Adonis Diaries

Archive for the ‘medicine/medical treatment’ Category

 

I have a patent for creating HIV/AIDS Virus: Dr. Robert Gallo

In April 1984, Dr. Robert Gallo filed a United States patent application for his invention, the HIV/AIDS Virus.

Normally, when a patent is filed and approved, as Dr. Gallo’s was, anyone who uses the product or invention owes a royalty payment to the inventor. Thus, holding the intellectual property laws to their fullest interpretations, one must only wonder why Dr. Gallo has yet to file a lawsuit seeking to recover damages from the usage of his invention?

As odd as this scenario may sound, it bears need for additional scrutiny.

The scientific evidence is complete and compelling, the AIDS Virus is a designer bi-product of the U.S. Special Virus program.

The Special Virus program was a federal virus development program that persisted in the United States from 1962 until 1978.

The U.S. Special Virus was then added as ‘compliment’ to vaccine inoculations in Africa and Manhattan.

Shortly thereafter the world was overwhelmed with mass infections of a human retrovirus that differed from any known human disease, it was highly contagious and more importantly, it could kill.

2045-Gallo NCI 1980
Image: Dr. Robert Gallo

A review of the Special Virus Flow Chart (“research logic”) reveals the United States was seeking a ‘virus particle’ that would negatively impact the defense mechanisms of the immune system.

The program sought to modify the genome of the virus particle in which to splice in an animal “wasting disease” called “Visna”.

According to the Proceedings of the United States of America, AIDS is an evolutionary, laboratory development of the peculiar Visna Virus, first detected in Icelandic sheep.

Recently, American and world scientists confirm with 100% certainty the laboratory genesis of AIDS.

This fact is further underscored when one reviews the ‘multiply-spliced’ nature of the HIV ‘tat’ gene and Dr. Gallo’s 1971 Special Virus paper, “Reverse Transcriptase of Type-C virus Particles of Human Origin”.

Dr. Gallo’s 1971 Special Virus paper is identical to his 1984 announcement of AIDS.

Upon further review the record reveals that he filed his patent on AIDS, before he made the announcement with Secretary Heckler. Earlier this year, Dr. Gallo conceded his role as a ‘Project Officer’ for the federal virus development program, the Special Virus.

The Flow Chart of the program and the 15 progress reports are irrefutable evidence of the United States’ secret plan to cull world populations via the unleashing of a stealth biological microorganism that would ‘waste’ humanity.

In light of this true genesis of the world’s most divesting biological scourge, it is the United States that owes ‘royal’ payments to the innocent victims.

Each and every victim of AIDS is deserving of a formal apology and a sense of economic closure for an invention of death and despair, perpetrated by the United States.

The eyes of the world are upon the General Accounting Office’s Health Care Team, under the direction of William J. Scanlon.

Between 1964 and 1978, the secret federal virus program spent $550 million dollars of taxpayer money to invent AIDS. It is now necessary to spend whatever it takes to dismantle an invention that has led to the greatest crime against humanity in the history of the world.

Note 1: Roger Hajjar  responded

Discovery is not equal to developing! Wallow! The disease had start spreading and Luc Montagnier identified, discovered the cause! and developed a test to identify it.

Max Gallo got samples from Montagnier before he publishes and jumped on the opportunity to try to get a share of the bounty coming from the test…

HIV is a strain from a virus that was know to infect monkeys in africa. It mutated and started infecting humans.

Note 2: Origin of AIDS

The origin of AIDS and HIV has puzzled scientists ever since the illness first came to light in the early 1980s.

For over 20 years it has been the subject of fierce debate and the cause of countless arguments, with everything from a promiscuous flight attendant to a suspect vaccine programme being blamed. So what is the truth?

Just where did AIDS come from?

The first recognised cases of AIDS occurred in the USA in the early 1980s.

A number of gay men in New York and California suddenly began to develop rare opportunistic infections and cancers that seemed stubbornly resistant to any treatment. At this time, AIDS did not yet have a name, but it quickly became obvious that all the men were suffering from a common syndrome.

The discovery of HIV, the Human Immunodeficiency Virus, was made soon after. While some were initially resistant to acknowledge the connection (and indeed some remain so today), there is now clear evidence to prove that HIV causes AIDS.

So, in order to find the source of AIDS, it is necessary to look for the origin of HIV, and find out how, when and where HIV first began to cause disease in humans. How?

What type of virus is HIV?HIV is a lentivirus, and like all viruses of this type, it attacks the immune system. Lentiviruses are in turn part of a larger group of viruses known as retroviruses.

The name ‘lentivirus’ literally means ‘slow virus’ because they take such a long time to produce any adverse effects in the body. They have been found in a number of different animals, including cats, sheep, horses and cattle.

However, the most interesting lentivirus in terms of the investigation into the origins of HIV is the Simian Immunodeficiency Virus (SIV) that affects monkeys, which is believed to be at least 32,000 years old.

1. So did HIV come from an SIV?It is now generally accepted that HIV is a descendant of a Simian Immunodeficiency Virus because certain strains of SIVs bear a very close resemblance to HIV-1 and HIV-2, the two types of HIV.HIV-2 for example corresponds to SIVsm, a strain of the Simian Immunodeficiency Virus found in the sooty mangabey (also known as the White-collared monkey), which is indigenous to western Africa.

The more virulent, pandemic strain of HIV, namely HIV-1, was until recently more difficult to place. Until 1999, the closest counterpart that had been identified was SIVcpz, the SIV found in chimpanzees. However, this virus still had certain significant differences from HIV.What happened in 1999?

In February 1999 a group of researchers from the University of Alabama 2 announced that they had found a type of SIVcpz that was almost identical to HIV-1. This particular strain was identified in a frozen sample taken from a captive member of the sub-group of chimpanzees known as Pan troglodytes troglodytes ( P. t. troglodytes), which were once common in west-central Africa.

The researchers (led by Paul Sharp of Nottingham University and Beatrice Hahn of the University of Alabama) made the discovery during the course of a 10-year long study into the origins of the virus. They claimed that this sample proved that chimpanzees were the source of HIV-1, and that the virus had at some point crossed species from chimps to humans.Their final findings were published two years later in Nature magazine 3.

In this article, they concluded that wild chimps had been infected simultaneously with two different simian immunodeficiency viruses which had “viral sex” to form a third virus that could be passed on to other chimps and, more significantly, was capable of infecting humans and causing AIDS.

These two different viruses were traced back to a SIV that infected red-capped mangabeys and one found in greater spot-nosed monkeys. They believe that the hybridisation took place inside chimps that had become infected with both strains of SIV after they hunted and killed the two smaller species of monkey.

They also concluded that all three ‘groups’ of HIV-1 – namely Group M, N and O (see our strains and subtypes page for more information on these) – came from the SIV found in P. t. troglodytes, and that each group represented a separate crossover ‘event’ from chimps to humans.How could HIV have crossed species?

It has been known for a long time that certain viruses can pass between species. Indeed, the very fact that chimpanzees obtained SIV from two other species of primate shows just how easily this crossover can occur. As animals ourselves, we are just as susceptible. When a viral transfer between animals and humans takes place, it is known as zoonosis.

Below are some of the most common theories about how this ‘zoonosis’ took place, and how SIV became HIV in humans:

The ‘hunter’ theory. The most commonly accepted theory is that of the ‘hunter’. In this scenario, SIVcpz was transferred to humans as a result of chimps being killed and eaten or their blood getting into cuts or wounds on the hunter. Normally the hunter’s body would have fought off SIV, but on a few occasions it adapted itself within its new human host and became HIV-1.

The fact that there were several different early strains of HIV, each with a slightly different genetic make-up (the most common of which was HIV-1 group M), would support this theory: every time it passed from a chimpanzee to a man, it would have developed in a slightly different way within his body, and thus produced a slightly different strain.“Retroviral transfer from primates to hunters is still occurring even today”

An article published in The Lancet in 2004 4, also shows how retroviral transfer from primates to hunters is still occurring even today. In a sample of 1099 individuals in Cameroon , they discovered (10%) were infected with SFV (Simian Foamy Virus), an illness which, like SIV, was previously thought only to infect primates.

All these infections were believed to have been acquired through the butchering and consumption of monkey and ape meat. Discoveries such as this have led to calls for an outright ban on bushmeat hunting to prevent simian viruses being passed to humans.

The oral polio vaccine (OPV) theorySome other rather controversial theories have contended that HIV was transferred iatrogenically (i.e. via medical interventions). One particularly well-publicised idea is that polio vaccines played a role in the transfer.

In his book, The River, the journalist Edward Hooper suggests that HIV can be traced to the testing of an oral polio vaccine called Chat, given to about a million people in the Belgian Congo, Ruanda and Urundi in the late 1950s.

To be reproduced, live polio vaccine needs to be cultivated in living tissue, and Hooper’s belief is that Chat was grown in kidney cells taken from local chimps infected with SIVcmz. This, he claims, would have resulted in the contamination of the vaccine with chimp SIV, and a large number of people subsequently becoming infected with HIV-1.

5. Many people have contested Hooper’s theories and insist that local chimps were not infected with a strain of SIVcmz that is closely linked to HIV. Furthermore, the oral administration of the vaccine would seem insufficient to cause infection in most people (SIV/HIV needs to get directly into the bloodstream to cause infection – the lining of the mouth and throat generally act as good barriers to the virus).

6. In February 2000 the Wistar Institute in Philadelphia (one of the original manufacturers of the Chat vaccine) announced that it had discovered in its stores a phial of polio vaccine that had been used as part of the program. The vaccine was subsequently analysed and in April 2001 it was announced that no trace had been found of either HIV or chimpanzee SIV.

7. A second analysis confirmed that only macaque monkey kidney cells, which cannot be infected with SIV or HIV, were used to make Chat. 8 While this is just one phial of many, it means that the OPV theory remains unproven.The fact that the OPV theory accounts for just one (group M) of several different groups of HIV also suggests that transferral must have happened in other ways too, as does the fact that HIV seems to have existed in humans before the vaccine trials were ever carried out.

More about when HIV came into being can be found below.The contaminated needle theoryThis is an extension of the original ‘hunter’ theory.

In the 1950s, the use of disposable plastic syringes became commonplace around the world as a cheap, sterile way to administer medicines. However, to African healthcare professionals working on inoculation and other medical programmes, the huge quantities of syringes needed would have been very costly. It is therefore likely that one single syringe would have been used to inject multiple patients without any sterilisation in between.

This would rapidly have transferred any viral particles (within a hunter’s blood for example) from one person to another, creating huge potential for the virus to mutate and replicate in each new individual it entered, even if the SIV within the original person infected had not yet converted to HIV.

The colonialism theory. The colonialism or ‘Heart of Darkness’ theory, is one of the more recent theories to have entered into the debate. It is again based on the basic ‘hunter’ premise, but more thoroughly explains how this original infection could have led to an epidemic. It was first proposed in 2000 by Jim Moore, an American specialist in primate behaviour, who published his findings in the journal AIDS Research and Human Retroviruses.

9. During the late 19th and early 20th century, much of Africa was ruled by colonial forces. In areas such as French Equatorial Africa and the Belgian Congo, colonial rule was particularly harsh and many Africans were forced into labour camps where sanitation was poor, food was scarce and physical demands were extreme.

These factors alone would have been sufficient to create poor health in anyone, so SIV could easily have infiltrated the labour force and taken advantage of their weakened immune systems to become HIV.

A stray and perhaps sick chimpanzee with SIV would have made a welcome extra source of food for the workers. “SIV could easily have infiltrated the labour force and taken advantage of their weakened immune systems”

Moore also believes that many of the labourers would have been inoculated with unsterile needles against diseases such as smallpox (to keep them alive and working), and that many of the camps actively employed prostitutes to keep the workers happy, creating numerous possibilities for onward transmission.

A large number of labourers would have died before they even developed the first symptoms of AIDS, and those that did get sick would not have stood out as any different in an already disease-ridden population. Even if they had been identified, all evidence (including medical records) that the camps existed was destroyed to cover up the fact that a staggering 50% of the local population were wiped out there.

One final factor Moore uses to support his theory, is the fact that the labour camps were set up around the time that HIV was first believed to have passed into humans – the early part of the 20th century.

The conspiracy theory. Some believe that HIV is a ‘conspiracy’ or that it is ‘man-made’. A recent survey carried out in the US for example, identified a significant number of African Americans who believe HIV was manufactured as part of a biological warfare programme, designed to wipe out large numbers of black and homosexual people.

10. Many say this was done under the auspices of the US federal ‘Special Cancer Virus Program’ (SCVP), possibly with the help of the CIA. Linked in to this theory is the belief that the virus was spread (either deliberately or inadvertently) to thousands of people all over the world through the smallpox inoculation programme, or to gay men through Hepatitis B vaccine trials.

While none of these theories can be definitively disproved, the evidence given to back them up is usually based upon supposition and speculation, and ignores the clear link between SIV and HIV or the fact that the virus has been identified in people as far back as 1959.

When?

During the last few years it has become possible not only to determine whether HIV is present in a blood or plasma sample, but also to determine the particular subtype of the virus. Studying the subtype of virus of some of the earliest known instances of HIV infection can help to provide clues about the time it first appeared in humans and its subsequent evolution.

Four of the earliest known instances of HIV infection are as follows:

A plasma sample taken in 1959 from an adult male living in what is now the Democratic Republic of the Congo.

11. A lymph node sample taken in 1960 from an adult female, also from the Democratic Republic of the Congo.

12. HIV found in tissue samples from an American teenager who died in St. Louis in 1969.

13. HIV found in tissue samples from a Norwegian sailor who died around 1976.

14. A 1998 analysis of the plasma sample from 1959 suggested that HIV-1 was introduced into humans around the 1940s or the early 1950s.

15. In January 2000, the results of a new study 16 suggested that the first case of HIV-1 infection occurred around 1931 in West Africa. This estimate (which had a 15 year margin of error) was based on a complex computer model of HIV’s evolution.

However, a study in 2008 17 dated the origin of HIV to between 1884 and 1924, much earlier than previous estimates. The researchers compared the viral sequence from 1959 (the oldest known HIV-1 specimen) to the newly discovered sequence from 1960.

They found a significant genetic difference between them, demonstrating diversification of HIV-1 occurred long before the AIDS pandemic was recognised.

The authors suggest a long history of the virus in Africa and call Kinshasa the “epicentre of the HIV/AIDS pandemic” in Central Africa.

They propose the early spread of HIV was concurrent with the development of colonial cities, in which crowding of people increased opportunities for HIV transmission. If accurate, these findings imply that HIV existed before many scenarios (such as the OPV and conspiracy theories) suggest.

What about HIV-2?

When did that get passed to humans? Until recently, the origins of the HIV-2 virus had remained relatively unexplored. HIV-2 is thought to come from the SIV in Sooty Mangabeys rather than chimpanzees, but the crossover to humans is believed to have happened in a similar way (i.e. through the butchering and consumption of monkey meat).

It is far rarer, significantly less infectious and progresses more slowly to AIDS than HIV-1. As a result, it infects far fewer people, and is mainly confined to a few countries in West Africa.

In May 2003, a group of Belgian researchers published a report 18 in Proceedings of the National Academy of Science.

By analysing samples of the two different subtypes of HIV-2 (A and B) taken from infected individuals and SIV samples taken from sooty mangabeys, Dr Vandamme concluded that subtype A had passed into humans around 1940 and subtype B in 1945 (plus or minus 16 years or so).

Her team of researchers also discovered that the virus had originated in Guinea-Bissau and that its spread was most likely precipitated by the independence war that took place in the country between 1963 and 1974 (Guinea-Bissau is a former Portuguese colony). Her theory was backed up by the fact that the first European cases of HIV-2 were discovered among Portuguese veterans of the war, many of whom had received blood transfusions or unsterile injections following injury, or had possibly had relationships with local women.

Where?

The question of exactly where the transfer of HIV to humans took place, and where the ‘epidemic’ officially first developed has always been controversial. Some have suggested that it is dangerous to even try to find out, as AIDS has frequently been blamed on an innocent person or group of individuals in the past.

However, scientists remain keen to find the true origin of HIV, as most agree it is important to understand the virus and its epidemiology in order to fight it. So did it definitely come from Africa?

Given the evidence we have already looked at, it seems highly likely that Africa was indeed the continent where the transfer of HIV to humans first occurred (monkeys from Asia and South America have never been found to have SIVs that could cause HIV in humans).

In May 2006, the same group of researchers who first identified the Pan troglodytes troglodytes strain of SIVcpz, announced that they had narrowed down the location of this particular strain to wild chimpanzees found in the forests of Southern Cameroon 19.

By analysing 599 samples of chimp droppings (P. T. troglodytes are a highly endangered and thus protected species that cannot be killed or captured for testing), the researchers were able to obtain 34 specimens that reacted to a standard HIV DNA test, 12 of which gave results that were virtually indistinguishable from the reactions created by human HIV.

The researchers therefore concluded that the chimpanzees found in this area were highly likely the origin of both the pandemic Group M of HIV-1 and of the far rarer Group N. The exact origins of Group O however remain unknown.

HIV Group N principally affects people living in South-central Cameroon, so it is not difficult to see how this outbreak started. Group M, the group that has caused the worldwide pandemic, was however first identified in Kinshasa, in the Democratic Republic of Congo.

It is not entirely clear how it transferred from Cameroon to Kinshasa, but the most likely explanation is that an infected individual travelled south down the Sangha river that runs through Southern Cameroon to the River Congo and then on to Kinshasa, where the Group M epidemic probably began.

Just as we do not know exactly who spread the virus from Cameroon to Kinshasa, how the virus spread from Africa to America is also not entirely clear.

However, recent evidence suggests that the virus may have arrived via the Caribbean island of Haiti.

Why is Haiti significant?

The AIDS epidemic in Haiti first came to light in the early 1980s, at around the same time that cases in the USA were being uncovered. Following the discovery of a number of Haitians with Kaposi’s Sarcoma and other AIDS-related conditions, medical journals and books began to claim that AIDS had come from Haiti, and that Haitians were responsible for the AIDS epidemic in the United States.

These claims, which were often founded on dubious evidence, fuelled pre-existing racism in the US and many Haitians suffered severe discrimination and stigma as a result. A large number of Haitian immigrants living in the US lost their jobs and were evicted from their homes as Haitians were added to homosexuals, haemophiliacs and heroin users to make the ‘Four-H Club’ of groups at high risk of AIDS.

20. The emotionally-charged culture of blame and prejudice that surrounded HIV and AIDS in the early years meant that it soon became politically difficult to present epidemiological findings in a neutral and objective way. For many years the link between Haiti and the US epidemic was therefore dropped as a subject. “Tracing HIV’s origins remains a politically sensitive exercise ”

In March 2007 however, it returned to the public eye at the Fourteenth Conference on Retroviruses and Opportunistic Infections (CROI) in Los Angeles. A group of international scientists presented data based on complex genetic analysis of 122 early samples of HIV-1, group M, subtype B (the most common strain found in the USA and in Haiti) showing that the strain had probably been brought to Haiti from Africa by a single person in around 1966; a time when many Haitians would have been returning from working in the Congo.

21. Genetic analysis then showed that subtype B spread slowly from person to person on the island, before being transferred to the US, again probably by a single individual, at some point between 1969 and 1972. A paper published in October 2007 by Worobey and colleagues gave a 99.7% certainty that HIV subtype B originated in Haiti before passing to the US.

22. It is possible that HIV had entered the US several times before subtype B took a firm hold (which would explain the infection of the St. Louis teenager in the early to mid-1960s), but it was the late 1960s / early 1970s transfer that is believed to be responsible for the widespread epidemic seen in the US today.

Once the virus had established itself in the gay community, it would have spread fairly rapidly (anal intercourse carries a very high transmission risk), with transmission occurring within and between the US and Haiti, and internationally, until the original route taken by the virus was largely obscured.

Dr Michael Worobey, lead researcher in the study, claimed that his data was not intended to place any blame on Haiti, or on Central Africans, and stressed that none of the people who first transmitted HIV would have been aware they were infected. His work still received strong protests from one Haitian delegate at the CROI conference however, demonstrating the extent to which tracing HIV’s origins remains a politically sensitive exercise.What caused the epidemic to spread so suddenly?

There are a number of factors that may have contributed to the sudden spread of HIV, most of which occurred in the latter half of the twentieth century.Travel International travel contributed to the rapid spread of HIV around the world.

Both national and international travel undoubtedly had a major role in the initial spread of HIV. In the US, international travel by young men making the most of the gay sexual revolution of the late 70s and early 80s would certainly have played a large part in taking the virus worldwide. In Africa, the virus would probably have been spread along truck routes and between towns and cities within the continent itself.

However, it is quite conceivable that some of the early outbreaks in African nations were not started by Africans infected with the ‘original’ virus at all, but by people visiting from overseas where the epidemic had been growing too. The process of transmission in a global pandemic is simply too complex to blame on any one group or individual.

Much was made in the early years of the epidemic of a so-called ‘Patient Zero’ who was the basis of a complex “transmission scenario” compiled by Dr. William Darrow and colleagues at the Centre for Disease Control in the US. This epidemiological study showed how ‘Patient O’ (mistakenly identified in the press as ‘Patient Zero’) had given HIV to multiple partners, who then in turn transmitted it to others and rapidly spread the virus to locations all over the world.

A journalist, Randy Shilts, subsequently wrote a book 23 based on Darrow’s findings, which named Patient Zero as a gay Canadian flight attendant called Gaetan Dugas. For several years, Dugas was vilified as a ‘mass spreader’ of HIV and the original source of the HIV epidemic among gay men.

However, four years after the publication of Shilts’ article, Dr. Darrow repudiated his study, admitting its methods were flawed and that Shilts’ had misrepresented its conclusions.While Gaetan Dugas was a real person who did eventually die of AIDS, the Patient Zero story was not much more than myth and scaremongering.

HIV in the US was to a large degree initially spread by gay men, but this occurred on a huge scale over many years, probably a long time before Dugas even began to travel.The blood industry Screening blood for HIV is essential for safe blood supplies

As blood transfusions became a routine part of medical practice, an industry to meet this increased demand for blood began to develop rapidly. In some countries such as the USA, donors were paid to give blood, a policy that often attracted those most desperate for cash; among them intravenous drug users.

In the early stages of the epidemic, doctors were unaware of how easily HIV could be spread and blood donations remained unscreened. This blood was then sent worldwide, and unfortunately most people who received infected donations went on to become HIV positive themselves.In the late 1960’s haemophiliacs also began to benefit from the blood clotting properties of a product called Factor VIII.

However, to produce this coagulant, blood from hundreds of individual donors had to be pooled. This meant that a single donation of HIV+ blood could contaminate a huge batch of Factor VIII. This put thousands of haemophiliacs all over the world at risk of HIV, and many subsequently became infected with the virus.

Drug use. The 1970s saw an increase in the availability of heroin following the Vietnam War and other conflicts in the Middle East, which helped stimulate a growth in intravenous drug use. As a result of sharing unsterilised needles and syringes, HIV was passed on among injecting drug users (IDUs).

Due to this repeated practice many IDUs continue to be infected with HIV.

Conclusions

It is likely that we will never know who the first person was to be infected with HIV, or exactly how it spread from that initial person. Scientists investigating the possibilities often become very attached to their individual ‘pet’ theories and insist that theirs is the only true answer, but the spread of AIDS could quite conceivably have been induced by a combination of many different events.

Whether through injections, travel, wars, colonial practices or genetic engineering, the realities of the 20th century have undoubtedly had a major role to play. Nevertheless, perhaps a more pressing concern for scientists today should not be how the AIDS epidemic originated, but how those it affects can be treated, how the further spread of HIV can be prevented and how the world can change to ensure a similar pandemic never occurs again

– See more at: http://www.avert.org/origin-hiv-aids.htm#sthash.MCcuPxlX.dpuf

 

 

This “Happy Cell”

“What is the truest form of human happiness?”  Steven Cole asks.

It’s a question he’s been considering for most of his career—but Cole is an immunologist, not a philosopher. To him, this question isn’t rhetoric or a thought experiment. It’s science—measureable and finite.

What a Happy Cell Looks Like

A growing field of research is examining how life satisfaction may affect cellular functioning and DNA.

Cole, a professor of medicine and psychiatry at the University of California, Los Angeles, has spent several decades investigating the connection between our emotional and biological selves.

“The old thinking was that our bodies were stable biological entities, fundamentally separate from the external world,” he says. “But the new thinking is that there is much more permeability and fluidity.”

Betty Nudler/Flickr

His latest project is the examination of happiness in biological terms.

“There’s an intrinsic connection between our direct experience of happiness and the perception of that experience in our bodies, as represented by changes in our biologic mechanisms. We’ve found that happiness can remodel our cellular composition,” he explains.

Specifically, Cole and his team of researchers at UCLA have found that happiness seems to alter the function of immune cells. “It’s no question that the mind and immune system are intrinsically linked,” he says. “Our body is a literal product of our environment.”

As he explains, the immune system has two primary functions: to fight infection and to cause inflammation.

The first function, known as the antiviral response, is generally considered positive because it helps ward off external threats, like viruses, that might otherwise harm the body.

The second function, known as the inflammatory response, is less positive because its efforts is to keep healthy immune cells circulating in the body can also cause tissue damage.

Cole has found that the balance of these two functions of the immune system may change based on life experiences.

His work has shown that negative experiences like a new cancer diagnosis, depression, post-traumatic stress disorder, and low socioeconomic status may cause changes to someone’s immunologic profile.

“Over the past 15 years, our work has shown us that diverse social and psychological experiences that cause a sense of threat or uncertainty can evoke a similar response in our immune cells,” he says.

Listening to him explain his work is part philosophy lesson, part cellular-biology lesson, a scientific discourse on la dolce vita.

“We’re beginning to understand that life experiences like chronic stress, loneliness, and social isolation negatively affect our immunologic profile. This gives us a sense of how not to live—but more importantly, it also tells us something about how to live, because there are concrete things we can do to actively promote a positive change in our immunology,” he says. “The biology of happiness is in our hands.”

But how exactly do our immune cells register this abstract concept of happiness? The answer depends on how “happiness” is defined.

“There are two distinct forms of happiness, hedonic happiness and eudaimonic happiness, and our bodies respond differently to each type,” Cole explains.

“Hedonic happiness is the elevated mood we experience after an external life event, like buying a new home,” while eudaimonic happiness “is our sense of purpose and direction in life, our involvement in something bigger than ourselves.”

Of the two, eudaimonic happiness in particular is associated with a better-functioning immune system, according to Cole.

To determine this effect, Cole and a team of researchers from the University of North Carolina, Chapel Hill, asked 80 healthy adults to fill out questionnaires about their well-being. The researchers then analyzed the volunteers’ answers to assess their levels of eudaimonic and hedonic happiness, and took blood samples to study the functioning of their immune cells.

They found that a high score of eudaimonic happiness, more than a high score of hedonic happiness, was correlated with a better genetic expression profile, meaning the immune cells showed high rates of the antiviral response and low rates of the inflammatory response.

The researchers posited that though both types of happiness may look similar on the outside, the corresponding genetic expression profiles are quite different. “When we asked people how happy they felt, both [the high eudaimonic and high hedonic] groups seemed about the same,”Cole says.

But when we looked at the cellular and molecular level, it looks like people with high levels of eudaimonic happiness are better off, immunologically speaking.”

“We already know ways to achieve hedonic happiness, but how can we live our lives to evoke a eudaimonic experience in our immune system?” he continues.

One way is through mind-body practices, like meditation, which “have been shown to cultivate positive and happy immune cells,” he says.

Research has linked meditation to reduced negative inflammatory activity, increased positive antiviral response, improved function of specific strains of immune cells, and higher antibody production.

But perhaps the most striking theory posed of meditation is that it could alter genetic material.

In recent years, a new field of study, known as mind-body genomics, has emerged.

Among the most well-known researchers in this area are Nobel laureate Elizabeth Blackburn, a biochemist at the University of California, San Francisco, and her colleague, psychiatrist Elissa Epel.

Through a series of studies, the two found that meditation could affect the ends of DNA known as the telomeres, which act as protective caps for genes. The longer the telomere, the greater the protection conferred for the DNA strand, and the longer that cell can survive.

And telomeres, like immune cells, seem to respond to emotional cues.

Negative external conditions like chronic stress that reduce eudaimonic happiness may shorten telomere length, while stress-reducing activities like meditation may help to maintain it.

“Telomeres are affected by many things, but they are directly affected by stress. So we can see how improvements in our mental health, through the practice of meditation, might be linked to improvements in our telomeres,” Epel explains. “They offer us a window and some insight into how we are living, and help us appreciate how what we do today can affect our health tomorrow.”

As the field of mind-body genomics matures, the focus is moving towards gaining a better understanding of not only how DNA could be structurally changed by meditation, but also whether meditation can alter DNA functionally, through changes in how genes are expressed.

In one recent study, for example, meditation was linked to enhanced expression of genes associated with insulin secretion, telomere structure, and cellular energy and function, and decreased expression of genes linked to inflammation and stress.

What’s more, blood samples collected during the study found that experienced meditators showed changes in their genetic activity after just one meditation session.

With 21,000 genes in the human genome, Cole, Epel, and other researchers have just scratched the surface of the connection between our emotional and biological selves.

“We are an ever-changing conglomeration of cells very much influenced by our experience of the world around us,” Cole says. “At the rate we’re going, we have more data than we can make sense of. It’s this process that helps us get closer to understanding the black box. Who knows? Maybe in the future we may be able to sequence our own genes.” Epel agrees: “We don’t yet have the technology to monitor our telomeres, but it’s coming.”

In the meantime, though, the lessons of mind-body genomics still apply. “The experience you have today will influence your body composition for the next 80 days, because that’s how long most cellular processes hang around,” Cole says. “So plan your day accordingly.”

Note: And I thought that memory is confined in brain cells and nerves only

Nerves hardwired in steel?

Any Psychological effects of War on Gaza’s children?

The report is of 2009. It must be even worse as the children in Gaza witnessed three such massive preemptive wars on Gaza since 2008.

Gaza child looking at what is left of her baby sister
‎هذا ما تبقى من أختها كي تدفن،فهل تبقى من كرامتكم شيئا كي تحيا؟؟؟‎

The Psychological effects of War on Gaza’s children

Report by Dr. Yousef Mousa
Published: 15/02/2009

 

Is Life returning to normal? What about the visible scars on children?

The Palestinian Ministry of Health (MoH) estimated that 1,314 Palestinians were killed in the 23 days of the military operation in the Gaza Strip.

This statistics were only updated until Jan. 18th 2009, but after the Israeli ceasefire, many corpses were found under the debris and the demolished houses in many areas (Zeytoun, Al Atatra, Ezzbet Abed Rabo, and Beit Hanoun).

The bombing and shelling caused extensive damage to civilian facilities throughout the Gaza Strip. Supplies of basic food and fuel, and the provision of electricity, water and sanitation services remain critical.

“Civilians in Gaza bore the brunt of the conflict, with 412 children and 100 women killed and 5, 450 people wounded. Ten of thousands of people were rendered homeless after their areas were damaged or destroyed during bombing raids.”

UN Report – New York

Palestinian Children – A Special Consideration:

Children represent more than 50% of the Palestinian society, and the most vulnerable group of this society

Children have been critically affected by the daily violence, such as bombing, destruction of their houses and other measures.

Damages to residential property, schools, health clinics and water and electricity infrastructure by Israelis are still widespread.

45.2% of death occurrence among children was caused mainly by firearm missiles by Israeli occupation.

Up to 80% of Palestinian children suffer from behavioral problems, including:

  • Increasing level of violence.
  • Sleeping problems, with feelings of fear and anxiety.
  • Changes in attachment to family and community.
  • Various emotional and cognitive problems such as inability to concentrate.
  • Decreasing hope in the future

Palestinian children who experience armed conflict carry the heavy emotional, social, and spiritual burdens associated with death, separation from and loss of parents, attack and victimization, destruction of homes and communities, economic ruin, and disruption of the normal patterns of living.

The United Nations Committee on the Rights of the Child is deeply concerned at the devastating effects that the current military engagement in Gaza is having on children, ” the 18-member body said in a statement issued in Geneva, where it is currently in session.

Hundreds of children have been killed or injured, many seriously. Many others have lost their loved ones. The continuous fighting and destruction of livelihoods and basic infrastructures, severely compromise enjoyment of human rights especially in relation to health, education and family life.

The psycho-social need in Palestine has been realized most acutely during the past eight years of conflict, occupation and violence. Military incursions, movement restrictions, targeted killing, arrests, humiliation, spread of the terror acts, economic situation and poverty have affected every individual from children to the elderly.

The impact has resulted in children: being unable to attend school; sick and injured persons have been denied hospital access while attempting to cross Erez checkpoints.

Maher Wahba, a psychologist with Muslim Aid said that one of the first tasks would be to address the psychological trauma being suffered by children who had lost family members and friends. “These children have suffered a lot, we have seen many cases, many psychological disorders… aggressive behaviour, many nightmares, dreams” he added.

Dr. Samir Gota, a professor of psychology at the Islamic University of Gaza, said to Asharq Al-Awsat that there has been a significant increase in the number of parents visiting psychological health centers in the Gaza Strip enquiring about treatments for psychological breakdowns after having recognized these symptoms in their children following the bombings which have affected the cities, towns and refugee camps of the Gaza Strip.

Psychological problems such as depression and aggression are common in children who have lived through conflict. This is not a new phenomenon in Gaza as many children have lived through other periods of violence, but this latest crisis will have added to the mental health problems faced by Gaza’s children. However, families in Gaza are already struggling with the basics of life; getting enough water, food, fuel and shelter. Hidden psychological problems are not something they are able to deal with.Hatem Shurrab said.

According to WHO, the Psychological consequences of conflict situation in Gaza are, as follows:

Distress responses expressed as:

Insomnia
Sense of Vulnerability
Emotional liability

Behavioral changes expressed as:

Domestic Violence
Increased health care use
Smoking
Alcohol Consumption
Drug addict

Psychiatric illness expressed as:

Post Traumatic Stress Disorder
Major Depression

The unpredictability of the day-to-day situation further adds to the stress and anxiety felt by not having control over ones lives.

This is the current situation in Palestine but it comes with the memories of the conflicts of the past and ultimately with the loss of land and identity. Methods of coping with chronic instability tie into religious beliefs, community lifestyle and cultural traditions. One of the most dominant effects of the continued conflict is the loss of hope.

The affects on the individual, the family, and the community will be long lasting – finding ways to overcome the traumas of the past is the only way to a brighter future.

Psychosocial programs seek to limit these effects on children, prevent further harmful events, and strengthen the coping mechanisms of children, their families, and their communities.

Palestinian children experience many forms of violence from the current war, longest occupation in the world and continuous Palestinian-Israeli conflict. Those which are most likely to cause trauma among children are the death of a parent, relative or acquaintance, torture, witnessing an act of violence, separation from one or both parents for any period of time, injury, including those resulting in deformity or handicaps, engaging in violence, poverty and severe depravation, and shelling or demolition of their house.

Emotions and reactions of children are manifested in many ways including: Problems with speech, difficulty concentrating, learning difficulties, sleep related problems, bedwetting, loss of recently acquired skills, feelings of guilt, and variety of somatic complaints. Children must have safe places for healing and emotional support to be able to overcome these problems in order to continue to live normal, productive lives.

Currently Palestine has no comprehensive mental health services for children, resulting in a high level of need of such services in the community.

I have no concrete evidence of what I claim; only the anecdotes of friends and associates. Given that aid organizations and academics have yet to fully chronically the effects of the 2008-2009 war, I think anecdotal evidence will have to do for now.

Clenched Jaws and Chipped Teeth

I have heard many occurrences of jaw problems. Some residents of Gaza are clenching their teeth to the degree that it hurts to chew. I have heard many reports of jaw aches. A couple I know say each separately wake up at night because their spouse is grinding his/her teeth so loudly.

A dentist told me that he is making many night guards and repairing chipped teeth. He claims that Palestinians are giving themselves long-term tooth and jaw damage from stress. A friend started wearing a mouth guard when he runs because he can’t stop clenching his jaw. He already chipped away half a tooth.

Pills

A friend of mine in Rafah can’t sleep. His wife and daughter can’t sleep, either, he refuses to medicate. The rest of his family take pills. They can’t sleep without them. They began to take more as the battles bombs got louder.

Nightmares

It is not even worth cataloging the number of nightmares I’ve heard from others. Almost everyone I know tells me about a dream they’ve had recently. I’ve had many awkward and disturbing dreams, as well. I tend to have political dreams. Throughout the 2008-2009 war, I often dreamt of myself as a member of the Palestinian cabinet trying to resolve the conflict. Some of the dreams of my friends are too disturbing to recount.

Many of them involve lots of blood, dead bodies, and death. A woman tells me that she has dreams about saving her young daughter from dark, shadowy, faceless enemies. Another man dreams that he is a member of a South African private security corporation of ninjas that descends on Gaza and secretly and quietly kills all Israeli solders and politicians.

Weight Gains/Loss

Friends have visibly changed. Some people have gained significant amounts of weight. Others stopped eating, and look sickly thin and exhausted.

Conclusion

Many Palestinians, myself included, argue that this conflict did far more psychological damage than the all Israeli-Arab wars. The last wars are much harder psychologically than 1948 war.

Dr. Yousef Mousa
Executive Director
Union of Health Work Committess-Gaza
Tel: +970 8 2824272
Fax: +970 8 2869220
Mobile: +970 599 122211
Website: www.gaza-health.org
email: info@gaza-health.org

It is no dishonor to be in a minority in the cause of liberty and virtue

 

Letter from Gaza by a Norwegian doctor

Dearest friends,

The last night was extreme. The “ground invasion” of Gaza resulted in scores and carloads with maimed, torn apart, bleeding, shivering, dying – all sorts of injured Palestinians, all ages, all civilians, all innocent.

Dr Mads Frederick Gilbert (centre) at Al-Shifa hospital on July 17th, treating a wounded Palestinian child, after an Israeli air strike killed 4 children and wounded 5 others.

The heroes in the ambulances and in all of Gaza’s hospitals are working 12-24 hour shifts, grey from fatigue and inhuman workloads (without payment all in Shifa for the last 4 months), they care, triage, try to understand the incomprehensible chaos of bodies, sizes, limbs, walking, not walking, breathing, not breathing, bleeding, not bleeding humans. HUMANS!

Now, once more treated like animals by “the most moral army in the world” (sic!).

My respect for the wounded is endless, in their contained determination in the midst of pain, agony and shock; my admiration for the staff and volunteers is endless, my closeness to the Palestinian “sumud” gives me strength, although in glimpses I just want to scream, hold someone tight, cry, smell the skin and hair of the warm child, covered in blood, protect ourselves in an endless embrace – but we cannot afford that, nor can they.

Ashy grey faces – Oh NO! Not one more load of tens of maimed and bleeding, we still have lakes of blood on the floor in the ER, piles of dripping, blood-soaked bandages to clear out – oh – the cleaners, everywhere, swiftly shovelling the blood and discarded tissues, hair, clothes,cannulas – the leftovers from death – all taken away … to be prepared again, to be repeated all over.

More then 100 cases came to Shifa in the last 24 hrs.

Enough for a large well trained hospital with everything, but here – almost nothing: no electricity, water, disposables, drugs, OR-tables, instruments, monitors – all rusted and as if taken from museums of yesterday’s hospitals. But they do not complain, these heroes. They get on with it, like warriors, head on, enormously resolute.

And as I write these words to you, alone, on a bed, my tears flow, the warm but useless tears of pain and grief, of anger and fear. This is not happening!

An then, just now, the orchestra of the Israeli war-machine starts its gruesome symphony again, just now: salvos of artillery from the navy boats just down on the shores, the roaring F16, the sickening drones (Arabic ‘Zennanis’, the hummers), and the cluttering Apaches.

So much made in and paid by the US.

Mr. Obama – do you have a heart?

I invite you – spend one night – just one night – with us in Shifa. Disguised as a cleaner, maybe.

I am convinced, 100%, it would change history.

Nobody with a heart AND power could ever walk away from a night in Shifa without being determined to end the slaughter of the Palestinian people.

But the heartless and merciless have done their calculations and planned another “dahyia” onslaught on Gaza.

The rivers of blood will keep running the coming night. I can hear they have tuned their instruments of death.

Please. Do what you can. This, THIS cannot continue.

Mads Gilbert MD PhD
Professor and Clinical Head
Clinic of Emergency Medicine
University Hospital of North Norway

Note 1: Israel bombers targeted this hospital too

This is Dr. Mads Gilbert, a Norwegian surgeon who traveled to Gaza to help the injured and has been treating hundreds of victims wounded in Israel’s ongoing assault, including young children.
Dr. Gilbert says hospitals are operating without electricity, water and proper medical supplies, but
adds: “As a medical doctor, my appeal is don’t send bandages, don’t send syringes, don’t send medical teams. The most important medical thing you can do now is to force Israel to stop the bombing and lift the siege of Gaza.”
Gilbert recently recently submitted a report to the United Nations on the state of the Gaza health sector in 2014.
“Where is the decency in the U.S. government allowing Israel this impunity to punish the whole
civilian population in Gaza?”
Dr. Gilbert says hospitals are operating without electricity, water and proper medical supplies, but adds:
As a medical doctor, my appeal is don’t send bandages, don’t send syringes, don’t send medical teams. The most important medical thing you can do now is to force Israel to stop the bombing and lift the siege of Gaza.
Gilbert recently recently submitted a report to the United Nations on the state of the Gaza health sector in 2014.
“Where is the decency in the U.S. government allowing Israel this impunity to punish the whole civilian population in Gaza?”

– See more at: http://www.middleeastmonitor.com/articles/middle-east/12920-letter-from-gaza-by-a-norwegian-doctor#sthash.RBrA0XGH.Ct9cWQvu.dpuf

“Did not have choice or free will”? Phillip Seymour Hoffman 

What these people have in common with Phillip Seymour Hoffman (deceased-drug addiction)?

Actor Cory Monteith (deceased-drug addiction), singer Amy Winehouse (deceased-alcoholism), author David Foster Wallace (deceased-depression), actor Jon Hamm (depression), TV personality Nicole Richie (anorexia), actress Karla Alvarez (deceased-anorexia/bulimia), actress Amanda Byne (bi-polar disorder), actor Howie Mandel (ocd) , reality TV star Vinnie Guadagnino (anxiety disorder),  actress Brooke Shields (postpartum depression)?

In the wake of the tragic loss of Phillip Seymour Hoffman, a great artist, partner, father, brother, and son, I offer the following facts about the neurological disease of addiction.

The overwhelming majority of adults in the western world have passed through experimental stages in their lives where they have dabbled with some kind of brain altering addictive substance, i.e., cigarettes, alcohol, prescription pain killers, ADHD medication, anti-anxiety medication, marijuana (save the ‘it’s not addictive” arguments for later, please).

And the overwhelming majority of these adults will emerge from their experiments unscathed, believing that their free will and good choices are what saved them from becoming addicted.

The problem with this thinking is that it is factually incorrect, and all wrong.

Phillip Seymour Hoffman 1967-2014

Phillip Seymour Hoffman 1967-2014

debbie bayer blog

debbie bayer blog (selected as one of the top post today Feb. 3, 2014)

Phillip Seymour Hoffman did not have choice or free will and neither do you.

What saved the adults from becoming addicted is that their brains did not respond in the same way that an addict’s brain does. They were born with a resistance to addiction. Their free will and good choices had nothing to do with it.

It is time for all of us who got through unscathed to stop patting ourselves on the back for our genetic good luck, and it is time to stop judging those who were not born with the same good genes as defective.

About Phillip Seymour Hoffman, a relapsing drug addict, you may have had the thoughts, “He knew better.” or “Shame on him for throwing his life away.”

Let’s look at these ideas through the lens of how the brain actually works.

Phillip Seymour  “knew better.

He ‘knew better’ in the frontal lobes of his brain, where we all execute our better judgment and can make calculations of our behaviors and circumstances based on risk and reward.

Here’s the problem.

The activity of our frontal lobes can be shut down by the other parts of our brain when there is significant stress in our body. This comes from what is called the “fight, flight, freeze, or faint” mechanism.

This mechanism in the brain is hard-wired into each of us for survival purposes. It is the part of the brain that puts someone into shock when they have been injured and/or traumatized. It is also the part of the brain that can allow a person to lift a car by themselves if their loved one or someone they care about is in danger.

The brain does not analyze the type of stress it is experiencing, that is, this ‘fight or flight mechanism’ is binary.

The brain functions on a “yes” or “no” basis (a binary reaction as in computer).  ”Yes,” there is enough stress to activate the mechanism or “no,” there is not enough stress to activate the mechanism. Human beings have no control over when this mechanism is activated.

This is how PTSD works.

Seemingly innocuous sights, sounds, smells or sensations trigger this brain mechanism even when there is no actual threat to the person. The stress in the body is not even consciously recognizable to the person with PTSD.

The brain reacts to the trigger and the person is put into the experience of being threatened without choice or control because the frontal lobes cannot get their signals through. When this mechanism is activated, free will and choice become impossible. This is true for each and every human being on the planet, whether we like it or not.

The brain of an addict, Phillip Seymour Hoffman in this case, experiences withdrawal symptoms as stress. And since it operates on a binary system, it does not sort out “good” stress (I’m so sick because I’m kicking heroin-good for me!) from “bad” stress (I’m so sick because I’m kicking heroin I’d better call a doctor).

The brain only knows if the stress is present or not and how much stress is present.

When withdrawal symptoms, i.e., physical distress, anxiety caused by emotional stress, etc. reach a certain point in the brain, the brain automatically cuts off the access to the frontal lobes (in a manner of speaking) and begins to direct the body rebalance the stress, to find equilibrium, so that the brain can return to “normal” functioning.

“Normal” functioning to the brain of an addict is defined as having the addictive substance in the body. So while any relapsing addict “knows better,” the addict literally cannot access the part of his brain where his/her better judgment is stored.

The addict loses his choice and free will and is at the mercy of his brain which is in extreme stress and working to regain it’s equilibrium, at any cost, i.e., get more of the addictive substance.

The idea of losing choice, of relinquishing free will, is unthinkable to most of us, especially those of us fortunate enough to live in the U.S. where we have so many choices in so many areas of our lives.

Also, human consciousness defends heavily against the possibility of ‘no choice’ which is paradoxical considering we each carry a brain mechanism that removes choice, but I digress.

Suffice it to say that according to our brain physiology, choice and no choice are equally important to the survival of the species. The problem is that we humans are only conscious of the importance of choice (and the free will to make those choices).

Over the centuries, mankind has had tremendous difficulty acknowledging and treating brain disorders of all kinds.  And we haven’t made much progress in our supposed “enlightened” age of civil rights either.

Consider this, it was less than 50 years ago that 90+% of those born with Down’s syndrome were institutionalized for life.

Also, in spite of (or maybe because of?) a tremendous increase in the diagnoses of brain disorders in the last 40 years, all but a small percentage of treatment centers and publicly funded programs for treatment have been permanently shut down.

What we have on our hands in the U.S. is a mental health, i.e., brain health, crisis.

This is abundantly clear to us every time someone with a serious brain disorder buys an assault rifle.

Actually, those instances are but the tip of a gigantic iceberg. And even though we have had great breakthroughs in neuroscience, we are woefully lagging behind in treating people who suffer and offering support to their families.

How did this happen?

There are more than a few ways to answer that question.

One of the important answers is that we are naturally defensive against the idea that brain disorders which disconnect us from our free will exist. It’s too frightening an idea to consider, so we come up with stories.

A century or more ago our stories revolved around the idea that the person suffering was possessed by demons, and that these demons ran in the family. Perhaps the person’s mother was possessed? May she was a witch? Someone in that family must have sinned and now they are being punished, etc.

It was stories like these that ran so strongly through our cultures that families up until, well now, actually hid loved ones away in mental institutions and even disavowed knowledge or connection to them in order to avoid the stigma that would be placed on the healthy family members also.

We have made some progress, but as Mr. Hoffman’s death painfully points out, not nearly enough.

We seem to have compassion and some amount of treatment and support available for those who have schizophrenia, psychosis, delusional disorder, autism, and Downs syndrome.  (It’s not nearly enough treatment and support and the families and loved ones of those with these disorders suffer an enormous amount financially, emotionally, and physically with the burden of lifetime care of those who live with these challenges.)

Outside of these few of the many neurological disorders that exist we lose all compassion and concern for people and their families who are suffering, and we tell a modern day version of the demon possession story about them.

We continue to isolate and reject people suffering from a physiological disorder of the brain and force their families and loved ones to bear the lifetime burden of their care in shame and silence, in 2014, in the wealthiest nation the planet has ever known.

Our stories about these people who look so normal, so successful, on the outside but whose lives come crumbling down upon them or are cut ridiculously short no longer revolve around possession by evil spirits but by a defect in their character (selfish, lazy, greedy, arrogant, gluttonous, apathetic, hedonistic, etc.), a defect in their temperament (evil, violent, narcissistic, vain, eccentric, etc.) or a defect in their judgement or intelligence (immature, moron, idiot, being an a**hole).

In the absence of knowledge about how the brain functions these stories created theories about the causes of these behaviors (moral corruption, low character) and consequences which mirrored our cultural value system (it’s their own fault, they got what they deserved).

Out of our stories came ideas on how to avoid these behaviors (work hard, believe in God, be kind to others), consequences of these behaviors (why goes around comes around, God helps those who help themselves) and systems of support to uphold the implementation of these ideas (church, 12 step, therapy).

Sometimes the theories, ideas for correction and the support systems even work, but sadly, not most of the time.

All of the above stories/theories are normal individual and cultural adaptations to the unexplainable. This is how we humans learn and grow.

Gratefully, these days few if any people think a person with a phobia has had a spell cast upon him by a witch and now needs an exorcism while the family and neighbors have to find and lynch the witch.

Neither is a person with an addiction suffering from poor character, temperament, or judgment from which he can be cured with hard work, belief in God, attendance at church, 12 step and therapy. (Hang in there, recovered and recovering 12 steppers. I’m on your side. See ** below.)

What we fail to see is

a) how self-serving these old stories are, and

b) how ineffective our current treatment modalities are (see #a).

Our theories about addiction don’t really exist to explain the illogical behavior of someone who is suffering, but mostly to separate ourselves from that behavior with the assurance that what has happened to that “loser” won’t happen to us.

And when the need to distance ourselves from that “loser” is satisfied we don’t bother to fact check our theories.

Nor to we bother to notice if the treatment schemas we’ve created even work (they don’t).  Rather good proof that our theories are self-serving, don’t you think?

We also fail to notice the fear and sadness that comes up for us when we hear of the tragedies that befall those with high-functioning neurological disorders, especially now.

It’s 2014 and tragedies like the death of Phillip Seymour Hoffman have been happening steadily for 40+ years, with no end and no answer in sight. In light of this kind of repetitive hopelessness we are left with little choice but to blame the victims in order to soothe ourselves.

And it is difficult, if not impossible to create solutions in the presence of hopelessness.

The mental health/brain disorder crisis we are facing right now, this decades-long epidemic, is with the so-called high-functioning neurological disorders, i.e., depression, anxiety, bi-polar, ocd, anorexia, bulimia, and addiction (I have left out more than a few of the disorders, but these are the most familiar of the lot).

However, neuroscience is offering us the best reason to hope for good treatment outcomes in decades. The more we learn about how the brain works (like when the fight/flight mechanism is activated) and how it works when it is “broken” (fight/flight mechanism too easily triggered in addicts) the easier it will be for people who have these brain glitches to be identified and treated without shame and blame.

The first, most effective way to face our cultural crises of too many people with brain disorders being undiagnosed and untreated is to educate ourselves about these disorders and learn to spot the people who are suffering so that we can help them understand what is wrong with them and help them to agree to receive treatment.

We have to change our cultural view of addiction and the like before we can create more effective treatments for it and the other high-functioning neural disorders.

The change has to come from those of us who either do not have the disorders or have been successfully treated for the disorders because those with the disorders are not able to help themselves.

I like to say it this way, the last person to know that his brain is broken is the person with the broken brain.

This is just the way human consciousness works.

The only organ in the body that seems to make self-diagnosis impossible is the brain. I mean there is no mistaking a kidney stone trying to pass. When someone is in that kind of pain they don’t blame it on their lack of character. But the brain is expert at being able to reframe and explain away its own glitches.

Whatever isn’t working in a person’s brain is that person’s “normal.”  Over time people with high-functioning neurological disorders develop plausible explanations for their symptoms and adapt to them as best as they can.

And when life’s problems that are obviously (to those around them) connected to their neurological disorders become apparent on the outside of their lives (car accidents, drained bank accounts, lost jobs, broken marriages, etc.) they usually blame their own character defects or someone or something else.

Therefore, the person with the problem is the least likely to be able to get themselves the help they need.

Here is where the education begins, when otherwise high functioning people think and act in ways that defy facts and logic and threaten their well-being and the well-being of their loved ones, then we need to understand that they have a brain disorder, not a moral or character disorder; and they need medical treatment, not shaming, blaming, therapy or a sentence to a 12 step program.

This means that alcoholism, drug addiction, eating disorders, suicide attempts, phobias, adhd, anxiety and depression, et al are all disorders of the brain and as such need the treatment of a medical doctor first.

(Read that again. It’s a truth, not a theory. But since the truth is not widely known it will seem counter intuitive. You will want to say, “Yeah, but…..”  Read it again. Alcoholism is a brain disorder. Drug addiction is a brain disorder. Let it sink in.)

Here’s why this is true–otherwise high functioning people could not be high functioning without good judgment, good enough character, and at least average intelligence.  If they can hold down a job, go about the activities of daily living, have friendships and loved ones, and display empathy towards others before and during their lapses, melt downs, relapses, et al.,  then their frontal lobes are fully functioning.

The only explanation, for their behaviors then, is that their frontal lobes (where their high-functioning skills are located) have been hijacked by a different part of their brain.  When someone’s brain is highjacking their frontal lobes, they need medical treatment.

Blessedly, neuroscience is catching up with us and giving us facts about how our brains actually work.  So it is time NOW to drop those stories we have made up and begin to apply the facts of neuroscience as we understand them to the untimely deaths of addicts of all kinds and to the public meltdowns of otherwise functioning adults.

And it is way past time that we spread the word about what is really going on with these people who struggle mightily and their families who bear the burden of loving them and having to care for them.

Remember, these people don’t know that their brains are broken.  They are high-functioning and so they blame themselves. And they come to hate themselves for their problems more than you can imagine.  They live in a dark and self-loathing world where they come to believe that they don’t deserve any help which is why they don’t surrender themselves for treatment. They need the help of their friends and families and the world around them in order to get around the obstacles of their broken brains to get help.

When our entire culture understands as common sense that addiction is an individual neurological disorder that requires immediate medical attention then a person like Phillip Seymour Hoffman has a chance to understand that he has “one of those brains” that will shut down his frontal lobes and take away his ability to exercise good judgement and control of his behaviors.  And until he knows this fact about his brain in same the way that he knows a bone sticking out of his leg means he needs to go to the ER, then him and those like him will not be able to ask for help.

And a guy like Phillip Seymour Hoffman isn’t going to know these things until we all know them.  And that time is NOW.

Phillip Seymour Hoffman died from having a combination of sensitivities in his neural wiring that caused his brain to override his better judgement, take away his free will and caused him to take the actions that ultimately killed him.

It appears that these sensitivities were unknowingly activated by a prescription of pain killers that were necessary at the time to treat a different medical condition.  Because of his previous 23 years of being clean and sober he was presumed  safe to take the pain medication. And it looks like what he and maybe even his doctors didn’t know about how his brain worked kept him from staying in treatment long enough to allow his brain to rewire itself around those sensitivities and render him clean and sober again.

For this, like all addicts in this situation, he deserves our kindness and compassion.

If this post has helped you to understand addiction please do share it.  My passion is to help educate us all so that more people with neurological disorders will get the treatment they need.

Debbie Bayer, MA, MFTI

Note to my 12-step friends:  There are two caveats to the success of 12-step work
1) It works when you work it, and
2) You have to be honest, and some people are constitutionally incapable of being honest with themselves.
There is no doubt that over the last 70+ years the 12-step community has the highest success rate among alcoholics of any other treatment modality. This community is also incredibly successful in the support of sobriety among drug addicts of all kinds.
The problem lies in the millions of people who cannot meet the two criteria for success in a 12-step program due to other types of brain disorders.  Their suffering demands that health professionals continue to seek out effective treatment strategies for them.
I am certain that you have compassion for their plight and support these more unfortunate folks in their recovery.
DB

THE PSYCHIATRIC DRUG CRISIS

 
It’s been just over 25 years since Prozac came to market, and more than 20% of Americans now regularly take mind-altering drugs prescribed by their doctors.
Almost as familiar as brands like Zoloft and Lexapro is the worry about what it means that the daily routine in many households, for parents and children alike, includes a dose of medications that are poorly understood and whose long-term effects on the body are unknown.
 posted this Sept. 3, 2013:
Despite our ambivalence, sales of psychiatric drugs amounted to more than 7 billion dollars in 2010. They have become yet another commodity that consumers have learned to live with or even enjoy, like S.U.V.s or Cheetos.

Yet the psychiatric-drug industry is in trouble.

“We are facing a crisis,” the Cornell psychiatrist and New York Times contributor Richard Friedman warned last week. In the past few years, one pharmaceutical giant after another—GlaxoSmithKline, AstraZeneca, Novartis, Pfizer, Merck, Sanofi—has shrunk or shuttered its neuroscience research facilities. Clinical trials have been halted, lines of research abandoned, and the new drug pipeline has been allowed to run dry.

Why would an industry beat a hasty retreat from a market that continues to boom?

(Recent surveys indicate that mental illness is the leading cause of impairment and disability worldwide.)

The answer lies in the history of psychopharmacology, which is more deeply indebted to serendipity than most branches of medicine—in particular, to a remarkable series of accidental discoveries made in the fifteen or so years following the end of the Second World War.

In 1949, John Cade published an article in the Medical Journal of Australia describing his discovery that lithium sedated people who experienced mania. Cade had been testing his theory that manic people were suffering from an excess of uric acid by injecting patients’ urine into guinea pigs, who subsequently died.

When Cade diluted the uric acid by adding lithium, the guinea pigs fared better; when he injected them with lithium alone, they became sedated. He noticed the same effect when he tested lithium on himself, and then on his patients. Nearly twenty years after he first recommended lithium to treat manic depression, it became the standard treatment for the disorder.

In the 1940’sand 50’s,, schizophrenic patients in some asylums were treated with cold-induced “hibernation”—a state from which they often emerged lucid and calm.

In one French hospital, the protocol also called for chlorpromazine, a new drug thought to increase the hibernation effect. One day, some nurses ran out of ice and administered the drug on its own. When it calmed the patients, chlorpromazine, later named Thorazine, was recognized in 1952 as the first drug treatment for schizophrenia—a development that encouraged doctors to believe that they could use drugs to manage patients outside the asylum, and thus shutter their institutions.

In 1956, the Swiss firm Geigy wanted to be in the antipsychotics market, and it asked a researcher and asylum doctor, Roland Kuhn, to test out a drug that, like Thorazine, was an antihistamine—and thus was expected to have a sedating effect. The results were not what Kuhn desired: when the schizophrenic patients took the drug, imipramine, they became more agitated, and one of them, according to a member of the research team, “rode, in his nightshirt, to a nearby village, singing lustily.” He added, “This was not really a very good PR exercise for the hospital.”

But it was the inspiration for Kuhn and his team to reason that “if the flat mood of schizophrenia could be lifted by the drug, then could not a depressed mood be elevated also?” Under the brand name Tofranil, imipramine went on to become the first antidepressant—and one of the first blockbuster psychiatric drugs.

American researchers were also interested in antihistamines.

In 1957, Leo Sternbach, a chemist for Hoffmann-La Roche who had spent his career researching them, was about to throw away the last of a series of compounds he had been testing that had proven to be pharmacologically inert. But in the interest of completeness, he was convinced to test the last sample. “We thought the expected negative pharmacological results would cap our work on this series of compounds,” one of his colleagues later recounted. But the drug turned out to have muscle-relaxing and sedative properties.

Instead of becoming the last in a list of failures, it became the first in a series of spectacular successes—the benzodiazepenes, of which Sternbach’s Librium and Valium were the flagships.

By 1960, the major classes of psychiatric drugs—among them, mood stabilizers, antipsychotics, antidepressants, and anti-anxiety drugs, known as anxiolytics—had been discovered and were on their way to becoming a 70-billion-dollar market.

Having been discovered by accident, however, they lacked one important element: a theory that accounted for why they worked (or, in many cases, did not).

That didn’t stop drug makers and doctors from claiming that they knew.

Drawing on another mostly serendipitous discovery of the fifties—that the brain did not conduct its business by sending sparks from neuron to neuron, as scientists previously thought, but rather by sending chemical messengers across synapses—they fashioned an explanation: mental illness was the result of imbalances among these neurotransmitters, which the drugs treated in the same way that insulin treats diabetes.

The appeal of this account is obvious: it combines ancient notions of illness (specifically, the idea that sickness resulted from imbalanced humors) with the modern understanding of the molecular culprits that make us suffer—germs.

It held out the hope that mental illness could be treated in the same way as pneumonia or hypertension: with a single pill.

Drug companies wasted no time in promulgating it. Merck, the manufacturer of Elavil, commissioned the psychiatrist Frank Ayd to write a book called Recognizing the Depressed Patient, in which he extolled the “chemical revolution in psychiatry” and urged doctors to reassure patients they weren’t losing their minds, but rather suffering a “common illness” with a “physical basis” and a pharmacological cure.

Merck sent Ayd’s book to 50,000 doctors around the country.

In 1965, Joseph Schildkraut, a psychiatrist at the National Institute of Mental Health, reverse-engineered antidepressants and offered an actual theory: at least when it came to depression, the imbalances were to be found in the neurotransmitters he thought were affected by the drugs, dopamine and norepinephrine.

Seven years after antidepressants were invented, and five years after Ayd asserted that depression was a chemical problem, psychiatrists finally had a precise, scientific explanation for why they worked. The paper quickly became one of the most cited articles in the medical literature.

But Schildkraut was wrong.

Within a few years, as technology expanded our ability to peer into the brain, it became clear that antidepressants act mostly by increasing the availability of the neurotransmitter serotonin—rather than dopamine and norepinephrine, as previously thought.

A new generation of antidepressants—the selective serotonin reuptake inhibitors (S.S.R.I.s), including Prozac, Zoloft, and Paxil—was developed to target it. The ability to claim that the drugs targeted a specific chemical imbalance was a marketing boon as well, assuring consumers that the drugs had a scientific basis. By the mid-nineties, antidepressants were the best-selling class of prescription medications in the country.

Psychiatry appeared to have found magic bullets of its own.

The serotonin-imbalance theory, however, has turned out to be just as inaccurate as Schildkraut’s. While S.S.R.I.s surely alter serotonin metabolism, those changes do not explain why the drugs work, nor do they explain why they have proven to be no more effective than placebos in clinical trials.

In 1987, within a decade of Prozac’s approval by the F.D.A,, scientists had concluded that serotonin was only a finger pointing at one’s mood—that the causes of depression and the effects of the drugs were far more complex than the chemical-imbalance theory implied.

The ensuing research has mostly yielded more evidence that the brain, which has more neurons than the Milky Way has stars and is perhaps one of the most complex objects in the universe, is an elusive target for drugs.

Despite their continued failure to understand how psychiatric drugs work, doctors continue to tell patients that their troubles are the result of chemical imbalances in their brains. As Frank Ayd pointed out, this explanation helps reassure patients even as it encourages them to take their medicine, and it fits in perfectly with our expectation that doctors will seek out and destroy the chemical villains responsible for all of our suffering, both physical and mental. The theory may not work as science, but it is a devastatingly effective myth.

Whether or not truthiness, as one might call it, is good medicine remains to be seen. No one knows how important placebo effects are to successful treatment, or how exactly to implement them, a topic Michael Specter wrote about in the magazine in 2011.

But the dry pipeline of new drugs bemoaned by Friedman is an indication that the drug industry has begun to lose faith in the myth it did so much to create. As Steven Hyman, the former head of the National Institute of Mental Health, wrote last year, the notion that “disease mechanisms could … be inferred from drug action” has succeeded mostly in “capturing the imagination of researchers” and has become “something of a scientific curse.”

Bedazzled by the prospect of unraveling the mysteries of psychic suffering, researchers have spent recent decades on a fool’s errand—chasing down chemical imbalances that don’t exist. And the result, as Friedman put it, is that “it is hard to think of a single truly novel psychotropic drug that has emerged in the last thirty years.”

Despite the BRAIN initiative recently announced by the Obama Administration, and the N.I.M.H.’s renewed efforts to stimulate research on the neurocircuitry of mental disorder, there is nothing on the horizon with which to replace the old story. Without a new explanatory framework, drug-company scientists don’t even know where to begin, so it makes no sense for the industry to stay in the psychiatric-drug business.

And if loyalists like Hyman and Friedman continue to say out loud what they have been saying to each other for many years—that, as Friedman told Times readers, “just because an S.S.R.I. antidepressant increases serotonin in the brain and improves mood, that does not mean that serotonin deficiency is the cause of the disease”—then consumers might also lose faith in the myth of the chemical imbalance.

Gary Greenberg is a practicing psychotherapist and the author of “The Book of Woe: The DSM and the Unmaking of Psychiatry.”

Correction: Due to an editing error, the antidepressant Tofranil was originally identified as Elavil.

Photograph by Paul Skelcher/Science Faction/Corbis.

A kid “genetically ill”. And written by someone who has no kids…

There is this genetically transmitted disease called Myopathy, a  terminally deadly illness that afflict boys, and transmitted by the mothers.

The kid shows signs of incapacity to control his gripping muscles, holding firmly any object, and does fall down very frequently.

The kids will ultimately be handicapped in a wheelchair and his life expectancy barely exceed 20 of age.

The transmitted disease is acquired through generation of inbred marriages within closed communities, from repeated close relative intermarriages…

That is cause for a lot of blames to be spread around every which way

You blame your God, your community customs and habits,…

You blame ignorance and the failure of medical advances to finding a cure…

You may blame your God for punishing a kid instead of the real guilty and culprit…

You tend to blame your God to attacking a kid so that you are reduced to beg Him for a compassion that  is not of His nature…

A God playing the ultimate in politics game of afflicting your close family members in order to adore Him the harder…

The mother blame her mother and barely feels soothed that the grandmother is apologizing for her responsibilities in the matter…

We should know by now that we were born to die.

There are statistics of life expectancies for each incurable disease, life-style, “race”, genders, age…

There are statistics of life expectancies for every serious disease that is curable too, for every kinds of surgery…

Regardless, if you factor in the many dangers in modern life-style, you may die much earlier than “expected”

If you factor in the increased medical breakthrough whose time has come, you may live a while longer…

Too complicated a life to play the blame game…

If we could learn to display a genuine smile in a state of full joy and contentment… this moment is worth a lifetime of blame spreading to anyone observing you, worth a lifetime away from the long faces…

Do you think people marry in order to consciously increase its own species?

Do you think people marry and beget descendants with the full consciousness of the ultimate truth of death?

I doubt that anything we do or act upon is generated by a conscious awareness of our demise.

All we do and act upon is to please the community, to feel accepted and recognized as a “wise” member who agrees with the community vaster and deeper wise customs…

Pleasing our community is one of the thousand of unconscious orders that we all succumb to, even at very old age…

Note: Written by someone who never married, and who doesn’t have kids. Was it an act of tacit rebellion against obeying community forceful desires?

There are very rare cases where an awesome girl demands the hand of a plain-looking man. I am lucky to have survived that long, so far. Just playing it dumb. though I’m a terrible actor. A dumb face helps in the game.

Attention deficit hyperactivity disorder…Diagnosis of grieving Human

The news that 11% of school-age children now receive a diagnosis of attention deficit hyperactivity disorder — some 6.4 million — give the chill.

Ted Gup, an author and fellow of the Edmond J. Safra Center for Ethics at Harvard University, published this April 2, 2013

“My son David was one of those who received that diagnosis.

In his case, he was in the first grade.

Indeed, there were psychiatrists who prescribed medication for him even before they met him.

One psychiatrist said he would not even see him until he was medicated.

For a year I refused to fill the prescription at the pharmacy. Finally, I relented. And so David went on Ritalin, then Adderall, and other drugs that were said to be helpful in combating the condition.

In another age, David might have been called “rambunctious.” His battery was a little too large for his body. And so he would leap over the couch, spring to reach the ceiling and show an exuberance for life that came in brilliant microbursts.

As a 21-year-old college senior, he was found on the floor of his room, dead from a fatal mix of alcohol and drugs.

The date was Oct. 18, 2011.

No one made my son take the heroin and alcohol, and yet I cannot help but hold myself and others to account.

I had unknowingly colluded with a system that devalues talking therapy and rushes to medicate, inadvertently sending a message that self-medication, too, is perfectly acceptable.

My son was no angel (though he was to us) and he was known to trade in Adderall, to create a submarket in the drug among his classmates who were themselves all too eager to get their hands on it.

What he did cannot be excused, but it should be understood.

What he did was to create a market that perfectly mirrored the society in which he grew up, a culture where Big Pharma itself prospers from the off-label uses of drugs, often not tested in children and not approved for the many uses to which they are put.

And so a generation of students, raised in an environment that encourages medication, are emulating the professionals by using drugs in the classroom as performance enhancers.

And we wonder why it is that they use drugs with such abandon. As all parents learn, and to their chagrin, our children go to school not only in the classroom but also at home, and the culture they construct for themselves as teenagers and young adults is but a tiny village imitating that to which they were introduced as children.

The issue of permissive drug use and over-diagnosis goes well beyond hyperactivity.

In May, the American Psychiatric Association will publish its D.S.M. 5, the Diagnostic and Statistical Manual of Mental Disorders.

This voluminous book is called the bible of the profession.

Its latest iteration, like those before, is not merely a window on the profession but on the culture it serves, both reflecting and shaping societal norms. (For instance, until the 1970s, it categorized homosexuality as a mental illness.)

One of the new, more controversial provisions expands depression to include some forms of grief. On its face it makes sense.

The grieving often display all the common indicators of depression loss of interest in life, loss of appetite, irregular sleep patterns, low functionality, etc. But as others have observed, those same symptoms are the very hallmarks of grief itself.

Ours is an age in which the airwaves and media are one large drug emporium that claims to fix everything from sleep to sex.

I fear that being human is itself fast becoming a condition. It’s as if we are trying to contain grief, and the absolute pain of a loss like mine.

We have become increasingly disassociated and estranged from the patterns of life and death, uncomfortable with the messiness of our own humanity, aging and, ultimately, mortality.

Challenge and hardship have become pathologized and monetized.

Instead of enhancing our coping skills, we undermine them and seek shortcuts where there are none, eroding the resilience upon which each of us, at some point in our lives, must rely. Diagnosing grief as a part of depression runs the very real risk of delegitimizing that which is most human — the bonds of our love and attachment to one another.

The new entry in the D.S.M. cannot tame grief by giving it a name or a subsection, nor render it less frightening or more manageable.

The D.S.M. would do well to recognize that a broken heart is not a medical condition, and that medication is ill-suited to repair some tears.

Time does not heal all wounds, closure is a fiction, and so too is the notion that God never asks of us more than we can bear.

Enduring the unbearable is sometimes exactly what life asks of us.

But there is a sweetness even to the intensity of this pain I feel. It is the thing that holds me still to my son.

And yes, there is a balm even in the pain. I shall let it go when it is time, without reference to the D.S.M., and without the aid of a pill.

A version of this op-ed appeared in print on April 3, 2013, on page A27 of the New York edition with the headline: Diagnosis: Human.
Note: And billion of people go hungry, suffer malnutrition…and die of curable diseases before the age of 5.

Nurture “alters the epigenetic expressions of genes in the brain…”: Consider seriously Grandma’s Experiences

Trait vs. Fate? Nature versus Nurture?

Trust the nurturing processes: You are significantly how you have been nurtured, and the next generations…

Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles.

The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.”

“Bad inheritance,” says Darwin.

“Bad mothering,” says Freud.

For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations.

And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life

You may first read https://adonis49.wordpress.com/2012/05/11/genes-are-transformed-by-nurturing-genes-functioning-as-default-program/

Dan Hurley published on April 23, 2013 “Grandma’s Experiences Leave a Mark on Your Genes” on Discover Magazine (May issue, 2013).

The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application.

Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.

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Michael Meaney, neurobiologist. Owen Egan/McGill University

“I can still visualize the place — it was a corner bar that specialized in pizza,” Meaney says. “Moshe, being kosher, was interested in kosher calories. Beer is kosher. Moshe can drink beer anywhere. And I’m Irish. So it was perfect.”

The two engaged in animated conversation about a hot new line of research in genetics.

Since the 1970s, researchers had known that the tightly wound spools of DNA inside each cell’s nucleus require something extra to tell them exactly which genes to transcribe, whether for a heart cell, a liver cell or a brain cell.

One such extra element is the methyl group, a common structural component of organic molecules. The methyl group works like a placeholder in a cookbook, attaching to the DNA within each cell to select only those recipes (genes) necessary for that particular cell’s proteins.

Because methyl groups are attached to the genes, residing beside but separate from the double-helix DNA code, the field was dubbed epigenetics, from the prefix epi (Greek for over, outer, above).

Originally these epigenetic changes were believed to occur only during fetal development. But pioneering studies showed that molecular bric-a-brac could be added to DNA in adulthood, setting off a cascade of cellular changes resulting in cancer.

Sometimes methyl groups attached to DNA, thanks to changes in diet.  Other times, exposure to certain chemicals appeared to be the cause. Szyf showed that correcting epigenetic changes with drugs could cure certain cancers in animals.

Geneticists were especially surprised to find that epigenetic change could be passed down from parent to child, one generation after the next.

A study from Randy Jirtle of Duke University showed that when female mice are fed a diet rich in methyl groups, the fur pigment of subsequent offspring is permanently altered. Without any change to DNA at all, methyl groups could be added or subtracted, and the changes were inherited much like a mutation in a gene.

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Moshe Szyf, molecular biologist and geneticist. McGill University

At the bar in Madrid, Szyf and Meaney considered a hypothesis as improbable as it was profound: If diet and chemicals can cause epigenetic changes, could certain experiences — child neglect, drug abuse or other severe stresses — also set off epigenetic changes to the DNA inside the neurons of a person’s brain?

That question turned out to be the basis of a new field, behavioral epigenetics. This vibrant field of study has spawned dozens of studies and suggested profound new treatments to heal the brain.

According to the new insights of behavioral epigenetics, traumatic experiences in our past, or in our recent ancestors’ past, leave molecular scars adhering to our DNA. Jews whose great-grandparents were chased from their Russian shtetls; Chinese whose grandparents lived through the ravages of the Cultural Revolution; young immigrants from Africa whose parents survived massacres; adults of every ethnicity who grew up with alcoholic or abusive parents — all carry with them more than just memories.

Like silt deposited on the cogs of a finely tuned machine after the seawater of a tsunami recedes, our experiences, and those of our forebears, are never gone, even if they have been forgotten. They become a part of us, a molecular residue holding fast to our genetic scaffolding.

The DNA remains the same, but psychological and behavioral tendencies are inherited. You might have inherited not just your grandmother’s knobby knees, but also her predisposition toward depression caused by the neglect she suffered as a newborn.

Or not. If your grandmother was adopted by nurturing parents, you might be enjoying the boost she received thanks to their love and support. The mechanisms of behavioral epigenetics underlie not only deficits and weaknesses but strengths and resiliencies, too.

And for those unlucky enough to descend from miserable or withholding grandparents, emerging drug treatments could reset not just mood, but the epigenetic changes themselves. Like grandmother’s vintage dress, you could wear it or have it altered. The genome has long been known as the blueprint of life, but the epigenome is life’s Etch A Sketch: Shake it hard enough, and you can wipe clean the family curse.

Jay Smith/DISCOVER

Voodoo Genetics 

Twenty years after helping to set off a revolution, Meaney sits behind a wide walnut table that serves as his desk. A January storm has deposited half a foot of snow outside the picture windows lining his fourth-floor corner office at the Douglas Institute, a mental health affiliate of McGill. He has the rugged good looks and tousled salt-and-pepper hair of someone found on a ski slope — precisely where he plans to go this weekend. On the floor lays an arrangement of helium balloons in various stages of deflation. “Happy 60th!” one announces.

“I’ve always been interested in what makes people different from each other,” he says. “The way we act, the way we behave — some people are optimistic, some are pessimistic. What produces that variation? Evolution selects the variance that is most successful, but what produces the grist for the mill?”

Meaney pursued the question of individual differences by studying how the rearing habits of mother rats caused lifelong changes in their offspring. Research dating back to the 1950s had shown that rats handled by humans for as little as five to 15 minutes per day during their first three weeks of life grew up to be calmer and less reactive to stressful environments compared with their non-handled littermates.

Seeking to tease out the mechanism behind such an enduring effect, Meaney and others established that the benefit was not actually conveyed by the human handling. Rather, the handling simply provoked the rats’ mothers to lick and groom their pups more, and to engage more often in a behavior called arched-back nursing, in which the mother gives the pups extra room to suckle against her underside.

It’s all about the tactile stimulation,” Meaney says.

In a landmark 1997 paper in Science, Meaney showed that natural variations in the amount of licking and grooming received during infancy had a direct effect on how stress hormones, including corticosterone, were expressed in adulthood. The more licking as babies, the lower the stress hormones as grown-ups. It was almost as if the mother rats were licking away at a genetic dimmer switch. What the paper didn’t explain was how such a thing could be possible.

“What we had done up to that point in time was to identify maternal care and its influence on specific genes,” Meaney says. “But epigenetics wasn’t a topic I knew very much about.”

And then he met Szyf.

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Alison Mackey/DISCOVER

Postnatal Inheritance 

“I was going to be a dentist,” Szyf says with a laugh. Slight, pale and balding, he sits in a small office at the back of his bustling laboratory — a room so Spartan, it contains just a single picture, a photograph of two embryos in a womb.

Needing to write a thesis in the late 1970s for his doctorate in dentistry at Hebrew University of Jerusalem, Szyf approached a young biochemistry professor named Aharon Razin, who had recently made a splash by publishing his first few studies in some of the world’s top scientific journals. The studies were the first to show that the action of genes could be modulated by structures called methyl groups, a subject about which Szyf knew precisely nothing. But he needed a thesis adviser, and Razin was there. Szyf found himself swept up to the forefront of the hot new field of epigenetics and never looked back.

Until researchers like Razin came along, the basic story line on how genes get transcribed in a cell was neat and simple. DNA is the master code, residing inside the nucleus of every cell; RNA transcribes the code to build whatever proteins the cell needs. Then some of Razin’s colleagues showed that methyl groups could attach to cytosine, one of the chemical bases in DNA and RNA.

It was Razin, working with fellow biochemist Howard Cedar, who showed these attachments weren’t just brief, meaningless affairs. The methyl groups could become married permanently to the DNA, getting replicated right along with it through a hundred generations. As in any good marriage, moreover, the attachment of the methyl groups significantly altered the behavior of whichever gene they wed, inhibiting its transcription, much like a jealous spouse. It did so, Razin and Cedar showed, by tightening the thread of DNA as it wrapped around a molecular spool, called a histone, inside the nucleus. The tighter it is wrapped, the harder to produce proteins from the gene.

Consider what that means: Without a mutation to the DNA code itself, the attached methyl groups cause long-term, heritable change in gene function. Other molecules, called acetyl groups, were found to play the opposite role, unwinding DNA around the histone spool, and so making it easier for RNA to transcribe a given gene.

By the time Szyf arrived at McGill in the late 1980s, he had become an expert in the mechanics of epigenetic change. But until meeting Meaney, he had never heard anyone suggest that such changes could occur in the brain, simply due to maternal care.

“It sounded like voodoo at first,” Szyf admits. “For a molecular biologist, anything that didn’t have a clear molecular pathway was not serious science. But the longer we talked, the more I realized that maternal care just might be capable of causing changes in DNA methylation, as crazy as that sounded. So Michael and I decided we’d have to do the experiment to find out.”

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Thinkstock

Actually, they ended up doing a series of elaborate experiments. With the assistance of postdoctoral researchers, they began by selecting mother rats who were either highly attentive or highly inattentive. Once a pup had grown up into adulthood, the team examined its hippocampus, a brain region essential for regulating the stress response. In the pups of inattentive mothers, they found that genes regulating the production of glucocorticoid receptors, which regulate sensitivity to stress hormones, were highly methylated; in the pups of conscientious moms, the genes for the glucocorticoid receptors were rarely methylated.

Methylation just gums up the works. So the less the better when it comes to transcribing the affected gene.

In this case, methylation associated with miserable mothering prevented the normal number of glucocorticoid receptors from being transcribed in the baby’s hippocampus. And so for want of sufficient glucocorticoid receptors, the rats grew up to be nervous wrecks.

To demonstrate that the effects were purely due to the mother’s behavior and not her genes, Meaney and colleagues performed a second experiment. They took rat pups born to inattentive mothers and gave them to attentive ones, and vice versa. As they predicted, the rats born to attentive mothers but raised by inattentive ones grew up to have low levels of glucocorticoid receptors in their hippocampus and behaved skittishly. Likewise, those born to bad mothers but raised by good ones grew up to be calm and brave and had high levels of glucocorticoid receptors.

Before publishing their findings, Meaney and Szyf conducted a third crucial experiment, hoping to overwhelm the inevitable skeptics who would rise up to question their results. After all, it could be argued, what if the epigenetic changes observed in the rats’ brains were not directly causing the behavioral changes in the adults, but were merely co-occurring? Freud certainly knew the enduring power of bad mothers to screw up people’s lives. Maybe the emotional effects were unrelated to the epigenetic change.

To test that possibility, Meaney and Szyf took yet another litter of rats raised by rotten mothers. This time, after the usual damage had been done, they infused their brains with trichostatin A, a drug that can remove methyl groups. These animals showed none of the behavioral deficits usually seen in such offspring, and their brains showed none of the epigenetic changes.

It was crazy to think that injecting “trichostatin A” straight into the brain would work,” says Szyf. “But it did. It was like rebooting a computer.”

Jay Smith/DISCOVER

Despite such seemingly overwhelming evidence, when the pair wrote it all up in a paper, one of the reviewers at a top science journal refused to believe it, stating he had never before seen evidence that a mother’s behavior could cause epigenetic change.

“Of course he hadn’t,” Szyf says. “We wouldn’t have bothered to report the study if it had already been proved.”

In the end, their landmark paper, “Epigenetic programming by maternal behavior,” was published in June 2004 in the journal Nature Neuroscience.

Meaney and Szyf had proved something incredible. Call it postnatal inheritance: With no changes to their genetic code, the baby rats nonetheless gained genetic attachments due solely to their upbringing — epigenetic additions of methyl groups sticking like umbrellas out the elevator doors of their histones, gumming up the works and altering the function of the brain.

The Beat Goes On

Together, Meaney and Szyf have gone on to publish some two-dozen papers, finding evidence along the way of epigenetic changes to many other genes active in the brain. Perhaps most significantly, in a study led by Frances Champagne — then a graduate student in Meaney’s lab, now an associate professor with her own lab at Columbia University in New York — they found that inattentive mothering in rodents causes methylation of the genes for estrogen receptors in the brain. When those babies grow up, the resulting decrease of estrogen receptors makes them less attentive to their babies. And so the beat goes on.

As animal experiments continue apace, Szyf and Meaney have entered into the next great step in the study of behavioral epigenetics: human studies.

In a 2008 paper, they compared the brains of people who had committed suicide with the brains of people who had died suddenly of factors other than suicide. They found excess methylation of genes in the suicide brains’ hippocampus, a region critical to memory acquisition and stress response. If the suicide victims had been abused as children, they found, their brains were more methylated.

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Alison Mackey/DISCOVER

Why can’t your friend “just get over” her upbringing by an angry, distant mother? Why can’t she “just snap out of it”? The reason may well be due to methyl groups that were added in childhood to genes in her brain, thereby handcuffing her mood to feelings of fear and despair.

Of course, it is generally not possible to sample the brains of living people. But examining blood samples in humans is routine, and Szyf has gone searching there for markers of epigenetic methylation. Sure enough, in 2011 he reported on a genome-wide analysis of blood samples taken from 40 men who participated in a British study of people born in England in 1958.

All the men had been at a socioeconomic extreme, either very rich or very poor, at some point in their lives ranging from early childhood to mid-adulthood. In all, Szyf analyzed the methylation state of about 20,000 genes. Of these, 6,176 genes varied significantly based on poverty or wealth.

Most striking, however, was the finding that genes were more than twice as likely to show methylation changes based on family income during early childhood versus economic status as adults.

Timing matters.

Your parents winning the lottery or going bankrupt when you’re 2 years old will likely affect the epigenome of your brain, and your resulting emotional tendencies, far more strongly than whatever fortune finds you in middle age.

Last year, Szyf and researchers from Yale University published another study of human blood samples, comparing 14 children raised in Russian orphanages with 14 other Russian children raised by their biological parents. They found far more methylation in the orphans’ genes, including many that play an important role in neural communication and brain development and function.

“Our study shows that the early stress of separation from a biological parent impacts long-term programming of genome function. This might explain why adopted children may be particularly vulnerable to harsh parenting in terms of their physical and mental health,” said Szyf’s co-author, psychologist Elena Grigorenko of the Child Study Center at Yale. “Parenting adopted children might require much more nurturing care to reverse these changes in genome regulation.”

A case study in the epigenetic effects of upbringing in humans can be seen in the life of Szyf’s and Meaney’s onetime collaborator, Frances Champagne. “My mom studied prolactin, a hormone involved in maternal behavior. She was a driving force in encouraging me to go into science,” she recalls. Now a leading figure in the study of maternal influence, Champagne just had her first child, a daughter. And epigenetic research has taught her something not found in the What to Expect books or even her mother’s former lab.

The thing I’ve gained from the work I do is that stress is a big suppressor of maternal behavior,” she says. “We see it in the animal studies, and it’s true in humans. So the best thing you can do is not to worry all the time about whether you’re doing the right thing. Keeping the stress level down is the most important thing. And tactile interaction — that’s certainly what the good mother rats are doing with their babies. That sensory input, the touching, is so important for the developing brain.”

The Mark Of Cain 

The message that a mother’s love can make all the difference in a child’s life is nothing new. But the ability of epigenetic change to persist across generations remains the subject of debate.

Is methylation transmitted directly through the fertilized egg, or is each infant born pure, a methylated virgin, with the attachments of methyl groups slathered on solely by parents after birth?

Neuroscientist Eric Nestler of the Icahn School of Medicine at Mount Sinai in New York has been seeking an answer for years. In one study, he exposed male mice to 10 days of bullying by larger, more aggressive mice. At the end of the experiment, the bullied mice were socially withdrawn.

To test whether such effects could be transmitted to the next generation, Nestler took another group of bullied mice and bred them with females, but kept them from ever meeting their offspring.

trait-9
Alison Mackey/DISCOVER

Despite having no contact with their depressed fathers, the offspring grew up to be hypersensitive to stress. “It was not a subtle effect; the offspring were dramatically more susceptible to developing signs of depression,” he says.

In further testing, Nestler took sperm from defeated males and impregnated females through in vitro fertilization. The offspring did not show most of the behavioral abnormalities, suggesting that epigenetic transmission may not be at the root. Instead, Nestler proposes, “the female might know she had sex with a loser. She knows it’s a tainted male she had sex with, so she cares for her pups differently,” accounting for the results.

Despite his findings, no consensus has yet emerged. The latest evidence, published in the Jan. 25 issue of the journal Science, suggests that epigenetic changes in mice are usually erased, but not always. The erasure is imperfect, and sometimes the affected genes may make it through to the next generation, setting the stage for transmission of the altered traits in descendants as well.

What’s Next?

The studies keep piling on. One line of research traces memory loss in old age to epigenetic alterations in brain neurons. Another connects post-traumatic stress disorder to methylation of the gene coding for neurotrophic factor, a protein that regulates the growth of neurons in the brain.

If it is true that epigenetic changes to genes active in certain regions of the brain underlie our emotional and intellectual intelligence — our tendency to be calm or fearful, our ability to learn or to forget — then the question arises: Why can’t we just take a drug to rinse away the unwanted methyl groups like a bar of epigenetic Irish Spring?

The hunt is on. Giant pharmaceutical and smaller biotech firms are searching for epigenetic compounds to boost learning and memory. It has been lost on no one that epigenetic medications might succeed in treating depression, anxiety and post-traumatic stress disorder where today’s psychiatric drugs have failed.

But it is going to be a leap.

How could we be sure that epigenetic drugs would scrub clean only the dangerous marks, leaving beneficial — perhaps essential — methyl groups intact?

And what if we could create a pill potent enough to wipe clean the epigenetic slate of all that history wrote? If such a pill could free the genes within your brain of the epigenetic detritus left by all the wars, the rapes, the abandonments and cheated childhoods of your ancestors, would you take it?

[This article originally appeared in print as “Trait vs. Fate“]

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Dehydration? Resulting from catching a most resilient bacteria in the hospital?

Diary. Sunday, April 21, 2013

I woke up at 8 am. Mother (85 year-old) is already working since 6 am: doing dishes, cooking, sweeping, vacuuming in order to wake me up…

Yesterday was a hectic day: We sent dad to the hospital, and he ended in the intensive care by 5 pm.

Last night, I watched the old TV movie Boxcart Bertha, set during the US great depression of 1930.  The syndicates of workers are virulent and the institutions are disseminating the notion that the syndicates are Communist inspired plot, and sold out to Stalin Soviet Union.

Initially, the confrontations are physical and no live ammunitions are used against the demonstrators and strikers.

The situation deteriorates and companies start hiring armed private security, militias and mercenaries to tame the demonstrators.

The syndicated Shelly is nailed on a boxcart as Jesus was nailed on the cross…

My father is back to the intensive care unit, after residing at home for a month and slowly improving and walking on his own.

Last month, father got afflicted with pneumonia and bronchitis and his lungs have shriveled and are shot: He was a heavy smoker for over 70 years.

Father was making good progress and occasionally walking without the walker, and getting up 5 times in the night to fix himself sandwiches of jam, labneh… And emptying a bagful of candies (bonbons).

We were unable to sleep at night, fearing that he might fall as he did previously and get injured.

Mother refused to sleep in another room, just to have an eye on him.

Suddenly, at 5 am on Saturday, father started terrible and very frequent bouts of vomiting and diarrhea for over 5 hours. I changed his diapers and pajamas 4 times within half a hour, while he was in the restroom and I was completely exhausted and dejected.

I could not fathom how he accumulated so much water in his stomach. It was very warm, but father was shivering in his bed.

I called up the Red Cross of Kornet Chehwan: I initially thought it was merely a matter of dehydration and some plasma in the hospital would do by the end of the day.

We were lucky: The Red Cross sent us a team from the town of Bolonia very quickly, and we dispatched father to the hospital of Bhaness. The  Red Cross volunteers at the branch in Cornet Chehwan (mostly of university students) does not open during the day: It opens at 5:30 pm till 6 am. This branch already knows our address and mother visited the center for 2 months to change the wrapping of her 3rd degree burned arm…

It turned out that father has caught a most resilient bacteria that nested in the lungs during his last stay at the hospital last month. Does such a bacteria needs 30 days of gestation (incubation) before it hits full-blown and so suddenly?

After 3 hours in the emergency section for blood testing and other kinds of tests, a duration that any patient might die before receiving any kinds of prevention cure, father was sent to a room and plasma attached to his arm.

Initially father received a powerful antibiotics as during his last stay: His white blood counts was over 2,300, way above the normal 1,000.

By 5 pm, father was asphyxiating and barely could breath. Luckily, I was by his bed and noticed that he tried to sit in order to breath and his face darkened. I buzzed the emergency red button and began slapping his face and initiating chest-press technique, and was about to take out his tongue when the nurse emerged and looked dazzled and horrified.

The neighboring patient and his daughter were horrified and feeling helpless. The next patient had his urinary tract removed after 6 hours of surgery and a bag attached on his side in order to empty urine. This patient told me stoically that this was for the better: he had to go to the restroom every 10 minutes…

The physician reanimated father and ordered that he be sent to intensive unit.

The physician told me that father caught a most resilient bacteria from his previous 3-week stay in the hospital and that the most “powerful set” of antibiotics were injected, the most powerful arsenal available in the hospital…

Resilient bacteria are most likely inherited from residing in hospital: They accumulate and adhere to equipment, tubes and tools in the hospitals.

On this Sunday, the day after father was sent to hospital, I exercised, fed the chicken under the rain, cooked whatever mother has already started, shaved and dressed up. The odds that I might receive visits is very dim: The frequency of occurrences of guests paying me visit tells a long story.

Mother drove with my sister to church and would visit dad on her way back.

The visiting hours for patients in intensive care are from 11 to noon, and from 4 to 5 pm.

I was relieved that father is intensive care: Mother would have decided to sleep in the same room if he were not in intensive care unit.

Last evening, many came to visit father: Jihad and his wife Nada, Jean and his wife Joelle, Nassif…

My sister told me that all these cousins will meet for lunch somewhere on Sunday. Patrick is to arrive from France at night.

My niece Joanna called from London around 11 am and I told her to chat with mother around 7 pm as she might be back from the hospital.

Mother feels depressed, particularly in the evening: She is worried of what to do with dad when he returns from the hospital…

We had a bad month and this time around is going to be even a worse case of caring for dad.

Most patients who die after surgery is the consequence of catching resilient infection from the hospital.  Million die every year due to hospital infected environment.

Note: Dad stayed a week in intensive care without any anesthetic, and a week in a room. For an entire week, the nurses didn’t try to take dad for a short walk, fearing shortness of oxygen…

On Monday at 1 pm, the hospital called me and informed me that dad should be removed from the hospital. That was a very quick decision and took us all by surprise… I told the nurse that dad should at least be taken for a walk in order to check on his condition.  Two hours later, the nurse calls me and said that they took dad for a short walk and removed the mill… and that they didn’t administer him any antibiotics in the last three days (he is covered from infection), and that his blood test is good… And that dad cannot remain in the hospital. The nurse said  “It is better for him not to catch any infection while overstaying in the hospital“, but this was not convincing.

I later learned that my brother Ghassan (a dentist) visited dad at noon and got pretty upset because the nurses never attempted to walk my dad. I guess the physician got upset also from this outburst and signed on the exit papers


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