How Extreme Weather Is Shrinking the Planet

California is currently ablaze, after a record hot summer and a dry fall set the stage for the most destructive fires in the state’s history. Above: The Woolsey fire, near Los Angeles, seen from the West Hills.

Photograph by Kevin Cooley for The New Yorker

Thirty years ago, this magazine published “The End of Nature,” a long article about what we then called the greenhouse effect. I was in my twenties when I wrote it, and out on an intellectual limb: climate science was still young. But the data were persuasive, and freighted with sadness. We were spewing so much carbon into the atmosphere that nature was no longer a force beyond our influence—and humanity, with its capacity for industry and heedlessness, had come to affect every cubic metre of the planet’s air, every inch of its surface, every drop of its water. Scientists underlined this notion a decade later when they began referring to our era as the Anthropocene, the world made by man.

I was frightened by my reporting, but, at the time, it seemed likely that we’d try as a society to prevent the worst from happening. In 1988, George H. W. Bush, running for President, promised that he would fight “the greenhouse effect with the White House effect.” He did not, nor did his successors, nor did their peers in seats of power around the world, and so in the intervening decades what was a theoretical threat has become a fierce daily reality. As this essay goes to press, California is ablaze. A big fire near Los Angeles forced the evacuation of Malibu, and an even larger fire, in the Sierra Nevada foothills, has become the most destructive in California’s history. After a summer of unprecedented high temperatures and a fall “rainy season” with less than half the usual precipitation, the northern firestorm turned a city called Paradise into an inferno within an hour, razing more than ten thousand buildings and killing at least sixty-three people; more than six hundred others are missing. The authorities brought in cadaver dogs, a lab to match evacuees’ DNA with swabs taken from the dead, and anthropologists from California State University at Chico to advise on how to identify bodies from charred bone fragments.

For the past few years, a tide of optimistic thinking has held that conditions for human beings around the globe have been improving. Wars are scarcer, poverty and hunger are less severe, and there are better prospects for wide-scale literacy and education. But there are newer signs that human progress has begun to flag. In the face of our environmental deterioration, it’s now reasonable to ask whether the human game has begun to falter—perhaps even to play itself out. Late in 2017, a United Nations agency announced that the number of chronically malnourished people in the world, after a decade of decline, had started to grow again—by thirty-eight million, to a total of eight hundred and fifteen million, “largely due to the proliferation of violent conflicts and climate-related shocks.” In June, 2018, the Food and Agriculture Organization of the U.N. found that child labor, after years of falling, was growing, “driven in part by an increase in conflicts and climate-induced disasters.”

In 2015, at the U.N. Climate Change Conference in Paris, the world’s governments, noting that the earth has so far warmed a little more than one degree Celsius above pre-industrial levels, set a goal of holding the increase this century to 1.5 degrees Celsius (2.7 degrees Fahrenheit), with a fallback target of two degrees (3.6 degrees Fahrenheit). This past October, the U.N.’s Intergovernmental Panel on Climate Change published a special report stating that global warming “is likely to reach 1.5 C between 2030 and 2052 if it continues to increase at the current rate.” We will have drawn a line in the sand and then watched a rising tide erase it. The report did not mention that, in Paris, countries’ initial pledges would cut emissions only enough to limit warming to 3.5 degrees Celsius (about 6.3 degrees Fahrenheit) by the end of the century, a scale and pace of change so profound as to call into question whether our current societies could survive it.

Scientists have warned for decades that climate change would lead to extreme weather. Shortly before the I.P.C.C. report was published, Hurricane Michael, the strongest hurricane ever to hit the Florida Panhandle, inflicted thirty billion dollars’ worth of material damage and killed forty-five people. President Trump, who has argued that global warming is “a total, and very expensive, hoax,” visited Florida to survey the wreckage, but told reporters that the storm had not caused him to rethink his decision to withdraw the U.S. from the Paris climate accords. He expressed no interest in the I.P. C.C. report beyond asking “who drew it.” (The answer is ninety-one researchers from forty countries.) He later claimed that his “natural instinct” for science made him confident that the climate would soon “change back.” A month later, Trump blamed the fires in California on “gross mismanagement of forests.”

Human beings have always experienced wars and truces, crashes and recoveries, famines and terrorism. We’ve endured tyrants and outlasted perverse ideologies. Climate change is different. As a team of scientists recently pointed out in the journal Nature Climate Change, the physical shifts we’re inflicting on the planet will “extend longer than the entire history of human civilization thus far.”

“His last words were ‘Yodel-ay-he-hoo.’ ”

The poorest and most vulnerable will pay the highest price. But already, even in the most affluent areas, many of us hesitate to walk across a grassy meadow because of the proliferation of ticks bearing Lyme disease which have come with the hot weather; we have found ourselves unable to swim off beaches, because jellyfish, which thrive as warming seas kill off other marine life, have taken over the water. The planet’s diameter will remain eight thousand miles, and its surface will still cover two hundred million square miles. But the earth, for humans, has begun to shrink, under our feet and in our minds.

“Climate change,” like “urban sprawl” or “gun violence,” has become such a familiar term that we tend to read past it. But exactly what we’ve been up to should fill us with awe. During the past two hundred years, we have burned immense quantities of coal and gas and oil—in car motors, basement furnaces, power plants, steel mills—and, as we have done so, carbon atoms have combined with oxygen atoms in the air to produce carbon dioxide. This, along with other gases like methane, has trapped heat that would otherwise have radiated back out to space.

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There are at least four other episodes in the earth’s half-billion-year history of animal life when CO2 has poured into the atmosphere in greater volumes, but perhaps never at greater speeds. Even at the end of the Permian Age, when huge injections of CO2 from volcanoes burning through coal deposits culminated in “The Great Dying,” the CO2 content of the atmosphere grew at perhaps a tenth of the current pace. Two centuries ago, the concentration of CO2 in the atmosphere was two hundred and seventy-five parts per million; it has now topped four hundred parts per million and is rising more than two parts per million each year. The extra heat that we trap near the planet every day is equivalent to the heat from four hundred thousand bombs the size of the one that was dropped on Hiroshima.

As a result, in the past thirty years we’ve seen all twenty of the hottest years ever recorded. The melting of ice caps and glaciers and the rising levels of our oceans and seas, initially predicted for the end of the century, have occurred decades early. “I’ve never been at . . . a climate conference where people say ‘that happened slower than I thought it would,’ ” Christina Hulbe, a New Zealand climatologist, told a reporter for Grist last year. This past May, a team of scientists from the University of Illinois reported that there was a thirty-five-per-cent chance that, because of unexpectedly high economic growth rates, the U.N.’s “worst-case scenario” for global warming was too optimistic. “We are now truly in uncharted territory,” David Carlson, the former director of the World Meteorological Organization’s climate-research division, said in the spring of 2017, after data showed that the previous year had broken global heat records.

We are off the literal charts as well. In August, I visited Greenland, where, one day, with a small group of scientists and activists, I took a boat from the village of Narsaq to a glacier on a nearby fjord. As we made our way across a broad bay, I glanced up at the electronic chart above the captain’s wheel, where a blinking icon showed that we were a mile inland. The captain explained that the chart was from five years ago, when the water around us was still ice. The American glaciologist Jason Box, who organized the trip, chose our landing site. “We called this place the Eagle Glacier because of its shape,” he said. The name, too, was five years old. “The head and the wings of the bird have melted away. I don’t know what we should call it now, but the eagle is dead.”

There were two poets among the crew, Aka Niviana, who is Greenlandic, and Kathy Jetnil-Kijiner, from the low-lying Marshall Islands, in the Pacific, where “king tides” recently washed through living rooms and unearthed graveyards. A small lens of fresh water has supported life on the Marshall Islands’ atolls for millennia, but, as salt water intrudes, breadfruit trees and banana palms wilt and die. As the Greenlandic ice we were gazing at continues to melt, the water will drown Jetnil-Kijiner’s homeland. About a third of the carbon responsible for these changes has come from the United States.

A few days after the boat trip, the two poets and I accompanied the scientists to another fjord, where they needed to change the memory card on a camera that tracks the retreat of the ice sheet. As we took off for the flight home over the snout of a giant glacier, an eight-story chunk calved off the face and crashed into the ocean. I’d never seen anything quite like it for sheer power—the waves rose twenty feet as it plunged into the dark water. You could imagine the same waves washing through the Marshalls. You could almost sense the ice elevating the ocean by a sliver—along the seafront in Mumbai, which already floods on a stormy day, and at the Battery in Manhattan, where the seawall rises just a few feet above the water.

When I say the world has begun to shrink, this is what I mean. Until now, human beings have been spreading, from our beginnings in Africa, out across the globe—slowly at first, and then much faster. But a period of contraction is setting in as we lose parts of the habitable earth. Sometimes our retreat will be hasty and violent; the effort to evacuate the blazing California towns along narrow roads was so chaotic that many people died in their cars. But most of the pullback will be slower, starting along the world’s coastlines. Each year, another twenty-four thousand people abandon Vietnam’s sublimely fertile Mekong Delta as crop fields are polluted with salt. As sea ice melts along the Alaskan coast, there is nothing to protect towns, cities, and native villages from the waves. In Mexico Beach, Florida, which was all but eradicated by Hurricane Michael, a resident told the Washington Post, “The older people can’t rebuild; it’s too late in their lives. Who is going to be left? Who is going to care?”

In one week at the end of last year, I read accounts from Louisiana, where government officials were finalizing a plan to relocate thousands of people threatened by the rising Gulf (“Not everybody is going to live where they are now and continue their way of life, and that is a terrible, and emotional, reality to face,” one state official said); from Hawaii, where, according to a new study, thirty-eight miles of coastal roads will become impassable in the next few decades; and from Jakarta, a city with a population of ten million, where a rising Java Sea had flooded the streets. In the first days of 2018, a nor’easter flooded downtown Boston; dumpsters and cars floated through the financial district. “If anyone wants to question global warming, just see where the flood zones are,” Marty Walsh, the mayor of Boston, told reporters. “Some of those zones did not flood thirty years ago.”

According to a study from the United Kingdom’s National Oceanography Centre last summer, the damage caused by rising sea levels will cost the world as much as fourteen trillion dollars a year by 2100, if the U.N. targets aren’t met. “Like it or not, we will retreat from most of the world’s non-urban shorelines in the not very distant future,” Orrin Pilkey, an expert on sea levels at Duke University, wrote in his book “Retreat from a Rising Sea.” “We can plan now and retreat in a strategic and calculated fashion, or we can worry about it later and retreat in tactical disarray in response to devastating storms. In other words, we can walk away methodically, or we can flee in panic.”

But it’s not clear where to go. As with the rising seas, rising temperatures have begun to narrow the margins of our inhabitation, this time in the hot continental interiors. Nine of the ten deadliest heat waves in human history have occurred since 2000. In India, the rise in temperature since 1960 (about one degree Fahrenheit) has increased the chance of mass heat-related deaths by a hundred and fifty per cent. The summer of 2018 was the hottest ever measured in certain areas. For a couple of days in June, temperatures in cities in Pakistan and Iran peaked at slightly above a hundred and twenty-nine degrees Fahrenheit, the highest reliably recorded temperatures ever measured. The same heat wave, nearer the shore of the Persian Gulf and the Gulf of Oman, combined triple-digit temperatures with soaring humidity levels to produce a heat index of more than a hundred and forty degrees Fahrenheit. June 26th was the warmest night in history, with the mercury in one Omani city remaining above a hundred and nine degrees Fahrenheit until morning. In July, a heat wave in Montreal killed more than seventy people, and Death Valley, which often sets American records, registered the hottest month ever seen on our planet. Africa recorded its highest temperature in June, the Korean Peninsula in July, and Europe in August. The Times reported that, in Algeria, employees at a petroleum plant walked off the job as the temperature neared a hundred and twenty-four degrees. “We couldn’t keep up,” one worker told the reporter. “It was impossible to do the work.”

This was no illusion; some of the world is becoming too hot for humans. According to the National Oceanic and Atmospheric Administration, increased heat and humidity have reduced the amount of work people can do outdoors by ten per cent, a figure that is predicted to double by 2050. About a decade ago, Australian and American researchers, setting out to determine the highest survivable so-called “wet-bulb” temperature, concluded that when temperatures passed thirty-five degrees Celsius (ninety-five degrees Fahrenheit) and the humidity was higher than ninety per cent, even in “well-ventilated shaded conditions,” sweating slows down, and humans can survive only “for a few hours, the exact length of time being determined by individual physiology.”

“Right now, they think they have amouse.”

As the planet warms, a crescent-shaped area encompassing parts of India, Pakistan, Bangladesh, and the North China Plain, where about 1.5 billion people (a fifth of humanity) live, is at high risk of such temperatures in the next half century. Across this belt, extreme heat waves that currently happen once every generation could, by the end of the century, become “annual events with temperatures close to the threshold for several weeks each year, which could lead to famine and mass migration.” By 2070, tropical regions that now get one day of truly oppressive humid heat a year can expect between a hundred and two hundred and fifty days, if the current levels of greenhouse-gas emissions continue. According to Radley Horton, a climate scientist at the Lamont-Doherty Earth Observatory, most people would “run into terrible problems” before then. The effects, he added, will be “transformative for all areas of human endeavor—economy, agriculture, military, recreation.”

Humans share the planet with many other creatures, of course. We have already managed to kill off sixty per cent of the world’s wildlife since 1970 by destroying their habitats, and now higher temperatures are starting to take their toll. A new study found that peak-dwelling birds were going extinct; as temperatures climb, the birds can no longer find relief on higher terrain. Coral reefs, rich in biodiversity, may soon be a tenth of their current size.

As some people flee humidity and rising sea levels, others will be forced to relocate in order to find enough water to survive. In late 2017, a study led by Manoj Joshi, of the University of East Anglia, found that, by 2050, if temperatures rise by two degrees a quarter of the earth will experience serious drought and desertification. The early signs are clear: São Paulo came within days of running out of water last year, as did Cape Town this spring. In the fall, a record drought in Germany lowered the level of the Elbe to below twenty inches and reduced the corn harvest by forty per cent. The Potsdam Institute for Climate Impact Research concluded in a recent study that, as the number of days that reach eighty-six degrees Fahrenheit or higher increases, corn and soybean yields across the U.S. grain belt could fall by between twenty-two and forty-nine per cent. We’ve already overpumped the aquifers that lie beneath most of the world’s breadbaskets; without the means to irrigate, we may encounter a repeat of the nineteen-thirties, when droughts and deep plowing led to the Dust Bowl—this time with no way of fixing the problem. Back then, the Okies fled to California, but California is no longer a green oasis. A hundred million trees died in the record drought that gripped the Golden State for much of this decade. The dead limbs helped spread the waves of fire, as scientists earlier this year warned that they could.

Thirty years ago, some believed that warmer temperatures would expand the field of play, turning the Arctic into the new Midwest. As Rex Tillerson, then the C.E.O. of Exxon, cheerfully put it in 2012, “Changes to weather patterns that move crop production areas around—we’ll adapt to that.” But there is no rich topsoil in the far North; instead, the ground is underlaid with permafrost, which can be found beneath a fifth of the Northern Hemisphere. As the permafrost melts, it releases more carbon into the atmosphere. The thawing layer cracks roads, tilts houses, and uproots trees to create what scientists call “drunken forests.” Ninety scientists who released a joint report in 2017 concluded that economic losses from a warming Arctic could approach ninety trillion dollars in the course of the century, considerably outweighing whatever savings may have resulted from shorter shipping routes as the Northwest Passage unfreezes.

Churchill, Manitoba, on the edge of the Hudson Bay, in Canada, is connected to the rest of the country by a single rail line. In the spring of 2017, record floods washed away much of the track. OmniTrax, which owns the line, tried to cancel its contract with the government, declaring what lawyers call a “force majeure,” an unforeseen event beyond its responsibility. “To fix things in this era of climate change—well, it’s fixed, but you don’t count on it being the fix forever,” an engineer for the company explained at a media briefing in July. This summer, the Canadian government reopened the rail at a cost of a hundred and seventeen million dollars—about a hundred and ninety thousand dollars per Churchill resident. There is no reason to think the fix will last, and every reason to believe that our world will keep contracting.

All this has played out more or less as scientists warned, albeit faster. What has defied expectations is the slowness of the response. The climatologist James Hansen testified before Congress about the dangers of human-caused climate change thirty years ago. Since then, carbon emissions have increased with each year except 2009 (the height of the global recession) and the newest data show that 2018 will set another record. Simple inertia and the human tendency to prioritize short-term gains have played a role, but the fossil-fuel industry’s contribution has been by far the most damaging. Alex Steffen, an environmental writer, coined the term “predatory delay” to describe “the blocking or slowing of needed change, in order to make money off unsustainable, unjust systems in the meantime.” The behavior of the oil companies, which have pulled off perhaps the most consequential deception in mankind’s history, is a prime example.

As journalists at InsideClimate News and the Los Angeles Times have revealed since 2015, Exxon, the world’s largest oil company, understood that its product was contributing to climate change a decade before Hansen testified. In July, 1977, James F. Black, one of Exxon’s senior scientists, addressed many of the company’s top leaders in New York, explaining the earliest research on the greenhouse effect. “There is general scientific agreement that the most likely manner in which mankind is influencing the global climate is through carbon-dioxide release from the burning of fossil fuels,” he said, according to a written version of the speech which was later recorded, and which was obtained by InsideClimate News. In 1978, speaking to the company’s executives, Black estimated that a doubling of the carbon-dioxide concentration in the atmosphere would increase average global temperatures by between two and three degrees Celsius (5.4 degrees Fahrenheit), and as much as ten degrees Celsius (eighteen degrees Fahrenheit) at the poles.

Exxon spent millions of dollars researching the problem. It outfitted an oil tanker, the Esso Atlantic, with CO2 detectors to measure how fast the oceans could absorb excess carbon, and hired mathematicians to build sophisticated climate models. By 1982, they had concluded that even the company’s earlier estimates were probably too low. In a private corporate primer, they wrote that heading off global warming and “potentially catastrophic events” would “require major reductions in fossil fuel combustion.”

An investigation by the L.A. Times revealed that Exxon executives took these warnings seriously. Ken Croasdale, a senior researcher for the company’s Canadian subsidiary, led a team that investigated the positive and negative effects of warming on Exxon’s Arctic operations. In 1991, he found that greenhouse gases were rising due to the burning of fossil fuels. “Nobody disputes this fact,” he said. The following year, he wrote that “global warming can only help lower exploration and development costs” in the Beaufort Sea. Drilling season in the Arctic, he correctly predicted, would increase from two months to as many as five months. At the same time, he said, the rise in the sea level could threaten onshore infrastructure and create bigger waves that would damage offshore drilling structures. Thawing permafrost could make the earth buckle and slide under buildings and pipelines. As a result of these findings, Exxon and other major oil companies began laying plans to move into the Arctic, and started to build their new drilling platforms with higher decks, to compensate for the anticipated rises in sea level.

The implications of the exposés were startling. Not only did Exxon and other companies know that scientists like Hansen were right; they used his nasaclimate models to figure out how low their drilling costs in the Arctic would eventually fall. Had Exxon and its peers passed on what they knew to the public, geological history would look very different today. The problem of climate change would not be solved, but the crisis would, most likely, now be receding. In 1989, an international ban on chlorine-containing man-made chemicals that had been eroding the earth’s ozone layer went into effect. Last month, researchers reported that the ozone layer was on track to fully heal by 2060. But that was a relatively easy fight, because the chemicals in question were not central to the world’s economy, and the manufacturers had readily available substitutes to sell. In the case of global warming, the culprit is fossil fuel, the most lucrative commodity on earth, and so the companies responsible took a different tack.

A document uncovered by the L.A. Times showed that, a month after Hansen’s testimony, in 1988, an unnamed Exxon “public affairs manager” issued an internal memo recommending that the company “emphasize the uncertainty” in the scientific data about climate change. Within a few years, Exxon, Chevron, Shell, Amoco, and others had joined the Global Climate Coalition, “to coordinate business participation in the international policy debate” on global warming. The G.C.C. coördinated with the National Coal Association and the American Petroleum Institute on a campaign, via letters and telephone calls, to prevent a tax on fossil fuels, and produced a video in which the agency insisted that more carbon dioxide would “end world hunger” by promoting plant growth. With such efforts, it ginned up opposition to the Kyoto Protocol, the first global initiative to address climate change.

In October, 1997, two months before the Kyoto meeting, Lee Raymond, Exxon’s president and C.E.O., who had overseen the science department that in the nineteen-eighties produced the findings about climate change, gave a speech in Beijing to the World Petroleum Congress, in which he maintained that the earth was actually cooling. The idea that cutting fossil-fuel emissions could have an effect on the climate, he said, defied common sense. “It is highly unlikely that the temperature in the middle of the next century will be affected whether policies are enacted now, or twenty years from now,” he went on. Exxon’s own scientists had already shown each of these premises to be wrong.

On a December morning in 1997 at the Kyoto Convention Center, after a long night of negotiation, the developed nations reached a tentative accord on climate change. Exhausted delegates lay slumped on couches in the corridor, or on the floor in their suits, but most of them were grinning. Imperfect and limited though the agreement was, it seemed that momentum had gathered behind fighting climate change. But as I watched the delegates cheering and clapping, an American lobbyist, who had been coördinating much of the opposition to the accord, turned to me and said, “I can’t wait to get back to Washington, where we’ve got this under control.”

“I hope this visit from your king has brightened your outlook on things.”

He was right. On January 29, 2001, nine days after George W. Bush was inaugurated, Lee Raymond visited his old friend Vice-President Dick Cheney, who had just stepped down as the C.E.O. of the oil-drilling giant Halliburton. Cheney helped persuade Bush to abandon his campaign promise to treat carbon dioxide as a pollutant. Within the year, Frank Luntz, a Republican consultant for Bush, had produced an internal memo that made a doctrine of the strategy that the G.C.C. had hit on a decade earlier. “Voters believe that there is no consensus about global warming within the scientific community,” Luntz wrote in the memo, which was obtained by the Environmental Working Group, a Washington-based organization. “Should the public come to believe that the scientific issues are settled, their views about global warming will change accordingly. Therefore, you need to continue to make the lack of scientific certainty a primary issue in the debate.”

The strategy of muddling the public’s impression of climate science has proved to be highly effective. In 2017, polls found that almost ninety per cent of Americans did not know that there was a scientific consensus on global warming. Raymond retired in 2006, after the company posted the biggest corporate profits in history, and his final annual salary was four hundred million dollars. His successor, Rex Tillerson, signed a five-hundred-billion-dollar deal to explore for oil in the rapidly thawing Russian Arctic, and in 2012 was awarded the Russian Order of Friendship. In 2016, Tillerson, at his last shareholder meeting before he briefly joined the Trump Administration as Secretary of State, said, “The world is going to have to continue using fossil fuels, whether they like it or not.”

It’s by no means clear whether Exxon’s deception and obfuscation are illegal. The company has long maintained that it “has tracked the scientific consensus on climate change, and its research on the issue has been published in publicly available peer-reviewed journals.” The First Amendment preserves one’s right to lie, although, in October, New York State Attorney General Barbara D. Underwood filed suit against Exxon for lying to investors, which is a crime. What is certain is that the industry’s campaign cost us the efforts of the human generation that might have made the crucial difference in the climate fight.

Exxon’s behavior is shocking, but not entirely surprising. Philip Morris lied about the effects of cigarette smoking before the government stood up to Big Tobacco. The mystery that historians will have to unravel is what went so wrong in our governance and our culture that we have done, essentially, nothing to stand up to the fossil-fuel industry.

There are undoubtedly myriad intellectual, psychological, and political sources for our inaction, but I cannot help thinking that the influence of Ayn Rand, the Russian émigré novelist, may have played a role. Rand’s disquisitions on the “virtue of selfishness” and unbridled capitalism are admired by many American politicians and economists—Paul Ryan, Tillerson, Mike Pompeo, Andrew Puzder, and Donald Trump, among them. Trump, who has called “The Fountainhead” his favorite book, said that the novel “relates to business and beauty and life and inner emotions. That book relates to . . . everything.” Long after Rand’s death, in 1982, the libertarian gospel of the novel continues to sway our politics: Government is bad. Solidarity is a trap. Taxes are theft. The Koch brothers, whose enormous fortune derives in large part from the mining and refining of oil and gas, have peddled a similar message, broadening the efforts that Exxon-funded groups like the Global Climate Coalition spearheaded in the late nineteen-eighties.

Fossil-fuel companies and electric utilities, often led by Koch-linked groups, have put up fierce resistance to change. In Kansas, Koch allies helped turn mandated targets for renewable energy into voluntary commitments. In Wisconsin, Scott Walker’s administration prohibited state land officials from talking about climate change. In North Carolina, the state legislature, in conjunction with real-estate interests, effectively banned policymakers from using scientific estimates of sea-level rise in the coastal-planning process. Earlier this year, Americans for Prosperity, the most important Koch front group, waged a campaign against new bus routes and light-rail service in Tennessee, invoking human liberty. “If someone has the freedom to go where they want, do what they want, they’re not going to choose public transit,” a spokeswoman for the group explained. In Florida, an anti-renewable-subsidy ballot measure invoked the “Rights of Electricity Consumers Regarding Solar Energy Choice.”

Such efforts help explain why, in 2017, the growth of American residential solar installations came to a halt even before March, 2018, when President Trump imposed a thirty-per-cent tariff on solar panels, and why the number of solar jobs fell in the U.S. for the first time since the industry’s great expansion began, a decade earlier. In February, at the Department of Energy, Rick Perry—who once skipped his own arraignment on two felony charges, which were eventually dismissed, in order to attend a Koch brothers event—issued a new projection in which he announced that the U.S. would go on emitting carbon at current levels through 2050; this means that our nation would use up all the planet’s remaining carbon budget if we plan on meeting the 1.5-degree target. Skepticism about the scientific consensus, Perry told the media in 2017, is a sign of a “wise, intellectually engaged person.”

Of all the environmental reversals made by the Trump Administration, the most devastating was its decision, last year, to withdraw from the Paris accords, making the U.S., the largest single historical source of carbon, the only nation not engaged in international efforts to control it. As the Washington Postreported, the withdrawal was the result of a collaborative venture. Among the anti-government ideologues and fossil-fuel lobbyists responsible was Myron Ebell, who was at Trump’s side in the Rose Garden during the withdrawal announcement, and who, at Frontiers of Freedom, had helped run a “complex influence campaign” in support of the tobacco industry. Ebell is a director of the Competitive Enterprise Institute, which was founded in 1984 to advance “the principles of limited government, free enterprise, and individual liberty,” and which funds the Cooler Heads Coalition, “an informal and ad-hoc group focused on dispelling the myths of global warming,” of which Ebell is the chairman. Also instrumental were the Heartland Institute and the Koch brothers’ Americans for Prosperity. After Trump’s election, these groups sent a letter reminding him of his campaign pledge to pull America out. The C.E.I. ran a TV spot: “Mr. President, don’t listen to the swamp. Keep your promise.” And, despite the objections of most of his advisers, he did. The coalition had used its power to slow us down precisely at the moment when we needed to speed up. As a result, the particular politics of one country for one half-century will have changed the geological history of the earth.

We are on a path to self-destruction, and yet there is nothing inevitable about our fate. Solar panels and wind turbines are now among the least expensive ways to produce energy. Storage batteries are cheaper and more efficient than ever. We could move quickly if we chose to, but we’d need to opt for solidarity and coördination on a global scale. The chances of that look slim. In Russia, the second-largest petrostate after the U.S., Vladimir Putin believes that “climate change could be tied to some global cycles on Earth or even of planetary significance.” Saudi Arabia, the third-largest petrostate, tried to water down the recent I.P.C.C. report. Jair Bolsonaro, the newly elected President of Brazil, has vowed to institute policies that would dramatically accelerate the deforestation of the Amazon, the world’s largest rain forest. Meanwhile, Exxon recently announced a plan to spend a million dollars—about a hundredth of what the company spends each month in search of new oil and gas—to back the fight for a carbon tax of forty dollars a ton. At a press conference, some of the I.P.C.C.’s authors laughed out loud at the idea that such a tax would, this late in the game, have sufficient impact.

The possibility of swift change lies in people coming together in movements large enough to shift the Zeitgeist. In recent years, despairing at the slow progress, I’ve been one of many to protest pipelines and to call attention to Big Oil’s deceptions. The movement is growing. Since 2015, when four hundred thousand people marched in the streets of New York before the Paris climate talks, activists—often led by indigenous groups and communities living on the front lines of climate change—have blocked pipelines, forced the cancellation of new coal mines, helped keep the major oil companies out of the American Arctic, and persuaded dozens of cities to commit to one-hundred-per-cent renewable energy.

Each of these efforts has played out in the shadow of the industry’s unflagging campaign to maximize profits and prevent change. Voters in Washington State were initially supportive of a measure on last month’s ballot which would have imposed the nation’s first carbon tax—a modest fee that won support from such figures as Bill Gates. But the major oil companies spent record sums to defeat it. In Colorado, a similarly modest referendum that would have forced frackers to move their rigs away from houses and schools went down after the oil industry outspent citizen groups forty to one. This fall, California’s legislators committed to using only renewable energy by 2045, which was a great victory in the world’s fifth-largest economy. But the governor refused to stop signing new permits for oil wells, even in the middle of the state’s largest cities, where asthma rates are high.

New kinds of activism keep springing up. In Sweden this fall, a one-person school boycott by a fifteen-year-old girl named Greta Thunberg helped galvanize attention across Scandinavia. At the end of October, a new British group, Extinction Rebellion—its name both a reflection of the dire science and a potentially feisty response—announced plans for a campaign of civil disobedience. Last week, fifty-one young people were arrested in Nancy Pelosi’s office for staging a sit-in, demanding that the Democrats embrace a “Green New Deal” that would address the global climate crisis with policies to create jobs in renewable energy. They may have picked a winning issue: several polls have shown that even Republicans favor more government support for solar panels. This battle is epic and undecided. If we miss the two-degree target, we will fight to prevent a rise of three degrees, and then four. It’s a long escalator down to Hell.

“Oh, yes. Definitely a forgery. Hope it didn’t cost you much.”

Last June, I went to Cape Canaveral to watch Elon Musk’s Falcon 9 rocket lift off. When the moment came, it was as I’d always imagined: the clouds of steam venting in the minutes before launch, the immensely bright column of flame erupting. With remarkable slowness, the rocket began to rise, the grip of gravity yielding to the force of its engines. It is the most awesome technological spectacle human beings have produced.

Musk, Jeff Bezos, and Richard Branson are among the billionaires who have spent some of their fortunes on space travel—a last-ditch effort to expand the human zone of habitability. In November, 2016, Stephen Hawking gave humanity a deadline of a thousand years to leave Earth. Six months later, he revised the timetable to a century. In June, 2017, he told an audience that “spreading out may be the only thing that saves us from ourselves.” He continued, “Earth is under threat from so many areas that it is difficult for me to be positive.”

But escaping the wreckage is, almost certainly, a fantasy. Even if astronauts did cross the thirty-four million miles to Mars, they’d need to go underground to survive there. To what end? The multimillion-dollar attempts at building a “biosphere” in the Southwestern desert in 1991 ended in abject failure. Kim Stanley Robinson, the author of a trilogy of novels about the colonization of Mars, recently called such projects a “moral hazard.” “People think if we fuck up here on Earth we can always go to Mars or the stars,” he said. “It’s pernicious.”

The dream of interplanetary colonization also distracts us from acknowledging the unbearable beauty of the planet we already inhabit. The day before the launch, I went on a tour of the vast grounds of the Kennedy Space Center with nasa’s public-affairs officer, Greg Harland, and the biologist Don Dankert. I’d been warned beforehand by other nasa officials not to broach the topic of global warming; in any event, nasa’s predicament became obvious as soon as we climbed up on a dune overlooking Launch Complex 39, from which the Apollo missions left for the moon, and where any future Mars mission would likely begin. The launchpad is a quarter of a mile from the ocean—a perfect location, in the sense that, if something goes wrong, the rockets will fall into the sea, but not so perfect, since that sea is now rising. nasa started worrying about this sometime after the turn of the century, and formed a Dune Vulnerability Team.

In 2011, Hurricane Sandy, even at a distance of a couple of hundred miles, churned up waves strong enough to break through the barrier of dunes along the Atlantic shoreline of the Space Center and very nearly swamped the launch complexes. Dankert had millions of cubic yards of sand excavated from a nearby Air Force base, and saw to it that a hundred and eighty thousand native shrubs were planted to hold the sand in place. So far, the new dunes have yielded little ground to storms and hurricanes. But what impressed me more than the dunes was the men’s deep appreciation of their landscape. “Kennedy Space Center shares real estate with the Merritt Island Wildlife Refuge,” Harland said. “We use less than ten per cent for our industrial purposes.”

“When you look at the beach, it’s like eighteen-seventies Florida—the longest undisturbed stretch on the Atlantic Coast,” Dankert said. “We launch people into space from the middle of a wildlife refuge. That’s amazing.”

The two men talked for a long time about their favorite local species—the brown pelicans that were skimming the ocean, the Florida scrub jays. While rebuilding the dunes, they carefully bucket-trapped and relocated dozens of gopher tortoises. Before I left, they drove me half an hour across the swamp to a pond near the Space Center’s headquarters building, just to show me some alligators. Menacing snouts were visible beneath the water, but I was more interested in the sign that had been posted at each corner of the pond explaining that the alligators were native species, not pets. “Putting any food in the water for any reason will cause them to become accustomed to people and possibly dangerous,” it went on, adding that, if that should happen, “they must be removed and destroyed.”

Something about the sign moved me tremendously. It would have been easy enough to poison the pond, just as it would have been easy enough to bulldoze the dunes without a thought for the tortoises. But nasa hadn’t done so, because of a long series of laws that draw on an emerging understanding of who we are. In 1867, John Muir, one of the first Western environmentalists, walked from Louisville, Kentucky, to Florida, a trip that inspired his first heretical thoughts about the meaning of being human. “The world, we are told, was made especially for man—a presumption not supported by all the facts,” Muir wrote in his diary. “A numerous class of men are painfully astonished whenever they find anything, living or dead, in all God’s universe, which they cannot eat or render in some way what they call useful to themselves.” Muir’s proof that this self-centeredness was misguided was the alligator, which he could hear roaring in the Florida swamp as he camped nearby, and which clearly caused man mostly trouble. But these animals were wonderful nonetheless, Muir decided—remarkable creatures perfectly adapted to their landscape. “I have better thoughts of those alligators now that I’ve seen them at home,” he wrote. In his diary, he addressed the creatures directly: “Honorable representatives of the great saurian of an older creation, may you long enjoy your lilies and rushes, and be blessed now and then with a mouthful of terror-stricken man by way of dainty.”

That evening, Harland and Dankert drew a crude map to help me find the beach, north of Patrick Air Force Base and south of the spot where, in 1965, Barbara Eden emerged from her bottle to greet her astronaut at the start of the TV series “I Dream of Jeannie.” There, they said, I could wait out the hours until the pre-dawn rocket launch and perhaps spot a loggerhead sea turtle coming ashore to lay her eggs. And so I sat on the sand. The beach was deserted, and under a near-full moon I watched as a turtle trundled from the sea and lumbered deliberately to a spot near the dune, where she used her powerful legs to excavate a pit. She spent an hour laying eggs, and even from thirty yards away you could hear her heavy breathing in between the whispers of the waves. And then, having covered her clutch, she tracked back to the ocean, in the fashion of others like her for the past hundred and twenty million years. ♦

This article appears in the print edition of the November 26, 2018, issue, with the headline “Life on a Shrinking Planet.”

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Imuno – The Solution

What is imuno – The Solution®?

  • imuno™ is a revolutionary immune support formula with a patented component which is twice as effective as comparable formulas.
  • imuno™ is finely filtered, powerful, and pure.  It has the ability to get into deeply hidden congestion and move it out in its entirety.
  • imuno™  is a micro-sized, blended molecule of vegan chondroitin sulfate, a pre-cursor of acytle-choline, and Vit D for brain & gut.
  • Imuno™ was designed by quantum molecular biologist and immunotherapist Dr. Marco Ruggiero, MD. Ph.D., from Florence, Italy
  • Dr. Ruggiero recommends combining imuno™, Bravo Yogurt, and a ketogenic diet to get set for success.

imuno – The Solution® – Bioavailable  & molecularly organized ingredients:

  1. Chondroitin Sulfate – no animal ingredients, vegan, and finely filtered x3
  2. Phosphatidylcholine – lipid (fat) cleaner accuring on cell walls
  3. Cholecalciferol – type of Vit D3 used in skin and cell walls

Building a stronger immune system is science that delivers.

Designed in 2018, imuno – The Solution® is set apart from its predecessors. Its ingredients have been carefully crafted to deliver a powerful action of removing what the immune system doesn’t want.

  • Micro-sized  ingredient action of chondroitin sulfate, phosphatidylcholine, cholecalciferol which are bonded together at a low-molecular weight.
  • More efficiency and power from a proprietary algorithm which is based on biologic negentropy; which means that things become more organized.

The end result is an unexpected empowerment of the immune system to remove congestion within the body.

___________________________________________________________________________

How someone feels about using imuno™

Using imuno has raised the bar in my mind about how clean a body can be!  imuno is cleaning my body to a higher level than I expected and with each dose I take, that brightness keeps manifesting.  It’s so hopeful! I can’t wait to get more clean to see what that is like!

____________________________________________________________________________

Quick Start Instructions:

  • Shake before using & refrigerate after opening
  • Extract each use with a sterile needle syringe so the jar will last for 6 months after opening
  • Imuno™ is a sterile injectable solution. It can also be applied topically, sublingually, or with a nebulizer for systemic issues.
  • Start slowly to make sure detox pathways are open. At first, take 1-3 drops 1x per week. Work up to your dose! More is not better.
  • When your dose is sufficient, the product provides a lift.
  • Uncomfortable detox is rare.  Reduce or spread out doses & take more protein.
  • if you have severity health conditions consult a practitioner for assistance on how to detoxify.

Using imuno – The Solution®

imuno – The Solution® is a sterile solution which comes in a 3 ml vial. Individuals who are appropriately licensed, can injections of imuno – The Solution® into the body:

  1. To put the solution into a specific congested area of tissue
  2. To apply to a specific tissue subcutaneously and put small amounts of the solution as a reservoir under the skin.

It can also be applied topically, sublingually, or with a nebulizer for systemic issues.

  • The adult serving size: 0.2 ml (4 drops) daily.
    • (maximum dose 0.5 ml daily)
  • The child serving size: 0.1 ml (2 drops) once per week.
    • (maximum dose .25 ml daily)

Each 3 ml vial contains 15 x 0.2 ml servings

Precautions:

Chondroitin Sulfate, an ingredient in imuno which has a blood thinning effect similar to the drug heparin.  Take precautions when taking large doses that it may have an anti-coagulant effect and medical supervision is advised.

See the pamphlets and box inserts:

  1. Box Insert
  2. Health Flyer
  3. Beauty Flyer
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Vegetable compound could have a key role in ‘beeting’ Alzheimer’s disease

Vegetable compound could have a key role in ‘beeting’ Alzheimer’s disease

Note to journalists: Please report that this research will be presented at a meeting of the American Chemical Society.

A press conference on this topic will be held Tuesday, March 20, at 9 a.m. Central time in the Ernest N. Morial Convention Center. Reporters may check-in at the press center, Great Hall B, or watch live on YouTube http://bit.ly/ACSLive_NOLA. To ask questions online, sign in with a Google account.

NEW ORLEANS, March 20, 2018 — A compound in beets that gives the vegetable its distinctive red color could eventually help slow the accumulation of misfolded proteins in the brain, a process that is associated with Alzheimer’s disease. Scientists say this discovery could lead to the development of drugs that could alleviate some of the long-term effects of the disease, the world’s leading cause of dementia.

The researchers are presenting their work today at the 255th National Meeting & Exposition of the American Chemical Society (ACS). ACS, the world’s largest scientific society, is holding the meeting here through Thursday. It features more than 13,000 presentations on a wide range of science topics.

“Our data suggest that betanin, a compound in beet extract, shows some promise as an inhibitor of certain chemical reactions in the brain that are involved in the progression of Alzheimer’s disease,” says Li-June Ming, Ph.D. “This is just a first step, but we hope that our findings will encourage other scientists to look for structures similar to betanin that could be used to synthesize drugs that could make life a bit easier for those who suffer from this disease.”

More than 5 million Americans have Alzheimer’s disease, according to the National Institute on Aging. Its incidence rises with age, affecting one in 10 Americans 65 and older, and one in three by age 85. Scientists are still trying to figure out what causes this progressive and irreversible brain disorder. But one prime suspect is beta-amyloid, a sticky protein fragment, or peptide, that accumulates in the brain, disrupting communication between brain cells called neurons. Much of this damage occurs, Ming says, when beta-amyloid attaches itself to metals such as iron or copper. These metals can cause beta-amyloid peptides to misfold and bind together in clumps that can promote inflammation and oxidation — a process similar to rusting — in nearby neurons, eventually killing them.

Previous research conducted by other scientists suggests that beetroot juice can improve oxygen flow to the aging brain and possibly improve cognitive performance. Building on this work, Ming, Darrell Cole Cerrato and colleagues at the University of South Florida wanted to find out if betanin, a beet compound used in commercial dyes that readily binds to metals, could block the effects of copper on beta-amyloid and, in turn, prevent the misfolding of these peptides and the oxidation of neurons.

In laboratory studies, the researchers conducted a series of experiments involving 3,5 di-tert-butylcatechol, or DTBC, a compound that is used as a model substance for tracking the chemistry of oxidation. Using visible spectrophotometry, the scientists measured the oxidative reaction of DTBC when exposed to beta-amyloid only, beta-amyloid bound to copper, and copper-bound beta-amyloid in a mixture containing betanin.

On its own, beta-amyloid caused little or no oxidation of DTBC. However, as expected, beta-amyloid bound to copper induced substantial DTBC oxidation. But when betanin was added to the copper-bound beta-amyloid mixture, the researchers found oxidation dropped by as much as 90 percent, suggesting that misfolding of the peptides was potentially suppressed.

“We can’t say that betanin stops the misfolding completely, but we can say that it reduces oxidation,” Cerrato says. “Less oxidation could prevent misfolding to a certain degree, perhaps even to the point that it slows the aggregation of beta-amyloid peptides, which is believed to be the ultimate cause of Alzheimer’s.”

Ming acknowledges funding from the National Science Foundation.

The American Chemical Society, the world’s largest scientific society, is a not-for-profit organization chartered by the U.S. Congress. ACS is a global leader in providing access to chemistry-related information and research through its multiple databases, peer-reviewed journals and scientific conferences. ACS does not conduct research, but publishes and publicizes peer-reviewed scientific studies. Its main offices are in Washington, D.C., and Columbus, Ohio.

This is something I just ‘picked up’ when reading “The Week” news magazine!  There was a short write-up that suggests new breakthroughs in medical brain studies (April 6, p. 21) to help ward off Alzheimer’s disease.  The article states that:

     Scientists at the University of South Florida found that betanin,
     the compound that gives the beet root vegetable its rich red color,
     could help prevent protein pieces called beta-amyloid from forming           harmful plaque in the brain—a hallmark of the neuro-degenerative             disease.  This plaque usually occurs when beta-amyloid binds to               metals in the brain such as iron and copper; these metals cause the         protein to form clumps that can trigger inflammation and oxidation,
     which destroys nerve cells.  In a series of esperiments, the           researchers found that when beta-amyloid bound to copper was exposed       to betanin, oxidation dropped by up to 90 percent.
They are hopeful that other scientists look further into thisl
Now my footnote!  I have always had an appreciation of pickled beets and keep an open jar in my frig.  Very often I will eat a few—almost as an appetizer while cooking dinner, as Andy doesn’t care for beets!  This might be a glimmer of a reason why I have been spared up to this point!!
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Vectors for healing fibromyalgia

This is a communication on email with someone who has concerns.  I thought I would publish it for those who want to know about how to heal the deepest parts of their energy dysfunction.  I touch on the points as bullet points but I get through it to show you how to do it.  With a little study and elbo grease you could get yourself started.
Check out www.bravocoop.com and www.imunothesolution.com
Hello Mimi,
I have a few more questions for you as I am going along in my treatment. I am still using the yogurt only topically 1 tsp twice a day. I have continually adjusted the dosage sometimes higher and sometimes lower because it does seem like I have some reactions if it is too high.

Well done.  This is a very good lifetime health habit that will clear many things over time.

I am wondering how to determine the correct dosage.

Your correct dosage is determined by finding how much energy you have to heal yourself.  You need energy to run your body and your life, and to have fun.

Budgeting energy can come from your various accounts.
If it is life threatening, then you use more and take more rests on the couch.
But in general your dosage is best when you are moving, in an upward path and feeling great.
I find that I get in trouble only when my general nutrition is low.  If I crave or get bad microbes, if I increase the quality of my food and supplements, I am back on course.
It seems as though I may have some die-off from candida or something.

Very possibly.  Usually under the candida is some sort of parasitic condition.  Again, good habits will pull you through.

I have some itchiness on my skin and even in my intimate areas and constant draining down my throat (sometimes it’s even green or yellow which makes me think there is some infection or something?)
I would say that you are detoxing!  Make sure that your protein is high enough to keep you grounded and you should be able to “slow down” the rate of detox by digesting that protein.  (Lighter food will make you go too fast.  Like a light sled on ice.  This is not advisable unless you want to put yourself at risk.  Bobsledding can cause other damage to yourself in the area of not being safe on your feet.). so grounded, safe and feeling great.
Minerals are also important.
Meanwhile beside the detox, you also have two symptoms.
Itching is the removal of heavy metals.  This is held in place by bad habits.  They will be reflected by the type of metals that get caught inside.  Like ironing filings on a magnet, there are many different types of magnets that are in the body.
The best way to release heavy metal is let go of your bad habits.  Like the seven deadly sins.
Greed, lust, averse, sloth, anger, etc.  the list is long and it is not something we want to do or know we do.
But regardless of the bind, taking good care of ourselves and letting go of what we used to “hold on to” and getting “better friends” is the key.
I call them good habits.
You will want to take lots of greens specifically cilantro and chlorella to bind the heavy metals.
Also, if you “meditate or pray” and consciously release the electro magnetic charge from the metal particles, it will stop the itching and it will leave through proper channels.  This being the spine to the end and then it is passed through the colon and out the feces.
When it is coming out of everywhere, it is too much detox and not enough exit.
That’s why we go slowly and condition the exits before we start going on the “double diamond” runs.
Slow down your dose and increase meat.
If you are a vegetarian, you still need to increase your protein so that you stay grounded.
Minerals.  Lots of them.  This will help the spine to build containment for your heavy load.
You probably want to keep this email and make an appt with me to figure out how to work this all out.
What minerals, greens and proteins  work and how many.  You can pick up on the accessories page.  It is called an energetic healing session.
It’s not required, and I am not licensed to “tell you what to do”. But I can help with over the counter type choices and save you lots of time and money.

Green would be infection.

and some headaches.Are these normal detox reactions?

No.  You shouldn’t be having headaches.  This is an indication of the parasitic condition.  If the headache is a low dull throb in the back of the head, near the neck area.

If not, describe headache.
I have found that on this dose I feel more energetic but I still have pain from the fibromyalgia.

One thing at a time.  The FM is from loss of energy in the cell cycle.  That can be too many things and it is best to get some of these layers off before we can get that whole picture into scope.

It’s kind of like layers of lasagna.  Yeast candida on top. Then parasitic condition, if there is a lack of oxygen the cells will turn blue.
Look under your tongue.  AT mirror, look at your tongue and lift it up.  Are the blood vessels blue?  That is a good reading of your gut under there.  Get yourself breathing and exercising so that you are getting oxygen to your body.  Detox baths help but breathing is the best way to get your pH, hormones, and oxygen cycles balanced.  It also cuts through the layers and gets you closer to the FM.
There are also things you can do that will bring the cells back into balance faster.  You can login to the site and look in the search for Yew capsules.  Or just Yew and pick the capsules.  This is a very good way to get the cells into balance as quickly as possible.  It clears the heavy metals out of the cells and then the imuno can turn on the energy.
Again, how and when and how much need to be designed.
I am unsure if I should up the dose and risk more detox symptoms.

No.  You are already releasing, more will only release potentially magnetized metals and make you miserable

Or kill more parasites than you can get out the door.
They would be dead and start to become septic before you released it causing infection that is harder to deal with than what you are doing.
Go slowly, get some movement.
Remove the carbs from diet to not invite them to relocate and have food.
Go into the burning oil diet with a few tablespoons of oil per day.  FRESH ORGANIC oils.  Not too much.  Just enough to make a light oil/water emollient lotion out of your body.  One that is delicious and happy to live in.
Think of oil as clothing, it needs to be comfortable, breathable and healthy.  The body uses it as soap to clean the cells.  It has been reviewed and rewritten that healthy fats actually cause you to loose weight and gain clarity but it has to be right.  Not too much or too little.
It can do a lot of good on all levels since we can use it for fuel and our hitchhikers cannot.  They go elsewhere.
Or go dormant
I also began taking the psyllium husk powder and bentonite which seems to be aiding in the detox.

Not too much pls.

How can I aid the detox in the most painless way so that I feel the best I can from a fibro point of view?

Follow what I am saying here.  Make your own notes.

Track how you feel about each of these baselines and see what your adjustments do to you.
Keep watching for your break in power.  Most of it for the FM is that people are doing too much.  There is so much work piled on top of them that they can’t do it and don’t see that.  They use it to distract from feelings of emptiness, etc.
It is far better to have the feelings than use all your life energy to distract and then wallow in the uncleaned up mess.  It is better to have the feelings, get them out, and then use all the newly recovered energy for healthy habits and getting through your housework so you can live a clean happy, well adjusted life.
It seems that when I was taking more I had less fibro pain

That’s important to track and find those balances.

Do you understand tracking.  1-10 on a scale and check a box everyday.
Do it on a spreadsheet with the symptom on the vertical and the dates across the top.
You will have to test al the things I am talking about
Including grounding, how much pain, how clean your house is, how happy you are.  All the habits you are building, etc.
but I am scared I will unleash some scary virus or something.

You probably do have a scary virus that wants to come out of you.  It is scary because your body takes lots of energy to contain it.

Stop feeding it.  No carbs.  Then it will at least weaken and you won’t be scared.
Oil pulling as a consistent habit will be the eventual area where you handle this.
Don’t judge about being scared.
It’s like getting old, it will happen.  But if you build your habits to take care of the viruses then less fear and more happiness.
Is that something I should be concerned about?

Ask yourself again after reading what I have begun to build for you.  You let me know if you can shift into confidence.

Your immune system can’t take out a virus if you have built it stronger than it by eating sugar and carbs.
It will get too big to get it out.
You have to get it to go dormant,  put it in jail and then do the prisoner transport to get it out.
The fear and concern is from letting it get too powerful and not containing it.
Containing it is not eating sugars and carbs.
Balancing your food, water and supplements, oils
And movement and breathing.  Track it all.
Soon, you will see the tool Good habits and taking very good care of yourself and letting the feelings out from underneath that you are distracting yourself from.
We all do this.  I am not singling you out.
I also was wondering about taking probiotics seperately since I am only taking the yogurt topically at the moment? Would there be a conflict?

Yes.  The probiotics could alter the formula since it is built on a ratio.  Besides, more probiotics are not necessary.  If they are, take more topically and soon you will want to take some internally as well.  That’s fine but once you get your tracking going, you will begin to understand what is too much.  You will see it multidimensionally since all these things relate.

It is more work but very, very enlightening.
I have seen some food intolerances come back since I took the antibiotics in August

Yes. The antibiotics will damage the digestion because you don’t have what you need to digest your food.

If you are done with the need for antibiotics, consider rebuilding your good gut flora with Bravo internally at very small doses, like put a spoon into the yogurt and swish it in water.  It is a very, very small amount but your shouldn’t react to it.
That and all the other things here to look at.  This is when I can best help you.  When you start turning all the systems into the right direction and stop resisting the simple feeling that we all repress, we can get the wind back into our sails.
and I can tell my gut has regressed and I feel the need to give it some attention. I am worried to use the suppositories because I don’t want to have a detox reaction to it. Is that a concern I should have?

Maybe…. We know your gut is in need of rebuilding.

We know. You are already at your rate of detoxing.
Suppositories can be a good idea if
They are very gentle and low in potency
Not used very often
You see, they are a different place than skin.
So you can take a little bit and not rock the boat.
With FM it’s all about balancing the boat and you wanting to rock it really hard to distract from things that you don’t want to feel.
And usually, there is a spiky defense.  Meaning you will bite anyone who wants to get near those hurtful feelings.  You want a life, in this lifetime?  Deal with the painfulness.  It is a much more direct, fully lined up way to deal with the symptoms than anything else.  It is dead on.  The feelings are hurtful but once you connect with them they clear in a few minutes and you are free.
You have let go of all the energy that was used to hold them down and keep them “safe”.
“Safety”/defensive patterns take the place of healthy patterns.  If you can really find the courage to connect and let them up, you will “know”.
It’s a reckoning inside but all the tracking will help.
Here is an incomplete example:
Yes, you put more energy into the right direction and all things start to level out and head up.
It keeps you honest.
It keeps you focused on where you want to be.
It acknowledges where you are.
But there is one thing that happens that is unexpected:
You start to realize that you ARE changing.
Usually we aren’t paying enough attention so this becomes a vital redirection of the energy into NEW GROWTH.
🙂
Mimi
The vectors of Tabatha’s healing
Sun 9/29/18
1-10
10 highest
Transient things that are popping up right now
?
?
?
Abnormalities
green mucus in throat
4
Headaches
Strengtheners in the food department
dark green leafy vegetables. (percentage of goal. goal = 10 oz)
4
meats or proteins (percentage of goal. goal = 10 oz)
5
Strengtheners in the supplement department
Amino Acids
?
Minerals
?
vitamins
?
 
The emollient cleansing
Water (percentage of goal. goal = ? oz)
?
Oil (also known as cellular soap) (percentage of goal. goal = 1 oz)
?
Stress
Holding of repressed emotion
?
amount of work piled on top of repressed emotions
?
defensive patterns that hide the hurt
?
energy used to provide safety from defended territory
?
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Is chondroitin sulfate responsible for the biological effects attributed to the GC protein-derived Macrophage Activating Factor (GcMAF)?

Is chondroitin sulfate responsible for the biological effects attributed to the GC protein-derived Macrophage Activating Factor (GcMAF)?

Abstract

We hypothesize that a plasma glycosaminoglycan, chondroitin sulfate, may be responsible for the biological and clinical effects attributed to the Gc protein-derived Macrophage Activating Factor (GcMAF), a protein that is extracted from human blood. Thus, Gc protein binds chondroitin sulfate on the cell surface and such an interaction may occur also in blood, colostrum and milk. This interpretation would solve the inconsistencies encountered in explaining the effects of GcMAF in vitro and in vivo. According to our model, the Gc protein or the GcMAF bind to chondroitin sulfate both on the cell surface and in bodily fluids, and the resulting multimolecular complexes, under the form of oligomers trigger a transmembrane signal or, alternatively, are internalized and convey the signal directly to the nucleus thus eliciting the diverse biological effects observed for both GcMAF and chondroitin sulfate.

Introduction: A brief history of GcMAF research and controversies

The group-specific component (Gc) protein-derived Macrophage Activating Factor (GcMAF), a protein that is extracted from human blood, has received a great deal of attention in the past few years because of its proposed therapeutic use in the immunotherapy of cancer and other diseases ranging from autism and AIDS to multiple sclerosis and lupus [1], [2], [3], [4], [5], [6], [7], [8], [9], [10].

GcMAF derives from the Gc protein, also know as vitamin D binding protein, a carrier protein highly represented in plasma, and, in lower concentration, in colostrum and milk. The Gc protein was first described in 1959 and it is endowed with multiple functions [11]. The role of the Gc protein as precursor of the GcMAF, however, was described only in 1995, when it was postulated that reduced conversion of the Gc protein into the active GcMAF was associated with immunosuppression in AIDS patients [1]. In this paper, it was hypothesized that the conversion of the Gc protein into the GcMAF occurred via deglycosylation at the level of the Threonine in position 420 of the Gc protein. In particular, it was hypothesized that the Gc protein could be selectively deglycosylated by beta-galactosidase of stimulated B lymphocytes, and by sialidase of T lymphocytes. Removal of Galactose and Sialic Acid would convert the Gc protein into the active GcMAF, that is nothing else than a Gc protein with only N-acetylgalactosamine (GalNAc) as the remaining sugar moiety covalently attached to Threonine 420 [1]. It was later demonstrated that the three sugar moieties attached to Threonine 420 are indeed arranged in a linear fashion with GalNAccovalently bound to Threonine, and Galactose and Sialic Acid attached to the GalNAc in this order (Fig. 1). Thus, the resulting linear trisaccharide is arranged as GalNAc-Galactose-Sialic Acid [12].

Fig. 1. Proposed structures of Gc protein and GcMAF. Panel A: Structure proposed by Yamamoto et al. in 2005 [1]. According to this early model, N-acetylgalactosamine (GalNAc) is covalently bound to Threonine (Thr) 420 of the Gc protein. Galactose and Sialic Acid are bound to GalNAc in a Y-branched arrangement; therefore, according to this model, the sequence of deglycosylation by the enzymes beta-galactosidase and sialidase is not critical for the preparation of GcMAF and treatment of Gc protein with immobilized beta-galactosidase may precede treatment with sialidase [30]. Removal of Galactose and Sialic Acid exposes the GalNAc moiety and leads to the formation of GcMAF. Panel B: Structure proposed by Ravnsborg et al. in 2010 [12]. According to this model the three sugar moieties attached to Threonine 420 are arranged in a linear fashion with GalNAc covalently bound to Threonine, and Galactose and Sialic Acid attached to the GalNAc in this order. At variance with the early model, the linear arrangement of the three sugar moieties was confirmed by mass spectrometry. According to the results reported by Ravnsborg et al. [12], treatment with sialidase must precede treatment with beta-galactosidase; if the Gc protein is treated only with beta-galactosidase, GalNAc would remain “covered” by the other two sugars and no GcMAF would be formed.

Three types of observation led to propose a critical role for the GalNAc moiety attached to Threonine 420, lending credit to the hypothesis that GalNAc was responsible for the binding to the putative receptor and/or for the activation of macrophages and, hence, for the observed immune stimulating and anticancereffects.

1.

When the GalNAc is not exposed, as it is in the Gc protein because it is “covered” by the two other sugars (i.e. Galactose and Sialic Acid), the Gc protein is not endowed with macrophage stimulating activity [1].

2.

Small synthetic peptides comprising and exposing the GalNAc moiety exerted in vitro the same effect of the full-length GcMAF [13].

3.

When the GalNAc is removed from the Threonine 420 by action of the enzyme alpha-N-acetylgalactosaminidase (nagalase), the Gc protein could not be converted to the active GcMAF, and it was postulated that such a lack of conversion led to immunodeficiency [1], [14].

As a logical consequence deriving from this latter point, it was hypothesized that elevated serum levels of nagalase would prevent the formation of GcMAF from the Gc protein, and measure of nagalase was proposed as a method to assess relative immunodeficiency due to deficient production of GcMAF in patients with AIDS, cancer, systemic lupus erythematosus, or autism [1], [10], [14], [15], [16], [2].

Since the serum nagalase seems to be an endo-nagalase and does not act as an exo-enzyme under colloidal serum environment, it was postulated that the administration of exogenous GcMAF extracted from the blood of healthy individuals to patients with elevated nagalase, would restore macrophage activity [17]. According to this hypothesis, exogenously administered GcMAF was not to be affected by the patient’s serum nagalase [18], bypassed the inactive Gc protein devoid of the GalNAc moiety because of the nagalase, and directly acted on macrophages for an extensive activation.

This theory led numerous research groups to study the effects of exogenously administered GcMAF in vitro and in vivo with very encouraging results. In most studies, the Gc protein was extracted from human blood using 25-hydroxyvitamin D affinity chromatography, and then it was treated enzymatically with beta-galactosidase and sialidase in order to expose the GalNAc moiety and thus to convert it into the active GcMAF (for exemplificative reference on the extraction procedure and the subsequent enzymatic conversion of the Gc protein into GcMAF, please see references: [17], [19], [20]. In some clinical studies, the passage involving vitamin D affinity chromatography was skipped, and GcMAF was prepared by enzymatic treatment of human serum without purification by vitamin D affinity chromatography [6].

Exogenously administered GcMAF, thus proved effective in inhibiting the proliferation of human prostate and breast cancer cells in vitro[21], [22]. Consistent with the results observed in cell cultures, GcMAF extracted from human blood inhibited angiogenesis and tumor growth in the experimental animal [19], [20], [23], [24]. It is interesting to notice that human blood-derived GcMAF appeared to work in animals, thus lending credit to the hypothesis that its effects on macrophages, tumor growth and angiogenesis were not specie-specific.

The clinical results of GcMAF-based immunotherapy, however, have been the object of intense scrutiny and some of the papers reporting such results have been questioned [25], [26], [27], with the consequent withdrawal of three papers from the same research group that had reported very encouraging clinical results in HIV and cancer patients [28], [29], [30]. It should be noticed, however, that the retraction of these three papers was due to “irregularities in the documentation for institutional review board approval” and not to questions concerning the validity of the clinical observations.

Thus, despite such concerns, the clinical efficacy of GcMAF-based immunotherapy has been independently confirmed by other research groups that have published clinical observations that seem to indicate that human blood-derived GcMAF is indeed effective in the immunotherapy of cancer [3], [4], [5], [6], [9], autism [10], and a miscellanea of other conditions associated with immune system dysfunction [8]. According to a recent paper, “By March 2014, Saisei Mirai (a clinic in Japan specialized in immunotherapy with human blood-derived GcMAF, non purified by vitamin D-binding chromatography) will have treated more than 1000 patients with GcMAF, both with and without conventional therapies, proving its safety as a therapy” [3].

In sum, in the past 20 years, solid evidence has accumulated demonstrating that GcMAF, extracted from human blood, inhibits cancer cell proliferation in vitro, angiogenesis and tumor growth in the experimental animal, and may have a role in the immunotherapy of a variety of conditions. In addition, we recently demonstrated that human blood-derived GcMAF may also have a role in reducing the damage inflicted by chemotherapy in neurons and glial cells in vitro[31], [32], thus proposing an additional role for GcMAF in counteracting some of the side effects of conventional chemotherapy of cancer.

Inconsistencies in the current hypothesis concerning the interpretation of the observed results

Despite the encouraging evidences concerning the effectiveness of human blood-derived GcMAF, there are significant inconsistencies at the molecular and clinical level that force us to question the interpretation of the results reported above, which include our own results, and to propose a novel hypothesis that may help solving such inconsistencies.

Inconsistencies concerning the role of GalNAc

One of the most striking inconsistencies concerns the cancer risk in individuals harboring the Gc2 allele only (Gc2 homozygotes) of the Gc protein. These individuals are unable to glycosylate the Gc protein on Threonine 420 due to its substitution by lysine. Thus, there is no GalNAc in position 420. In other words, Gc2 homozygotes are unable to produce one single molecule of GcMAF but, despite this fact, the risk of cancer in these individuals is decreased rather than increased as one would have expected given the absence of bona fide GcMAF [33]. It should be noticed that this inconsistency refers to breast cancer that is one of the types of cancer where GcMAF had proven effective in vitro[22], [34], and in vivo[3].

From this observation it appears that the presence or the absence of GalNAc in position 420 of the Gc protein is rather irrelevant in determining immune competency and/or cancer risk, and this observation is clearly at odds with the proposed critical role of GalNAc and, consequently, of nagalase, the enzyme that, by removing GalNAc, would prevent the conversion of the Gc protein into the active GcMAF.

It should be noticed, however, that the risk to develop breast cancer is not associated with one single factor and, therefore, it would be too simplistic to assume that the absence of bona fide GcMAF is responsible for the observed decrease risk of breast cancer in Gc2 homozygotes. Nevertheless, this observation leads to question the proposed role for GalNAc in position 420 of the Gc protein as far as breast cancer risk is concerned.

Another observation by a research group that has published several papers on GcMAF, further questions such a critical role for the GalNAc moiety. In a paper published in 2013, the Authors demonstrated that removal of the Galactose, but not of the Sialic Acid, by beta-galactosidase alone, was sufficient to confer antitumor activity to the Gc protein with a potency comparable to that of GcMAF [35]. It is worth noticing that treatment of the Gc protein with beta-galactosidase alone does not lead to the formation of GcMAF and, on the contrary, leaves the molecular structure of the Gc protein unaltered as demonstrated by Ravnsborg et al. in 2010 [12].

In this study, the Authors used mass spectrometry to demonstrate that treatment of Gc protein with beta-galactosidase alone did not change the glycosylation status of the Gc protein. In other words, the Authors demonstrated that, in order to remove the Sialic Acid and the Galactose and, therefore, to expose the GalNAc, treatment with sialidase must precede treatment with beta-galactosidase. If the Gc protein is treated only with beta-galactosidase, GalNAc would remain “covered” by the other two sugars and, therefore, not available for binding. It is therefore possible that the anti-tumor activity described by Hirota et al. [35] may be ascribed to the Gc protein itself or to its association with chondroitin sulfate as we shall propose in the following paragraphs.

Inconsistencies concerning the role of nagalase in immune deficiency or cancer risk

Another inconsistency refers to the amount of endogenous GcMAF that, at variance with what had been hypothesized, is not decreased in cancer patients, and it actually is much higher than the amount of exogenous GcMAF that has been administered in the immunotherapy of cancer as demonstrated by Rehder et al. in 2008 [36]. In this paper, the Authors examined the glycosylation status of the Gc protein in 56 patients with breast, colorectal, pancreatic, and prostate cancer (i.e. those cancers that had been successfully treated with GcMAF), and observed that there was no significant depletion of GcMAF in the 56 cancer patients examined relative to healthy controls. This observation clearly disproves the theory that cancer patients have decreased production of endogenous GcMAF because of elevated nagalase and, therefore, the entire rational for treating patients with exogenous GcMAF appears to be flawed.

Such an inconsistency concerning the role of nagalase, is further corroborated by the observation that autistic children may show levels of serum nagalase higher than those of HIV or cancer patients but, nevertheless, show no signs of immunodeficiency [5], [10], [30].

A novel hypothesis concerning the interpretation of the results reported for GcMAF

In order to solve the inconsistencies described above, we reconsidered the molecular structure of GcMAF and its mode of action. In fact, despite the wealth of information on this molecule, the details of its interaction with specific, or non-specific, cellular receptors are still missing. It is worth noticing that a receptor for GcMAF has never been described in molecular detail.

However, several years ago, it was demonstrated that the Gc protein binds to a variety of cells that include cells of the immune system, possibly influencing their function. In 1999, DiMartino and Kew studied the interaction of the Gc protein with the cellular membrane of neutrophils and demonstrated that the Gc protein did not bind to a specific cellular receptor, but formed oligomers and interacted with a chondroitin sulfate proteoglycan on the cell surface [37]. According to these Authors, large heterogenous macromolecules, such as cell surface proteoglycans containing chondroitin sulfate, would certainly explain the unusual cell-binding characteristics of the Gc protein. It did not escape our attention that chondroitin sulfate is composed of a chain of alternating sugars that are GalNAcand glucuronic acid.

According to the molecular model that may be derived from such an observation, several molecules of Gc protein would be assembled as oligomers thanks to their binding to the chondroitin sulfate that is present in the extracellular matrixsurrounding the cellular membrane. It is conceivable that the assembly of oligomers of Gc protein may trigger a transmembrane cell signaling mechanism. This mode of action would be analogous to that described for the epidermal- or the platelet-derived growth factors that have to oligomerize in order to trigger their specific signals [38], [39]. The formation of such a multimolecular complex comprising oligomers of the Gc protein and chondroitin sulfate, that is inherently rich in GalNAc, might help explaining the paradoxes and inconsistencies reported in the preceding paragraph.

The observation that the Gc protein binds to chondroitin sulfate, also supports the hypothesis that such a binding between Gc protein (or GcMAF) and chondroitin sulfate may occur also in serum, colostrum or milk, i.e. in fluids where both the Gc protein and chondroitin sulfate are present in relatively high amount [40], [41], [42].

Therefore, since the Gc protein used in the studies in vitro and in vivo to produce GcMAF was extracted from human blood using vitamin D affinity chromatography(and in certain cases even without such a step), and no other purification step was performed (i.e. a step using chondroitinases that would have removed chondroitin sulfate), it is almost certain that chondroitin sulfate remained associated with the Gc protein when it was extracted from human blood and, therefore, with the GcMAF that was enzymatically produced from the Gc protein. In fact, in human plasma, the Gc protein is present in fraction IV of Cohn-Oncley fractionation [43], and we demonstrated that chondroitin sulfates (i.e. chondroitin sulfate A, B and C) are highly represented in this very Cohn-Oncley fraction [44], thus making the interaction between the Gc protein and chondroitin sulfate highly probable if not certain.

Interestingly, chondroitin sulfate shows all the biological and clinical features that have been attributed to GcMAF. In fact, chondroitin sulfate activates macrophages and induces the synthesis and release of nitric oxide in a manner superimposable to that described for GcMAF [4], [45]. In analogy with the reported effects of GcMAF, activation of macrophages by chondroitin sulfate is not accompanied by the release of pro-inflammatory cytokines or Prostaglandin E2[45], further highlighting its role as an immune modulator with no pro-inflammatory activity. Activation of macrophages by chondroitin sulfate may occur also through the modulation of the signaling pertinent to the Macrophage Colony Stimulating Factor (CSF-1) [46]. In other words, chondroitin sulfate appears to be involved in the activation of macrophages not only when such an activation is exerted by GcMAF, but also when other macrophage activators are involved.

In addition to the activation of macrophages, chondroitin sulfate exhibits most of, if not all, the other effects attributed to GcMAF in vitro and in vivo. For example, it inhibits mitogenic signaling in human breast cancer cells [47], and it shows antitumor activity when administered alone or in combination with known chemotherapeutic agents [48].

Consistent with these observations in vitro, the efficacy of chondroitin sulfate in the treatment of a variety of diseases associated with dysregulation of the immune system is well proven. Experimental and clinical data suggest that chondroitin sulfate might be a useful therapeutic agent in diseases as diverse as osteoarthritis, psoriasis, inflammatory bowel diseases, atherosclerosis, Parkinson’s and Alzheimer’s diseases, multiple sclerosis, amyotrophic lateral sclerosis, rheumatoid arthritis and systemic lupus erythematosus, i.e. many of the conditions that have been reported to respond to GcMAF treatment [49].

Moreover, in analogy with GcMAF, chondroitin sulfate has been reported to be effective in HIV infection since 1998, when it was demonstrated that sulfated polysaccharides such as chondroitin sulfate, are potent inhibitors of HIV [50]. Further stressing the role of chondroitin sulfate as an immune stimulant agent with effects superimposable to those reported for GcMAF, in 1999 Di Caro et al. demonstrated that sulfated glycosaminoglycans were effective not only against HIV-1, but also against herpes simplex virus type 1 and human cytomegalovirus, two agents responsible for opportunistic infections in HIV-infected people. The Authors concluded that: “In view of the absence of the side-effects typical of heparin-like compounds, a combination of these derivatives could have therapeutic potential” [51]. Furthermore, chondroitin sulfate, but not other glycosaminoglycans, appears to specifically inhibit the binding of HIV glycoprotein gp120 to its host cell CD4 receptor, thus emphasizing the potential for chondroitin sulfate as an anti-HIV remedy [52].

Also the neuroprotective properties of GcMAF that we have recently described [31], [32] are mimicked by chondroitin sulfate [53].

Such a plethora of actual and potential therapeutic effects of chondroitin sulfate is widely recognized by the medical scientific community. The Mayo Clinic of the United States of America, for example, states that there is strong scientific evidence for the clinical use of chondroitin sulfate in osteoarthritis. In conditions as diverse as coronary artery disease, psoriasis, muscle soreness or interstitial cystitis, the web site of the Mayo Clinic reports that there are clinical studies supporting its use, although further studies need to be performed. However, most interesting is the list of the uses for chondroitin sulfate based on tradition or scientific theories reported by the Mayo Clinic. Such a list encompasses: “aging, allergies, Alzheimer’s disease, amyotrophic lateral sclerosis, antioxidant, antiviral, blood clots, bone healing, breast cancer, burns, cervical disc disease, chest pain, chronic venous ulcers, clogged arteries, colorectal cancer, diabetes, gout, gum disease, headaches, heart attack prevention, heart diseaseprevention, HIV/AIDS, hyperglycemia, high cholesterol, inflammation, inflammatory bowel disease, joint problems, kidney stones, leukemia, lung cancer, malaria, mouth and throat infections, multiple sclerosis, nerve damage, nerve regeneration, neuroblastoma, osteoporosis, pain, Parkinson’s disease, premature birth prevention, quality of life (osteoarthritis), rheumatoid arthritis, snoring, soft tissue injury, spinal cord injury, spine problems, surgery, systemic lupus erythematosus, temporomandibular joint disorder (TMJ), transplants, wound healing” [54].

It is evident that such a diversity in the possible indications for the use of chondroitin sulfate implies effects at the most basic levels of system physiology, most likely at the level of the immune system.

A molecular model of interaction between chondroitin sulfate and the Gc protein

It can be hypothesized that the interaction between the Gc protein and chondroitin sulfate occurs both at the level of the plasma membrane, as demonstrated by DiMartino and Kew [37], as well as in serum, colostrum and milk. Thus, given the abundance of Gc protein and chondroitin sulfate in the same fraction of plasma, an interaction between the two circulating macromolecules appears almost certain and it is conceivable that such an interaction may confer novel biological properties to the complexes deriving from such an interaction.

Consistent with this hypothesis, we demonstrated that when circulating sulfated glycosaminoglycans, in that case heparin, interact with plasma proteins, novel biological properties emerge from such an interaction, and these novel properties depend on the ratio and on the nature of the interaction between the macromolecules. For example, it is known that the effects of heparin on angiogenesis are controversial, with some studies claiming stimulatory and other studies claiming inhibitory effects. Since heparin in human plasma is complexed with basic peptides and proteins, we studied, in the chorioallantoic membrane assay, the angiogenic effect of complexes resulting by mixing poly-l-lysine (a basic heparin-binding polypeptide) with heparin. Our results demonstrated that the angiogenic effect of heparin was associated with the neutralization of its electric charges when the polysaccharide was complexed with a basic peptide [55]. We observed qualitatively identical results when we purified, from human blood, neutral complexes formed by endogenous heparin and basic plasma proteins, thus lending credit to the hypothesis that interaction between heparin and certain plasma proteins led to the formation of multimolecular complexes endowed with biological activities that were not present neither in the isolated proteins, nor in the isolated glycosaminoglycan [56]. Interestingly, not all the complexes between heparin and plasma proteins showed the same biological effects and, for example, only when the ratio poly-l-lysine and heparin was 20/1 (w/w), significant stimulation of angiogenesis occurred. Conversely, a ratio 1/1, that is a ratio that was not sufficient to neutralize all the negative charges on the heparin molecule, was ineffective [55].

Since the chemical-physical characteristics of chondroitin sulfate are similar to those of heparin as far as the interactions with proteins are concerned, it can be hypothesized that specific interactions between the Gc protein and chondroitin sulfate may lead to the formation of multimolecular complexes endowed with properties different from those of the two types of macromolecules taken separately. Thus, it is conceivable that these multimolecular complexes exert the immunological effects that had been attributed to GcMAF.

Furthermore, the complexes between the Gc protein and chondroitin sulfate may also be internalized and interact with the DNA of target cells. The rationale to propose such a mechanism of action lays in the recent observation that chondroitin sulfate favors the intracellular delivery of arginine-rich peptide-DNA complexes by coating the surface of these complexes through electrostatic interactions which improves their extracellular stability and subsequent cellular entry [57]. The efficiency of chondroitin sulfate in enhancing the intracellular delivery of charged molecules is such that the addition of chondroitin sulfate appears to be a promising strategy to enhance the transfection efficiency of cationic arginine-rich peptides in multiple cell types [57].

The possibility that chondroitin sulfate is internalized and conveys signals to the nucleus appears to be analogous to what we previously observed for heparin, thus further highlighting the analogies between the modes of action of these two glycosaminoglycans. Thus, more than thirty years ago, we and others demonstrated that heparin is internalized in different cell types, and internalization leads to a plethora of biological effects that are independent from its well known anticoagulant role [58], [59]. It is conceivable that the biological effects of the multimolecular complexes between the Gc protein and chondroitin sulfate may be different according to whether the complexes remain on the cell surface or are internalized; this would explain the numerous and diverse effects reported for GcMAF and chondroitin sulfate.

Implications and predictions deriving from this novel hypothesis

Our hypothesis concerning the role of chondroitin sulfate in the effects attributed to GcMAF, leads to two different implications that may be rather easily proven by future experiments:

1.

Chondroitin sulfate per se is responsible for all the biological effects attributed to GcMAF.

2.

Alternatively, it is the complex formed between the Gc protein (deglycosylated or not) and chondroitin sulfate that is responsible for the biological effects attributed to GcMAF.

Both predictions could be easily evaluated, at least in vitro; thus, the effects of GcMAF on human macrophages have been widely described at the cellular and molecular level, and an experiment to prove or disprove our hypothesis could be the following:

First, compare the effects of GcMAF extracted from human blood as described above [6], [17], [19], [20], with the effects of a GcMAF that is not extracted from human blood or other biological fluids so that there is no risk of contamination with chondroitin sulfate or other glycosaminoglycans. Such a “pure” GcMAF could be the one described by Bogani et al. in 2006 [13], or a GcMAF extracted and purified from human blood and exhaustively treated with enzymes to remove all possible contamination with glycosaminoglycans.

Then, compare the biological effects of such a “pure” preparation of GcMAF with those of chondroitin sulfate and with those of complexes formed between purified Gc protein and chondroitin sulfate.

In addition, since it is known that the Gc protein and GcMAF bind vitamin D3 and fatty acids such as oleic acid [4], [34], another experiment could be performed to compare the biological effects of “pure” GcMAF with the biological effects of:

i.

Human blood-derived GcMAF plus vitamin D3 and oleic acid;

ii.

“Pure” GcMAF plus vitamin D3 and oleic acid;

iii.

Chondroitin sulfate plus vitamin D3 and oleic acid;

iv.

A combination of the Gc protein, chondroitin sulfate, vitamin D3 and oleic acid.

As far as the parameters to be studied are concerned, we propose to study the pattern of gene expression elicited by human blood-derived GcMAF in human macrophages as it was demonstrated by Siniscalco et al. [7]. Such an experiment would demonstrate which molecule, or which combination of molecules among those quoted above, is responsible for such a pattern of gene expression.

Conclusions

We show evidence supporting the hypothesis that a plasma glycosaminoglycan, chondroitin sulfate, may be responsible for the biological and clinical effects attributed to the GcMAF, a protein that is extracted from human blood. Thus, it is known that the precursor of GcMAF, the Gc protein, binds chondroitin sulfate on the cell surface and such an interaction may occur also in bodily fluids such as blood, colostrum and milk where both the Gc protein and chondroitin sulfate are present in relatively high amounts. This hypothesis would solve all the inconsistencies encountered in trying to explain the effects of GcMAF in vitro and in vivo and helps understanding the sometimes conflicting results independently observed by different research groups when administering GcMAF, extracted from human blood, to cell cultures, experimental animals or humans. According to our hypothesis, the Gc protein, whether deglycosylated or not, binds chondroitin sulfate both on the cell surface and in bodily fluids, and the resulting multimolecular complexes, under the form of oligomers trigger a transmembranesignal or, alternatively, are internalized and convey the signal directly to the nucleus thus eliciting the diverse biological effects observed for both GcMAF and chondroitin sulfate.

Conflict of interest

The Authors are affiliated with the company “dr. reinwald healthcare”, a private company that organizes seminars and trainings for therapists and commercializes nutritional supplements and therapy devices. None of the products or devices distributed by the company is explicitly mentioned in this article and the Authors have not received financial compensation for writing this article.

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N. Yamamoto, V.R. NaraparajuImmunotherapy of BALB/c mice bearing Ehrlich ascites tumor with vitamin D-binding protein-derived macrophage activating factor
Cancer Res, 57 (1997), pp. 2187-2192
[24]
O. Kisker, S. Onizuka, C.M. Becker, et al.Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice
Neoplasia, 5 (2003), pp. 32-40
[25]
A. Ugarte, G. Bouche, L. Meheus, et al.Inconsistencies and questionable reliability of the publication “immunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophages-activating, GcMAF” by Yamamoto et al
Cancer Immunol Immunother, 63 (2014), pp. 1347-1348
[26]
N. Yamamoto, H. Suyama, N. Yamamoto, N. UshijimaImmunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF)
Int J Cancer, 135 (2014), p. 1509
[27]
N. Yamamoto, N. Ushijima, Y. KogaImmunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor
J Med Virol, 2014 (1998), p. 86
(Retracted article)
[28]
N. Yamamoto, H. Suyama, H. Nakazato, N. Yamamoto, Y. KogaImmunotherapy of metastatic colorectal cancer with vitamin D-binding protein-derived macrophage-activating factor, GcMAF
Cancer Immunol Immunother, 57 (2008), pp. 1007-1016
[29]
N. Yamamoto, H. Suyama, N. Yamamoto, N. UshijimaImmunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF)
Int J Cancer, 122 (2008), pp. 461-467
[30]
N. Yamamoto, N. Ushijima, Y. KogaImmunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF)
J Med Virol, 81 (2009), pp. 16-26
[31]
G. Morucci, J.J. Branca, M. Gulisano, et al.Gc-protein-derived macrophage activating factor counteracts the neuronal damage induced by oxaliplatin
Anticancer Drugs, 26 (2015), pp. 197-209
[32]
J.J. Branca, G. Morucci, F. Malentacchi, S. Gelmini, M. Ruggiero, S. PaciniEffects of oxaliplatin and oleic acid Gc-protein-derived macrophage-activating factor on murine and human microglia
J Neurosci Res, 93 (2015), pp. 1364-1377
[33]
S. Abbas, J. Linseisen, T. Slanger, et al.The Gc2 allele of the vitamin D binding protein is associated with a decreased postmenopausal breast cancer risk, independent of the vitamin D status
Cancer Epidemiol Biomarkers Prev, 17 (2008), pp. 1339-1343
[34]
L. Thyer, E. Ward, R. Smith, et al.A novel role for a major component of the vitamin D axis: vitamin D binding protein-derived macrophage activating factor induces human breast cancer cell apoptosis through stimulation of macrophages
Nutrients, 5 (2013), pp. 2577-2589
[35]
K. Hirota, Y. Nakagawa, R. Takeuchi, et al.Antitumor effect of degalactosylated gc-globulin on orthotopic grafted lung cancer in mice
Anticancer Res, 33 (2013), pp. 2911-2915
[36]
D.S. Rehder, R.W. Nelson, C.R. BorgesGlycosylation status of vitamin D binding protein in cancer patients
Protein Sci, 18 (2009), pp. 2036-2042
[37]
S.J. DiMartino, R.R. KewInitial characterization of the vitamin D binding protein (Gc-globulin) binding site on the neutrophil plasma membrane: evidence for a chondroitin sulfate proteoglycan
J Immunol, 163 (1999), pp. 2135-2142
[38]
F.F. Barros, D.G. Powe, I.O. Ellis, A.R. GreenUnderstanding the HER family in breast cancer: interaction with ligands, dimerization and treatments
Histopathology, 56 (2010), pp. 560-572
[39]
T. Matsui, J.H. Pierce, T.P. Fleming, et al.Independent expression of human alpha or beta platelet-derived growth factor receptor cDNAs in a naive hematopoietic cell leads to functional coupling with mitogenic and chemotactic signaling pathways
Proc Natl Acad Sci USA, 86 (1989), pp. 8314-8318
[40]
F. Cecchi, S. Pacini, M. Gulisano, et al.Heparin/heparan sulfate anticoagulant glycosaminoglycans in human plasma of healthy donors: preliminary study on a small group of recruits
Blood Coagul Fibrinolysis, 19 (2008), pp. 349-354
[41]
H. Lu, L.M. McDowell, D.R. Studelska, L. ZhangGlycosaminoglycans in human and bovine serum: detection of twenty-four heparan sulfate and chondroitin sulfate motifs including a novel sialic acid-modified chondroitin sulfate linkage hexasaccharide
Glycobiol Insights, 2010 (2010), pp. 13-28
[42]
G.V. Coppa, O. Gabrielli, E. Bertino, et al.Human milk glycosaminoglycans: the state of the art and future perspectives
Ital J Pediatr, 39 (2013), p. 2
[43]
C.S. Jørgensen, M. Christiansen, I. Laursen, et al.Large-scale purification and characterization of non-glycosylated Gc globulin (vitamin D-binding protein) from plasma fraction IV
Biotechnol Appl Biochem, 44 (2006), pp. 35-44
[44]
F. Cecchi, M. Ruggiero, R. Cappelletti, F. Lanini, S. VannucchiImproved method for analysis of glycosaminoglycans in glycosaminoglycan/protein mixtures: application in Cohn-Oncley fractions of human plasma
Clin Chim Acta, 376 (2007), pp. 142-149
[45]
L.E. Wrenshall, R.B. Stevens, F.B. Cerra, J.L. PlattModulation of macrophage and B cell function by glycosaminoglycans
J Leukoc Biol, 66 (1999), pp. 391-400
[46]
S. Suzu, F. Kimura, J. Ota, et al.Biologic activity of proteoglycan macrophage colony-stimulating factor
J Immunol, 159 (1997), pp. 1860-1867
[47]
C.M. Willis, M. KlüppelChondroitin sulfate-E is a negative regulator of a pro-tumorigenic Wnt/beta-catenin-Collagen 1 axis in breast cancer cells
PLoS ONE, 9 (2014), p. e103966
[48]
M. Ferro, G. Giuberti, S. Zappavigna, et al.Chondroitin sulphate enhances the antitumor activity of gemcitabine and mitomycin-C in bladder cancer cells with different mechanisms
Oncol Rep, 27 (2012), pp. 409-415
[49]
M. Vallières, P. du SouichModulation of inflammation by chondroitin sulfate
Osteoarthritis Cartilage, 18 (2010), pp. 1-6
[50]
M. KonleeSulfated polysaccharides (chondroitin sulfate and carrageenan) plus glucosamine sulfate are potent inhibitors of HIV
Posit Health News Fall, 17 (1998), pp. 4-7
[51]
A. Di Caro, E. Perola, B. Bartolini, et al.Fractions of chemically oversulphated galactosaminoglycan sulphates inhibit three enveloped viruses: human immunodeficiency virus type 1, herpes simplex virus type 1 and human cytomegalovirus
Antivir Chem Chemother, 10 (1999), pp. 33-38
[52]
D.S. Newburg, R.J. Linhardt, S.A. Ampofo, R.H. YolkenHuman milk glycosaminoglycans inhibit HIV glycoprotein gp120 binding to its host cell CD4 receptor
J Nutr, 125 (1995), pp. 419-424
[53]
S. Miyata, H. KitagawaChondroitin sulfate and neuronal disorders
Front Biosci (Landmark Ed), 21 (2016), pp. 1330-1340
[54]
http://www.mayoclinic.org/drugs-supplements/chondroitin-sulfate/evidence/hrb-20058926.
[55]
S. Pacini, M. Gulisano, S. Vannucchi, M. RuggieroPoly-L-lysine/heparin stimulates angiogenesis in chick embryo chorioallantoic membrane
Biochem Biophys Res Commun, 290 (2002), pp. 820-823
[56]
S. Pacini, M. Ruggiero, F. Cecchi, B. Peruzzi, S. VannucchiProteolysis of human plasma reveals the presence of complexes formed by endogenous heparin and peptides that stimulate angiogenesis
Oncol Res, 14 (2004), pp. 501-511
[57]
R.J. Naik, R. Sharma, D. Nisakar, G. Purohit, M. GanguliExogenous chondroitin sulfate glycosaminoglycan associate with arginine-rich peptide-DNA complexes to alter their intracellular processing and gene delivery efficiency
Biochim Biophys Acta, 1848 (2015), pp. 1053-1064
[58]
J.J. Castellot Jr, K. Wong, B. Herman, et al.Binding and internalization of heparin by vascular smooth muscle cells
J Cell Physiol, 124 (1985), pp. 13-20
[59]
S. Vannucchi, F. Pasquali, V. Chiarugi, M. RuggieroInternalization and metabolism of endogenous heparin by cultured endothelial cells
Biochem Biophys Res Commun, 140 (1986), pp. 294-301
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Are you having trouble sleeping? Block the blue! Protect your Melatonin

Are you having trouble sleeping? Block the blue! Protect your Melatonin – just be careful with a few things

As an amateur astronomer, I’ve done a lot of research about light pollution. That led me to research on how light affects sleep. Here’s the summed-up version so you don’t need to read all those scientific papers I have:

– Blue light is great for being awake – that’s why you wake up with a blue sky (read about melanopsin and melatonin on Wikipedia)

– Blue light is not good for sleep; in the 470 nanometers range, that suppresses melatonin (a key hormone for sleeping well)

Buy them here:

https://www.amazon.com/gp/product/B07BRM9Z3M/ref=oh_aui_detailpage_o00_s00?ie=UTF8&psc=1

– Humans (and other animals) evolved to sleep in the dark – or, at the darkest, full Moonlight (just 0.1-0.3 lux of light)

– Longer wavelengths of light were the only source of light at night for most of human history (fire/candles)

– Tablets/phones/screens / LED’s and many CFL bulbs have strong blue wavelengths that are messing with our circadian rhythms and suppressing melatonin because they have wavelengths shorter than 530nm – 540nm

So what to do in our modern world? Wear these glasses before bed. Natural melatonin production would have occurred with our ancestors starting with the onset of sunset. Wavelengths of light from the setting sun would have shifted to red, and fire or candles were usually the only forms of light available. Those are both relatively dim and in longer wavelengths.

Today, our “connected” world has a LOT of blue light. It’s messing with our sleep patterns because our bodies evolved to only see red/orange/yellow light at night, NOT blue light/shorter wavelengths.

https://www.amazon.com/gp/product/B07BRM9Z3M/ref=oh_aui_detailpage_o00_s00?ie=UTF8&psc=1

THESE GLASSES BLOCK THOSE MELATONIN SUPPRESSING WAVELENGTHS.

Put them on a couple hours before bed. For me, I start getting drowsy about 90 minutes after wearing them. The trick is DO NOT take them off without closing your eyes or being in a dark room (a room with ONLY a dim red light would work too, as your melanopsin won’t trigger melatonin suppression with red light). So when changing for bed, close your eyes when removing your shirt if you have to pull it off over your head or put your nighttime clothing on.

Then leave these on until you turn out the light for sleep. And be sure to sleep in the dark too, or wear a sleep mask. Small amounts of light can still affect your melatonin (well, anything brighter then full Moonlight – yes, even a blue LED on your computer). You can watch TV with these on, check your phone, read your tablet, work on your laptop – just note that colors will look weird. Blue looks black. Yellow looks white. Greens look weird. And the glasses aren’t exactly stylish.

But if you sleep better, who cares? They work.

And while you’re at it, make sure your home’s lights (and business if you own one) aren’t shining into other people’s homes or apartments. Too much light at night is what makes these things necessary in the first place. We don’t need all this light at night; these glasses are just a band-aid to help; what we really need is smarter outdoor lighting – aimed down, at the ground, at the proper color(s) so we aren’t suppressing others melatonin. According to a Harvard study, the U.S. loses $63 BILLION dollars per year due to American’s insomnia. Artificial light at night messing up people’s sleep is undoubtedly part of that – let’s fix that so these glasses aren’t as necessary.

Oh, and did these glasses work for me? An emphatic YES, they did. 5 nights (so far) of excellent sleep and well-rested mornings. And I am NOT a morning person! They work – just use them the right way, and be sure you’re not doing other things that might hurt sleep (too much caffeine, lack of / too much exercise right before bed, sleep apnea, etc.) So if it’s not a medical condition, do the right things, wear these, and get better sleep.

https://www.amazon.com/gp/product/B07BRM9Z3M/ref=oh_aui_detailpage_o00_s00?ie=UTF8&psc=1

These are primarily protective glasses and they provide good “physical” protection against anything that can get into your eyes (e.g. in a lab or manufacturing area).

The secondary ‘property’ of this specific pair with an orange lens to block blue light. In certain industrial environments, continuous and/or high level of blue light is present which can cause damage to or at least fatigue of the eyes. So, the blue blocking property helps to mitigate that for the workers.

Now, most of the consumers here (me as well) are buying these for their blue blocking capability and not the physical protection. Generally, the blue (and green to some extent) light is one of the causes of eye fatigue for individuals who work in artificial light (e.g. fluorescent), and with computers (the monitor being the source); therefore, some people are getting the glasses for helping with that.

Another interesting advantage of wearing these is for those people like me who have delayed sleep phase syndrome: it has been found that these individuals can benefit from reduced blue light, a few hours before sleep. By reducing the blue light with these glasses, the amount of disturbance to the sleep is reduced – at least it is working for me.

– For reference on the protective property of the glasses please visit http://uvex.us/uploadedFiles/ProductConfiguration/ProductLiterature/skyperfamily.pdf

– For reference on the lens tint property please visit http://www.uvex.us/uvexlenstechnology.aspx?id=4178

– For delayed sleep phase syndrome and the effect of blue light please check: http://en.wikipedia.org/wiki/Delayed_sleep_phase_disorder#Non-pharmacologic

Buy the product:

https://www.amazon.com/gp/product/B07BRM9Z3M/ref=oh_aui_detailpage_o00_s00?ie=UTF8&psc=1

 

 

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Autism Recovery Summit 3: Potential, Performance & Possibility

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Dear Customer,

In our struggle to provide you with the latest developments in research that may be of your interest, I am bringing to your attention this invitation to the

Autism Recovery Summit 3: Potential, Performance & Possibility October 5th -14th
FREE online event!

REGISTER NOW

Please feel free to share this invitation: it is free. Over 25 doctors, scientists, holistic practitioners, and outside-the-box specialists will share methods, tips, practical actions, new perspectives, and stories of recovery.

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The intention of the Organizers of the Summit is to present cutting-edge information and strategies creating a significant leap in any child’s autism recovery process.

We kick off on October 5th!
Are you ready to see the changes in your child?“Yes! Sign me up for the Summit!”

In this Free Virtual Event you will receive information from 25 autism recovery experts who will talk about their experience of how an autistic child can:

★ Find calm within instead of anxiety and tantrums
★ Sleep well and wake up rested
★ Focus, pay attention. motivate
★ Become more sociable and integrated with friends and life★ Eliminate tummy and head pain to feel better overall

★ Be in a more connection with you and those around him/her★ Speak, express, communicate fully
★ Be happy, expressing who s/he really is
★ Eat a variety of healthy food without sensitivities

★ Make eye contact and say, “I love you, Mama”★ And so much more

The lineup of speakers is incredible. I’ll be joined by experts like Anat Baniel, Kate Wilde, Dr. Jerry Kartzinel, Dr. Dietrich Klinghardt, Maria Rickert Hong, Kristin Selby Gonzalez, Dr. Tom O’Bryan, Julie Matthews, Beth Lambert, Dr. Thomas Moorcroft, Dr. Darin Ingels, and many more experienced leaders in the field who have been helping kids for decades.

In my interview “The Brain Microbiota as it relates to Autism and Immune System Function”https://autismtransformed.simplero.com/S/https://www.autismrecoverytelesummit.com/?ref=13413-

Marco-Ruggiero

I shall describe some novel features of our probiotic products that may be interesting for all those who are interested in detoxifying the body of harmful toxicants. Whether you listen to some or all of these speakers, I am confident you will find the information interesting.

Very truly yours,
Marco Ruggiero
Founder and CEO of Silver Spring Sagl

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Imuno – The Solution® – An Introduction

imuno – The Solution® – An Introduction

We first learned about imuno in July 2018 and the first batch became available in mid-August 2018.  I have begun to cobble a presentation together for you to understand imuno™.  There is more information about its predecessor, Rerum, which explains the product’s ingredients and actions.  The new product, imuno™ has an improved molecular structure and manufacturing process. 

At the end of this information, you will find an offer to purchase and also an apply to be a wholesale reseller.  

Dr. Ruggiero “BootCamp” on Bravo and Rerum:

This video is a good place to learn about Rerum, imuno™’s predecessor.  It is not being manufactured and therefore not available right now.   https://www.youtube.com/watch?v=YIWNgxipvzY

Imuno and Bravo:

imuno works synergistically with Bravo.  Therefore, we need to know about Bravo, how to use it, and what to expect from it. 

Here is a video about how Bravo works.  Bravo is essential for turning on the immune system and moving the toxins out.  Please pay special attention to the Bravo Protocol at minutes 40 to 46.   https://www.youtube.com/watch?v=TPsVpuYw11c&t=2792s

To buy Bravo: Go to https://www.healthyenergetics.com/collections/bravo-prepared-gcmaf

To buy prepared Bravo Yogurt, or handcrafted caps and suppositories, make sure you have an account and log in.

  • A login icon (a person icon) is on the upper right corner of the navigation bar.
  • Make an account if you don’t have one.
  • Login
  • The alternate choices will appear after you Login
    • Alternate choices such as handcrafted products require agreeing with the terms and conditions for the sale.

Specifics on the elements and ingredients of imuno – The Solution®:

Imuno is a well put together molecular structure designed by Dr. Marco Ruggiero who is a molecular biologist specializing in oncology.  Here are a few specific articles on the design and features.

Journal Articles about ingredients: 

Preparation of Low Molecular Weight Chondroitin Sulfates, Screening of a High Anti-Complement Capacity of Low Molecular Weight Chondroitin Sulfate and Its Biological Activity Studies in Attenuating Osteoarthritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5085717/

The ingredients of Rerum and imuno and how they relate to cancer. Oleic Acid, deglycosylated vitamin D-binding protein, nitric oxide: a molecular triad made lethal to cancer.  https://www.ncbi.nlm.nih.gov/pubmed/24982371

Is chondroitin sulfate responsible for the biological effects attributed to the GC protein-derived Macrophage Activating Factor (GcMAF)? https://doi.org/10.1016/j.mehy.2016.07.012

 

Current Events: 

Dr. Marco Ruggiero and Dr. Deitrich Klinghardt are announcing the Ruggiero-Klinghardt Protocol in November at the ACIM Integrative medicine conference in San Diego and in Orlando.  We would like to get your practice started well in advance of everyone else!  Read about it, get some products.  Be ready for the demand they are creating.  Tell your friends.  http://thescipub.com/pdf/10.3844/ajisp.2017.114.126

 

Buy imuno – The Solution@

Go to https://www.healthyenergetics.com/collections/imuno-the-solution®

To buy prepared imuno products such as handcrafted caps and suppositories, make sure you have an account and log in.

  • A login icon, a person icon, is on the upper right of the navigation bar.
  • Make an account if you don’t have one.
  • Login
  • Alternate choices such as handcrafted products require agreeing with the terms and conditions for the sale at account creation and will appear after you LOGIN.

Practitioners  

Apply to become a wholesale reseller you need to be a practitioner or a store.  This link will allow you to do that.  

https://na3.docusign.net/Member/PowerFormSigning.aspx?PowerFormId=767e98ff-a5f5-4b56-9765-a64cc3d22696

There is one more very deep article on how imuno works that I can give you after sign-up.

Do you have questions? 

  • Check the Live Chat button on the site for a knowledge database
  • Email mimi@BravoCoop.com
  • Look on the Accessories tab on the navigation menu for the free 1-1 Consultation.

These products, protocols, and ingredients are not specifically approved by the FDA.  The ingredients of both Bravo and imuno™ are FDA approved individually.  This protocol is not intended to treat, diagnose or take the place of medical treatment.   Consult your healthcare professional when using any of our products.

🙂 Mimi

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The Ruggiero-Klinghart Protocol

http://thescipub.com/pdf/10.3844/ajisp.2017.114.126

This is a detailed description of how to get reservoirs of microbes to move out of hidden areas using ultrasound testing the particulates in urine after and instructions of how to proceed with this technique.

  • Page 114 describes Lyme in depth
  • Page 115 describes co-infections and idiosyncracies
  • Page 116 describes the new approach
  • Page 117 has a table of steps for RK protocol and even mentions Rerum on the bottom of the first column. This page goes on to discuss the congestion of the glymphatics
  • Page 118 discusses the steps and bringing the issue visible to the immune system and the release of deep congestion at many described layers of tissue. (This is what I understand the action of micronized Chondroitin Sulfate to be doing.)  
  • Page 119 we get into ultrasound pictures of affected tissue and a description of mobilizing pathogens and toxins into the urine for elimination and proving than they are there with lab tests and backing up that it works with research.
  • Page 120 deals with what the ultrasound can do
  • Page 121 describes restoring the flow of cerebral lymph and possibly ameliorating neurological symptoms.
  • Page 122 emphasizing the ability of the protocol to excel in other areas and conditions where chronic inflammation and neurodegeneration are found.
  • Page 123 broadens the methodology to include other issues and such therapeutic approaches. 
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MERCURY, TROUT AND YEW 
 (yes you!)

MERCURY, TROUT, AND YEW

Current world use of mercury is estimated to be 10,000 to 15,000 tons annually, of which the United States accounts for about 18 percent.
Fungicides in agriculture, slime control agents in the pulp and paper industry, plastics and electrical apparatus productions, mining, and smelting operations are some of mercury’s uses.  Due to its stability, mercury levels can remain elevated for as long as 100 years after the source of pollution has been discontinued.
Mercury has no known biological function and its presence in living organisms is undesirable and potentially hazardous.
Methylmercury can be bio-concentrated in organisms and bio-magnified through food chains, thus delivering mercury to man and other upper-level consumers in concentrated form.
In May of 1996, Cynthia Ann Evans was graduated from the University of Northern Colorado with a BA degree in chemistry.  During her studies, she had conducted mercury-contamination research for two years.  Cindy’s interest in the environment had led her to study why rainbow trout reproduced poorly in the Carson River of her home state of Nevada.  Over 7,000 tons of mercury was dumped by gold mining operations into the Carson River in the late 1800s, and Cindy’s research focused on the toxicological effects of mercury on freshwater trout embryo and a possible solution to the problem.
When Cindy went on to complete her master’s degree in biochemistry, her faculty advisor at UNC encouraged her to continue her research and use the findings to publish her thesis.  Cindy decided for her research to collect sand from the Carson River and to construct an apparatus in which trout embryos were allowed to develop in conditions similar to the mercury-contaminated river.  Since this was a first-time project, Cindy had to design the apparatus herself.  Cindy’s ingenuity led to a patent-pending for the unique design of the apparatus, but this was not to be the end of her talents or curiosity.
On a weekend visit home from college, her mother gave her a bottle of Montana YewTip™ tincture (Taxus brevifolia) for the cold and flu symptoms she was experiencing at the time and Cindy took the tincture back to school.  Cindy was pleased with the results of the tincture and one day in the laboratory, on a whim, she put some of it into a container with a batch of trout eggs.  To her amazement, she observed the trout eggs absorbing the Yew tincture.  The wall of a trout egg will ordinarily repel damaging molecules, but mercury’s unique molecular structure will penetrate the egg, causing most of them to die or to mutate the few that hatched.  Cindy then observed a substantial increase in the eggs that hatched and survived after having been treated with the Yew tincture.  She repeated the test to confirm her observations, achieving even better results.  Montana YewTip™ tincture was then included in her study in an effort to reduce the toxic effect of mercury on the fish embryos.
Immediately following fertilization and prior to placement of eggs into the tank, the embryos were placed in a 100 ml beaker and 0.5 ml of tincture was added.  Embryos were gently swirled for one minute, the solution was removed and embryos were then placed into the aquarium.  Each aquarium contained 3 liters of water and 0.5 ml of Yew tincture was added to specified tanks.  The first experiment conducted with the tincture involved treated embryos that were used in the control tank (no mercury).  All Yew-treated tanks had a 99% survival and up after fourteen days of development.  Control tanks with no tincture had an 88% and 70% survival percentage with eggs supplied by two different hatcheries.
The experiments conducted in the presence of various amounts of mercuric nitrate, metallic mercury, and mercury-contaminated soil showed embryo survival was severely compromised.  Embryos exposed to mercury without Yew tincture were found not only to have a high mortality but also, fish that survived suffered from a large number of deformities.  The survival percentage for embryos exposed to 200 grams of mercury-contaminated soil was 18%, however, the survival of embryos treated with the Yew tincture and exposed to the same amount of toxic soil increased to 94%, a 76% difference.  Embryos that were exposed to 6 milligrams per liter of metallic mercury dissolved in water yielded a survival percentage of 
42%, while those treated with the Yew tincture had a 64% survival rate, a 22% difference.
It has been theorized that the Yew tincture possibly contains a metal-binding site within its compounds that protect the embryos from mercury’s harmful effects.  Further studies could be performed to determine exactly how the Yew tincture protects the embryos from mercury, and whether its use as a protective agent would be feasible for hatcheries.
Toxic metals detoxification in humans is also a possibility and initial results with a few folks using Yew tincture for that purpose have been encouraging.
Cindy’s thesis, “The Toxic Effects of Elemental Mercury and Mercury Salts On Embryogenesis of Freshwater Trout” was published in May 2001 by the University of Northern Colorado, College of Art and Sciences, Department of Chemistry and Biochemistry.  She earned her master’s degree in 2001 and now works as a quality control specialist for the pharmaceuticals industry in California.

 

 

Yew Tip Products for sale

Go to www.bravocoop.com, hit the shop tab, make an account if you don’t have one, log in.   Then the product will open to you.  (secret menu)

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