a problem with their cortisol, so we’re not going to call it major depression, we’re going to call it cortisol disorder. But that’s what we cannot do yet. Even though we’ve begun to understand that there are complex overlaps in the biology of these disorders and within each disorder, we have not yet come up with anything frankly, better than the DSM. That’s why in our book, and this eventually is what the National Institute of Mental Health has recently decided too, is to recognize that the DSM with its description of things like major depression is a useful clinical document that helps people use the same language. You and I can diagnose the same thing if we see somebody with something like major depression. But that these are not disorders like rheumatoid arthritis or pneumococcal pneumonia. The

Dr. Dave: In fact, you talk about the National Institute of Mental Health and IMH in the book. You say that for the purposes of funding research, they’re sort of ignoring the DSM-5 and requiring a different type of research. Can you briefly characterize what that different type of research is?

Raison: Another colleague of mine, a very famous guy named Tom Insel became the head of NIMH. He is no longer there, but about 15 years ago, this brilliant, bold controversial man came in and said, “When we look at research in general, if we look at cancer, we see a significant decline in deaths from cancer over the last 20 years. If we look at heart disease, even more impressive. We look at, say, depression, let’s say suicide as a proxy for depression. Rates haven’t dropped, they’ve gone up. We are failing.” More recently he said, “I don’t know what the number was, like $20 billion during my tenure in IMH. We did some really cool work, but I don’t think we accomplished anything.” So he decided to take the bull by the horns and say he thought part of the problem was that we’re trying to study these DSM disorders and they don’t exist. That they don’t exist that way. They don’t have a single mechanism.

So they came up with a system called RDoC, which stands for Research Domain Criteria, and, basically, instead of reaching into the DSM, they said, “We’re going to have these domains that we think characterize mental disturbance more generally, so a cognitive function domain, a stress resilience domain, a negative affect valence domain.” You’re only going to get grants if they propose to study those domains. But you can see you’re now setting up another set of these sort of criteria. So if you take something like stress resilience, there are probably a hundred ways to get stress resilience, right? Calling that a sort of a mechanism, it’s a step forward, but the problem is we don’t know the hundred ways.

The brain and the body in these regards are so complex that although we’ve learned a lot, really trying to zero in, is always the problem. But yes, NIMH has really changed things in very interesting ways in terms of they will now really only fund projects that use these sort of criteria and try to look at a mechanism. So, if I got a new treatment for depression, they’re not very interested in me just trying it on depressed people. What they want is for me to say, “I think it works by blocking inflammation.” So first show me that it blocks inflammation and then show me that people get less depressed. It’s a very logical idea, right? They’re really trying to get to be like the rest of medicine and try to find mechanisms.

Dr. Dave: I’m thinking of phenomenology as the experience, the inside experience of depression.

Raison: Yes. It’s often used to mean a “descriptor of symptoms”, like a description of what is it that people that have depression experience. There is no doubt that we need that, and there is no doubt that I have no idea what it is.

Dr. Dave: Okay.

Raison: We all have some ideas, but this is the huge challenge and … It depends on how you look at it. This is one of the things the book says too? If you try to go in up close and really hone in on details, it sort of is like a Buddhist feel in the world when you try to find solid objects, things just vanish into these complex interrelationships. If you try to be very specific about the phenomenology of something like depression, you cannot figure out where it starts, where it ends, what is what. But one of the things that Vlad and I realized in writing this book, was that if you step way back, you actually can get a sense of the phenomenology of depression. Then we can say some things.

One is that it’s remarkably common. Two is that it doesn’t really tend to come out of the blue. Most of the time it is in response to certain types of environmental adversities. It tends to hit men and women in different ages. In general, it tends to have a set of symptoms. Not everybody has all the symptoms, so if you go back, that turns out to be quite useful. It’s different than a simpler medical illness and it’s got a code. Because if you look at it this way, it has a narrative. It turns out that it has causes. It has effects too, but it has causes.

One of the arguments in the book is that the causes of depression are fairly stereotyped, suggesting that they’re ancient in human evolution, and they’re not random. That gives you a sense that we can call it a disease. Pragmatically, it might as well be a disease, it wrecks lives. But it’s not just a disease, it actually turns out to be an evolved response to adversity and that opens some really interesting doors for thinking about it and for thinking about its phenomenology.

Dr. Dave: Yeah. You mentioned bipolar, and I was wondering where does that fit in? Does that complicate the picture?

Raison: It does.

Dr. Dave: So is it more of its own thing or is it part of this thing?

Raison: Yeah. Oh, yeah. Well, so in the old days, in the way old days, people would kind of lump everything together. They thought everything ran together. There are modern people who think that all disorders of mood are bipolar. Most of us don’t believe that, but I admire that position. I don’t agree with it fully, but I really admire it. It’s old, it’s an ancient, it goes back to the ancient world to that guy whose name I’m not thinking of from Turkey. But more recently, and certainly in the DSM, there was this sharp distinction. Unipolar disorders, just depression, is one thing. Bipolar disorder is something else. That’s not true. We know that’s not true. They’re clearly not the same thing. Because to have bipolar disorder, you have to have a manic episode or hypomanic episode. Those can take various flavors, but when they’re extreme, people are psychotic, they’re hearing voices, they don’t sleep, they can’t stop talking, all the time. It looks like the opposite of depression.

Clearly, it’s not the same thing as depression, but bizarrely, it’s not altogether different either. Many of the biologic changes you see in mania, you can see in depression. It’s weird. Many people that seem to have depression, specially when it’s recurrent, when it happens to somebody a lot over the years, many of those people will eventually have something like a manic episode. As we’ve learned more, we’ve understood less in some ways. That’s one of the ways we’ve understood less. The clear demarkation of just regular old depression from a bipolar disorder has softened a little bit. Now I’ll tell you one way I think about the distinction is that depression tends to be response to certain types of adversity, largely social and often immune infectious related adversity. Bipolar disorder is often a response to the adversity of time. Most of us don’t think of time as an adversity, but it is. It’s quite an adversity, actually.

Dr. Dave: Getting older?

Raison: No, not that. Getting up everyday, going through the day, going to sleep. The literal passage of circadian rhythms is a powerful stressor, right? The most stressful thing you do most days that aren’t terrible is get up in the morning and your body prepares for it a couple of hours. It activates the stress system. That’s why there’s a surfeit of death rate at dawn. The reason people die at dawn is because it’s really rough to get up. Ask any teenager, they know that. But it turns out to be true, right?
Dr. Dave: I was thinking of teenagers.

Raison: Most of us manage that. In bipolar disorder, one of the classic things that induces episodes in bipolar disorder is disruption of circadian functioning, so missing sleep. For people with a bipolar disorder, all you need do is keep them up for a night and they’ll frequently go fully manic. If you put them asleep for 12 hours … When I used to do a lot of clinical work I ran a large inpatient service in California. Several times we took people that were doing things like running around naked in public, screaming, and stuff like that. Put them to sleep for 12 hours and, literally, when the people woke up the next morning and said, “Oh my God. Where am I? What happened?”, they were perfectly normal.
Some manic people have outbreaks when they get on a plane and fly to Europe. Bipolar disorder is more of a brain disorder. When it’s really severe, it really looks like there’s something wrong with people’s brains. But it’s not just that, we also know that the episodes of bipolar disorder are sparked by the environment, but they’re also sparked by the stress of time, circadian time, in a way that depression, regular old depression is not.

Dr. Dave: Now one of the things that you emphasized in the book is that depression is not a unitary disorder, and that there’s a complex interaction between genetics and environment.

Raison: That’s right. Although, that’s not novel. I think the whole field now recognizes that psychiatric disorders arise at the interface of genetic vulnerability and environmental conditions. The conditions that produce depression are often conditions of adversity. It’s a continual model and a simple way to think about it is that there’s some people whose essential makeup is largely driven by genes and the way those genes are expressed through epigenetic changes. There’s other people that take a lot of grief to get unhappy and get depressed. There’s a famous story from ancient Athens about a king who had everything until the end of his life when he lost his wife, he lost his children, he lost his kingdom. On his deathbed he said, “Call no man be happy until he dies.” Meaning that there are things that can happen that can probably upset everybody, but some people need a lot of push from the environment.

Other people are genetically vulnerable. They’re more sensitive to environmental perturbations. They need much less push from the environment. Because life is difficult, as the Buddhist said, “All life is suffering,” you are going to suffer in life. The more you’re vulnerable to that, the more likely you are to get depressed because the world is just not … it’s not a bowl of cherries, right? Most of us fall somewhere in the middle, but that’s a way of thinking about a continuum where the genes and the environment talk to each other that way. One of the things we do in the book that’s really interesting is we raise the point that even the dichotomy of genes and the environment is in many ways false. Because if you think about what a gene is, it’s a chemical structure, but it’s really an encoding of information.

If you say, “Well, what’s that information?” It really isn’t encoding. It’s information about past environments. Because those genes are there mostly, not always, but mostly because they were selected by past environments. From a genes point of view, everything outside the gene is environment, right? If you’re a gene and you wanted to survive and reproduce, your body is outside environment. If you’re a human, then there’s a lot more on the inside. You think your guts are on the inside, and your genes are on the inside, and the environment starts with your skin. But it really turns out that there’s another continuum which is genes and environments. They’re also married to each other and they’re ciphers for each other. One element to environment is a new element to a gene.

Think about an individual gene. Its environment includes the chromosome. It includes the entire genome because it’s fighting with those other genes. They get along but they also fight. Then if you look at a chromosome, well, its environment is the cell. You look at the cell, its environment is the body. When you really get into it, you begin to realize that although it’s very difficult to model these things, what really is going on is that all these levels are in constant interaction with each other, and the interactions are largely bidirectional. You get these extreme, complex systems. When you get complex systems it’s hard to make simple predictions. That’s why we can’t accurately forecast the weather. They become so complex that actually finding what they’re doing becomes either intractable, meaning you don’t have enough computer power to do it, or nearly impossible. That’s one of the challenges for thinking about why depression is so difficult. The simplest thing to say, and when I started with this, we know the genes and environments interact with each other.

Dr. Dave: Are we talking about multiple causal pathways.

Raison: Yes. Multiple causal pathways that are also interacting with each other in ascending levels. You get 12 pathways and these 12 pathways interact with each other, then those interactions can interact with each other. Some levels are going to be much more important for intervention than others. That’s how we can do anything in life. But still, in this way, it’s a like a quantum understanding in that it’s a cloud of causes. Some of them are more important than others, but it’s very complicated. In some circumstances, a cause that wasn’t so relevant in another circumstance becomes very important. That’s another complication. I think one of the things writing the book did for me was making me realize, with a certain humility, that we’re learning a lot. What I’m saying to you now, wouldn’t have been said 20 years ago. Even the articulation of our ignorance has become more knowing, but it’s a very humbling thing.

Thursday, December 14, 2017

Bitcoin is not a Bubble

Bitcoin is not a Bubble

For the past three decades, i struggled to understand how we were going to resolve the looming difficulties brought on by the steady and persistent decline in interest rates.

You must first though understand that the value of all money is based on human demand for two things.  One of those happens to be ease of exchange and simple portability.  Cash does that admirably and back in the day bits of metal as well.  Thus the mythical adoration of gold.  Yet all this is based on human need.  Without it we are economically crippled.

The second need is as a convenient store of value.  It is here that our government issued currencies have become unraveled.  Negative interest rates tend to do that and it is becoming more and more widespread.  The fiat printing machine however disguised has saturated the market with a mountain of cash that now cannot be placed.

Add in that we have started the process of exiting the whole oil industry as well and huge amounts of money will come out of that sector of the economy.  This will take perhaps two decades at most but the trend will be abruptly apparent much sooner.

Then along comes Bitcoin.  Every bitcoin has a finite supply and a profitable cost of production that naturally produces a huge body of individual interest just like coinage.  That body of interest will slowly expand and the only way in which that demand can be satisfied is through either mining or price appreciation.

Thus we see today multiple bitcoin clones all been spun out to meet that demand for a store of value.  There remain any number of issues in terms of security and thieves have done the odd hit and run.  all irrelevant and those holes are been steadily been plugged..  Bitcoin essentially works and is slowly shaking off the obvious frauds as well.

That means that when we have surplus cash, we will dump it into a bitcoin clone or even Bitcoin itself secure that most of the time we will actually earn because of expanding demand.  That is a completely novel idea.

New Study Sheds Light On How Earliest Forms Of Life Evolved On Earth

No question that an active volcanic event interacting with the surface provides the massive laboratory for the fabrication of a replicating chemistry able to change the general environment.

I also observe that volcanic  ash is often containing solid crystalline acids which provides an immobile anvil for chemistry as well.  Thus acidic or alkaline pores act as natural test tubes.

Hydrogen peroxide is very small.  Thus it brings maximum mobility and reaction speed.

New Study Sheds Light On How Earliest Forms Of Life Evolved On Earth

A new study led by ANU has shed light on how the earliest forms of life evolved on Earth about four billion years ago.

In a major advance on previous work, the study found a compound commonly used in hair bleach, hydrogen peroxide, made the eventual emergence of life possible.

Lead researcher Associate Professor Rowena Ball from ANU said hydrogen peroxide was the vital ingredient in rock pores around underwater heat vents that set in train a sequence of chemical reactions that led to the first forms of life.

"The origin of life is one of the hardest problems in all of science, but it is also one of the most important," said Dr Ball from the Mathematical Sciences Institute and Research School of Chemistry at ANU.

The research team made a model using hydrogen peroxide and porous rock that simulated the dynamic, messy environment that hosted the origin of life.

"Hydrogen peroxide played multiple roles in the emergence of living systems, and this study investigated how it ensured the randomly fluctuating temperatures and pH levels necessary to energise the production of a chemical world that made life on Earth possible," Dr Ball said.

"Our simulations reveal the importance of long rock pores or lengthy, interconnected porous structures in enabling the creation of long, large molecules."

The research advances upon previous studies by modelling the flow of reactive species through porous rock rather than through a single pore.

Dr Ball said the high temperature fluctuations must not rise too high or occur too often.

"The system needs to spend enough time at higher temperatures to carry out essential synthetic reactions, but not so much that the reactants are totally consumed or destroyed. We call this the 'Goldilocks' distribution," she said.

"This effectively gives us the 'fundamental equation of life'. It says that for life to begin and persist, the habitat must exhibit a specific range of temperature fluctuations."

This result provides new and valuable guidelines in the search for extraterrestrial life.

Hydrogen peroxide also promoted the evolution of enzymes called catalases that prevented a second 'origin of life' event.

"The ubiquitous presence of life, and hence catalases, in all habitable environments prevent hydrogen peroxide from accumulating sufficiently anywhere to drive a second origin event," Dr Ball said.

"Evolution can be thought of as burning a succession of small bridges. But the first cellular life destroyed probably one of the most important bridges, the one that spanned the living and non-living molecular worlds.

"Any chance of rebuilding that bridge was permanently rubbed out by the persistence of catalases throughout subsequent evolution."

The study is published in the international journal Royal Society Open Science.


The Plague that brought down mighty empires is thousands of years older than thought

St Macarius of Ghent Giving Aid to the Plague Victims, 1673 painting by Jacob van Oost

That it was pervasive far back in time is a conformation that it needs ample travel opportunities in oreder to launch a pandemic.  Its actual elimination is mostly about sanitation.  That is why it has mostly disappeared.
Driving it to extinction will beyond our ability.
This still reminds us of our core vulnerability and that is travel from cocoon to cocoon.   Yet rigorous attention to sanitation makes it almost possible to see most disease off.

The Plague that brought down mighty empires is thousands of years older than thought

25 OCTOBER, 2015 - 03:09 MARK MILLER

The Plague is far older than previously known and later changed to become much more virulent—so virulent that it may have contributed to the decline of Classical Greece and the Roman and Byzantine empires and later killed off 30 to 50 percent of Europe’s population, a new study says.

The bacteria that causes the Plague, Yersinia pestis, diverged from the less-pathogenic Y. pseudotuberculosis bacterium about 5,783 year ago.
That divergence, and therefore the bacteria’s possibility of infecting humans, is much earlier than scholars previously estimated.

While the Plague would go on to kill tens of millions of people in Europe and Asia, researchers have found DNA of Y. pestis in the teeth of a Russian person who died 5,000 years ago. They say that although the plague doesn’t appear to have been as prevalent or as virulent in the Bronze Age, even then it may have triggered migrations of populations in Europe and Asia and caused population decreases.

Writing the in the journal Cell, biologist Simon Rasmussen of the University of Denmark and his team say: “Here, we report the oldest direct evidence of Yersinia pestis identified by ancient DNA in human teeth from Asia and Europe dating from 2,800 to 5,000 years ago. … We find the origins of the Yersinia pestis lineage to be at least two times older than previous estimates. … Our results show that plague infection was endemic in the human populations of Eurasia at least 3,000 years before any historical recordings of pandemics.”

The Plague, which can be transmitted from humans to humans or from fleas to humans, has broken out in three pandemics in history. They werexSee all ReferencesTreille and Yersin, 1894 the Plague of Justinian (541–544 AD), which continued intermittently until about 750 AD; the Black Death in Europe, which included the first pandemic from 1347–1351, the Great Plague from 1665–1666 and into the 18th century; and the Third Pandemic, which emerged in China in the 1850s and erupted into a major epidemic in 1894, then spread worldwide as a series of epidemics until the mid-20th century. Earlier plagues, from 430-427 BC in Athens and a plague in the Roman Empire from 165-180 AD may or may not have been caused by Y. pestis, the authors say.

Scanning electron micrograph of a flea, which carry disease, including the plague, that infect people when they bite them. (CDC photo/Wikimedia Commons)

By sequencing Y. pestis DNA, the researchers determined the bacterium underwent genetic changes that increased its virulence and led to far more deaths and catastrophic impacts on society that may even have contributed to the collapse of empires. The authors wrote in Cell:

The consequences of the plague pandemics have been well-documented and the demographic impacts were dramatic. The Black Death alone is estimated to have killed 30%–50% of the European population. Economic and political collapses have also been in part attributed to the devastating effects of the plague. The Plague of Justinian is thought to have played a major role in weakening the Byzantine Empire, and the earlier putative plagues have been associated with the decline of Classical Greece and likely undermined the strength of the Roman army.

They concluded in their article that plague was common 3,000 years earlier than historic texts indicate and may have caused die-offs of humans in the late fourth millennium BC and into the early third millennium BC across Eurasia.

“However, based on the absence of crucial virulence genes, unlike the later Y. pestis strains that were responsible for the first to third pandemics, these ancient ancestral Y. pestis strains likely did not have the ability to cause bubonic plague, only pneumonic and septicemic plague,” they wrote.

Bubonic plague is transmitted by fleas, so this means the Plague likely was transmitted solely by humans earlier in its epidemiology. Around the late second millennium and early first millennium BC, the plague began to be spread by fleas via rats—an extremely rapid mode of transmission. Pneumonic plague affects the lungs, and septicemic plague affects the blood., reporting on the new research, wrote that the Books of Samuel in the Old Testament of the Bible tell of a plague among the Philistines in 1320 BC. The people suffering from it had swellings in the groin. The World Health Organization says such swellings are consistent with bubonic plague. The authors say this may indicate that the highly lethal bubonic plague originated in the Middle East.

Featured image: St Macarius of Ghent Giving Aid to the Plague Victims, 1673 painting by Jacob van Oost (Wikimedia Commons)

By Mark Miller

New study: Massive Aluminum levels in Autism brains, is this the smoking gun for vaccines?

Here it is folks.  we always had the indicative meta statistics that showed a correlation between rising rates of autism and the application of vaccination.  We missed an understanding of the biological pathways.  Science was looking into the obvious though and we have hit pay dirt.  We now know exactly how this all works.

Add in our rising concerns regarding the validity of the whole vaccination meme as applied now for a century and the public health aspect is now a serious concern.  Recall that the alternate explanation for global disease suppression has been the steady rise of successful public sanitation more than anything else.

Then we have the promotion of nasty variants that somehow vaccination can address when that is very unlikely. Add in the plausible probability that the 1918 flue epidemic was caused by an end of war vaccination program used to blow of excess stocks and you really start looking for someone to hang.

 The whole meme is beginning to look like a commercial enterprise based mostly on junk science with scant ambassadress successes that are not seriously controversial...

New study: Massive Aluminum levels in Autism brains, is this the smoking gun for vaccines?

“These are some of the highest values for aluminium in human brain tissue yet recorded.” — Professor Chris Exley of Keele University, discussing new findings of Aluminum levels in the brains of people with autism

BY J.B. HANDLEY November 27, 2017

STAFFORDSHIRE, England — Professor Chris Exley is a formidable scientist, which is perhaps more important than you think, because a study he published today with his colleagues in the Journal of Trace Elements in Medicine and Biology may just be the “smoking gun” to prove that vaccines are triggering autism that we’ve all been waiting for. Professor Exley is a Professor of Bioinorganic Chemistry at Keele University in Staffordshire, England. He received a Ph.D. in a subject that makes him highly qualified to author this latest paper: “the ecotoxicology of aluminium.”

His biography explains how his career has been devoted to the topic of aluminum in the brain:


Professor Chris Exley

“My research career (1984-present) has focussed upon an intriguing paradox; ‘how come the third most abundant element of the Earth’s crust (aluminium) is non-essential and largely inimcal to life’. Investigating this mystery has required research in myriad fields from the basic inorganic chemistry of the reaction of aluminium and silicon to the potentially complex biological availability of aluminium in humans. I am also fascinated by the element silicon in relation to living things which, as the second most abundant element of the Earth’s crust, is also almost devoid of biological function. One possible function of silicon is to keep aluminium out of biology (biota) and this forms a large part of the research in our group. We are also interested in biological silicification.”

Brand new research: How Aluminum Triggers Autism

Back in February, I wrote an extensive article that detailed emerging research, most of it published since 2010, that appeared to explain exactly how, biologically, vaccines administered to babies could be causing Autism through something known as an “Immune Activation Event.” If you haven’t yet, I respectfully ask that you consider reading that article (more than 300,000 reads so far), because Professor Exley’s findings will make even more sense to you for how important this new paper really is:

Big picture, newly published research is demonstrating that the following process is involved with triggering autism (please see a much more extensive explanation of this process at the bottom of this post):


Source : Vaccine Papers

Looking at this chart for a moment, the point of my article was that new published science has provided us with clear, unassailable, scientific answers at EVERY STEP of this process. We know that aluminum adjuvant from vaccines goes straight to the brain, we know it triggers the production of a cytokine known as “IL-6” that has been implicated in autism, and we know it also triggers “Microglial Activation,” which also triggers autism.

I’ll review just a few of the most recent scientific studies that help paint the picture of how autism is created, and then explain how Professor Exley’s work takes things to a new level.

In 2015, a study from Université Paris Est Créteil (UPEC) in France bolstered our understanding that the aluminum adjuvant used in vaccines is a dangerous, biopersistent, and ultimately brain-injuring toxin. (The study demonstrated that aluminum adjuvant slowly makes its way to the brain, where it then stays, possibly forever.)


Click to read

The study explained that aluminum adjuvant can generate a long-term immune response because of its “biopersistence”, which basically means our body has no ability to rid itself of aluminum adjuvant, because its a man-made substance we have no natural designs to eliminate:

“Thus alum and other poorly biodegradable materials taken up at the periphery by phagocytes circulate in the lymphatic and blood circulation and can enter the brain using a Trojan horse mechanism similar to that used by infectious particles. Previous experiments have shown that alum administration can cause CNS dysfunction and damage, casting doubts on the exact level of alum safety.”

Last Fall in 2016, the most important and revealing study yet done on aluminum adjuvant provided more bad news, and more insight.

It’s safe to say that this study’s conclusions have revolutionized our understanding of aluminum adjuvant. From the journal Toxicology, the French study authors were very concerned about the widespread use of aluminum adjuvant:

“Concerns about its [aluminum adjuvant’s] safety emerged following recognition of its unexpectedly long-lasting biopersistence within immune cells in some individuals, and reports of chronic fatigue syndrome, cognitive dysfunction, myalgia, dysautonomia and autoimmune/inflammatory features temporally linked to multiple Al-containing vaccine administrations.”

They also discovered, through mouse-models, a deeply alarming unique characteristic of aluminum adjuvant: low, consistent doses were MORE neurotoxic than a single bolus dose:

“We conclude that Alhydrogel [aluminum adjuvant] injected at low dose in mouse muscle may selectively induce long-term Al cerebral accumulation and neurotoxic effects. To explain this unexpected result, an avenue that could be explored in the future relates to the adjuvant size since the injected suspensions corresponding to the lowest dose, but not to the highest doses, exclusively contained small agglomerates in the bacteria-size range known to favour capture and, presumably, transportation by monocyte-lineage cells. In any event, the view that Alhydrogel neurotoxicity obeys ‘the dose makes the poison’ rule of classical chemical toxicity appears overly simplistic.”

This is a confusing conclusion. The website Vaccine Papers provided further explanation:

“A new paper (Crepeaux et al.) by the Gherardi research group in France reports important results on the toxicity and transport of aluminum (Al) adjuvant in mice. This single study is especially valuable because it looked at many outcomes: behavioral effects, immune (microglial) activation in the brain, and Al transport into the brain. The study tested dosages of 200 , 400 and 800 mcg/Kg, injected intramuscularly (IM). The Al adjuvant used was AlOH (brand name Alhydrogel), the most common vaccine adjuvant in use today. It is used in the tetanus, Hep A, Hep B, HiB, pneumococcal, meningococcal, and anthrax vaccines.

Remarkably, the study found that the lowest dosage (200 mcg/Kg) was the most toxic! For many outcomes, the 400 and 800 mcg/Kg dosages had no observable adverse effects, but the 200 mcg/Kg dosage did.

The low toxicity of the higher dosages appears to be a consequence of dosage-dependent inflammation at the injection site. The high dosages caused intense inflammation at the injection site, forming “granulomas”. The 200 mcg/Kg dosage did not produce granulomas. Granulomas are hard nodules in tissue produced in response to injury, infection or foreign substances. Its a way the body “walls off” injured tissue and prevents the spread of infection or toxins. The granuloma appears to provide protection from Al adjuvant toxicity; apparently the granuloma prevented Al adjuvant particles from leaving the injection site. This explains why the 200 mcg/Kg dosage affected the brain and behavior, while the higher dosages did not. This suggests that it is more dangerous and harmful to administer numerous small injections of Al adjuvant, compared to a large single injection capable of inducing a granuloma.”

The study authors also disputed the way the FDA and CDC currently think about aluminum adjuvant toxicity, basically saying that the current approach is wrong:

“As a possible consequence, comparing vaccine adjuvant exposure to other non- relevant aluminium exposures, e.g. soluble aluminium and other routes of exposure, may not represent valid approaches.”

And, the French scientists finish with a conclusion that all parents should find very troubling:
“In the context of massive development of vaccine-based strategies worldwide, the present study may suggest that aluminium adjuvant toxicokinetics and safety require reevaluation.”

Meet Professor Romain K. Gherardi

There are some true heroes emerging as published research reaches scientific certainty about the vaccine-autism connection, and French researcher Romain K. Gherardi is certainly one of them. Not only were the two studies I just walked you through authored by him, but he appears ready, willing, and able to tell the truth in public, as this recent T.V. appearance demonstrates, just watch (in French with English subtitles):

I’m picturing a press conference with Professor Exley and Professor Gherardi, who’s with me?


Huge gratitude for your help.

2017: Aluminium in brain tissue in autism

The one thing missing from all the work done to date about aluminum and its possible role in autism? Actual brain tissue of people with autism. All the studies published that appeared to be demonstrating strong biological certainty of how the aluminum in vaccines could trigger autism were done with MICE, and Professor Exley and his colleagues’ new research studied the actual brains of people with autism. The conclusions should make you gasp.

Released today.

“The aluminium content of brain tissues from donors with a diagnosis of ASD [Autism] was extremely high…the mean aluminium content for each lobe across all 5 individuals was towards the higher end of all previous (historical) measurements of brain aluminium content, including iatrogenic disorders such as dialysis encephalopathy …We recorded some of the highest values for brain aluminium content ever measured in healthy or diseased tissues in these male ASD donors…Why, for example would a 15 year old boy have such a high content of aluminium in their brain tissues?”

The answer is pretty obvious

Where’s all this aluminum coming from that Professor Exley and his colleagues just found? What source may have experienced explosive growth in the last three decades, perfectly matching the autism epidemic?


Source: Aluminum in Childhood Vaccines Is Unsafe By Neil Z. Miller

I think the answer is fairly obvious. I think the CDC and public health officials from all over the world have some serious explaining to do.

(Please see below for some more background information.)

J.B. Handley is the father of a child with Autism. He and his wife co-founded Generation Rescue, a national autism charity. He spent his career in the private equity industry and received his undergraduate degree with honors from Stanford University. He is also the author of “Did Chinese scientists find autism’s missing puzzle piece?”, “The Only Vaccine Guide a New Parent Will Ever Need” , “An Angry Father’s Guide to Vaccine-Autism Science”, and “7 reasons CDC employees should be “crying in the hallways

Please find two slides developed by the website Vaccine Papers that help explain the aluminum-autism connection, you can get your own copy right HERE.

And another video from Professor Exley back in 2011 discussing aluminum toxicity:

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