Adonis Diaries

Archive for the ‘medicine/medical treatment’ Category

Skeptics? Not in relation to physical fact. Circumcision Not cutting it?

Circumcision has endured because of tradition, not because of rationale nor medical benefit.

Nor has it ever been successful as an anti-masturbatory measure, which is why it gained prominence in the West 150 years ago.

When a custom remains after its original intent has vanished, it has morphed into a ritual.

And ritual is one of the kinder words to describe removing highly-innervated tissue from the most vulnerable members of our species, without any benefit in return.

The relic rests in the same vein as coming-of-age rituals and other practices that involve cutting, slicing, burning, and flogging.

According to the American Academy of Pediatrics, one in 500 boys experience acute complications from circumcision. Even a 0.2% risk is Not acceptable when there is no chance of reward.

Still it endures because, to most Westerners, that’s the way it’s always been. But the appeal to tradition is a logical fallacy that, were it rigidly adhered to, would have us still with slavery and without women’s suffrage. 

Imagine if circumcision had never been practiced and someone proposed we begin fondling and mutilating the infant genitals. The collective response would be revulsion.  Yet the practice continues today because, well, just because.

Reasons include ensuring the infant conform to religious norms or so that they will look like their father.

But faith should be a personal choice and if a father was missing three fingers, no one would suggest lopping off the digits to ensure familial uniformity.

A third reason proponents give is because they think it looks unappealing. But that’s only because they are used to seeing circumcised penises.  Were every male intact, proponents would see circumcised members as the freaky outcasts. 

Parents deciding to circumcise their sons is distinct from having them vaccinated or given Vitamin K boosters, as these have identifiable benefits.

Chopping off someone else’s body part would mean prison time under any other circumstance, but exception made for the most vulnerable victim.

In a depressing display of bipartisanship, the practice remains prevalent among persons of all political leanings.

Conservatives still go for the religion and tradition angles, which is to be expected.

Harder to comprehend is the tepid response from liberals, who should be demanding bodily autonomy over the most defenseless of our species.

It has been pointed out that  we should never make Junior hug an aunt just because she’s visiting for Christmas if the child doesn’t wish too. Yet, somehow this mindset does not extend to control over the most private part.

With no medical benefit, circumcision is a solution in need of a problem.  Proponents sometimes cite hygiene, but this is no more logical that lopping off our ears to prevent dirt from accumulating within.

One seemingly more valid reason is the chance of reducing HIV infection.

But this is an untruth and based on studies that make such basic mistakes as assuming all transmission was due to heterosexual sex. Also, if the studies were correct, and the practice provided STD protection, there would be a wide difference in infection rates between the circumcised and intact. 

Note: I can speak from personal experience.

I decided for circumcision when I was 26 after a painful unachieved sexual encounter. I had never masturbated and was still physically a “virgin”.

When I checked with a female physician, she transferred me to a male physician, and for a good reason. The physician “recovered” my swollen penis and taught me how to retract and recover. I was to get it down by doing this exercise 3 times a day. And I reasoned that getting circumcised would same me from this tedious exercise.

Sure I suffered for 2 weeks of pain and inconvenience, but I am glad for taking this decision

And I am wondering: If I were circumcised, would I have masturbated much early on?

If were circumcised, wouldn’t I be bold enough to try sexual encounter much earlier?

And I feel circumcision is actually necessary for a normal growing up of males, and more hygienic too.

Many children had to be circumcised because they lacked the necessary training to clean their penis when taking showers.

How can a layperson differentiate between Alzheimer and other more confusing loss of memories?

Maybe it is Not Alzheimer, but the memory confusion maybe worse to everyone concerned

Are you afraid of having Alzheimer’s?

Or Someone close to be afflicted with Alzheimer?

Those who really suffer from a memory disease, like in Alzheimer, they do Not realize what is happening or that they forgot to do something or forgot a name…

Probably your perception of memory loss is Not due to Alzheimer’s?

If anyone is aware of his memory problems, he doesn’t have Alzheimer’s.

It often happens in people aged 60 and over that they complain that their memory is lacking: Like the information is still in the brain, but it is the ” Processor ” that is missing., or failing to function properly.. It is labeled “temporary oblivion“.

My memory difficulties with names of persons and objects and fruits and vegetables… is worrying me.

The instances that I am excited and talkative, I feel that I can be a stand up comic and all words are fluent and coming quickly.

My mother condition is much worse: She cannot form an entire sentence and she get terribly frustrated and start to cry.

Yes, mother is aware of the deteriorating condition of her memory.

Lately, the TV has become a live and living scenes: People on TV are actually talking to her, and any procession on TV is converging to her house. And she get busy arranging coffee cups… waiting for the arrival of the visitors.

Mother confuses names: her own daughter receives the name of her late oldest sister. Many times she calls me Georges, the name of my late father.

 Elie Bashour posted this following article on July 27, 2018 and I am re-editing it.

”There are times when I speak, I can stop and don’t know what I was talking about…
I was afraid it was a start of Alzheimer’s… but today, reading this article, I’m reassured.”

In the following analysis, French Professor Bruno Dubois Director of the institute of memory and Alzheimer’s disease (Imma) at mercy-Salpêtrière – Paris Hospitals / addresses the subject in a rather reassuring way:

”If anyone is aware of his memory problems, he doesn’t have Alzheimer’s. ” “

1. I forget family names…
2. I don’t remember where I tidied up some things…

Half of the people aged 60 and over present some symptoms that are rather due to age than to disease.

The most common cases are:
– Oblivion of a person’s name,
– the fact that we went to a room in the house and never remember why we were going…
– a white memory for a movie title or an actor, an actress,
– a waste of time looking where we left his glasses or keys…

After 60 years most people have such difficulty.

This indicates that this is not a disease but rather a characteristic due to the passage of the years…

Many people are concerned about these omissions and the importance of the following statement:

” those who are aware of these omissions have no serious problem of memory.

Professor Bruno Dubois, director of Imma, reassures the majority of people concerned by their omissions:

” the more you complain about memory loss, the less likely it is you suffer from a memory disease. ” ”

– Now a little neurological test.
Only use your eyes!

1-find the c in the table below!


2-if you already found the c, then find the 6 in the table below.


3-now find the n in the table below. Careful, it’s a little harder!


If you pass these three tests without problems:

– you can cancel your annual visit to the neurologist.
– your brain is in perfect shape!
– you’re far from having any relationship with Alzheimer’s.

So, circulate. Be reassure…

And why am I not reassured?

The consequences are as bad. Better Not know what’s going around me.

Are these the Covid-19 recommendations from Maryland University?

Most probably, we are set to live with the Covid-19 for a long time.

We have got to learn and train our daily habits to survive this pandemics without major health degradation.

Wear a mask made of 3 layers of different fabrics in enclosed environment

Frequently wash your hands with soap and Not with bacteria disinfectant liquids, as you touch objects

Learn to keep the distance of 2 meters, even inside your home

Frequently enjoy clean air outside spaces and let your system be contact with all kinds of outside bacteria to increase your immune system.

Fortifying your immune system is Not a cure for catching this virus

No, the visus does Not attach to your shoes, but learn to walk barefoot inside your home

Your skin is the best defense against all kinds of viruses and bacterias

بيان من عيادة الأمراض المعدية في جامعة ميريلاند الأمريكية:

1. قد نضطر إلى العيش مع C19 لشهور أو سنوات، دعونا لا ننكره أو نذعر، دعونا نتعلم كيف نتعايش مع هذه الحقيقة.

2. لا يمكنك تدمير فيروسات C19 التي اخترقت جدران الخلايا، حتى لو شربت غالونات من الماء الساخن؛ فقط ستذهب إلى الحمام كثيرا.

3. غسل اليدين والمحافظة على مسافة جسدية بطول مترين ( 2 m) هي أفضل طريقة لحمايتك.

4. إذا لم يكن لديك مريض C19 في المنزل ، فلا حاجة لتطهير الأسطح في منزلك.

5. البضائع المعبأة ومضخات الغاز وعربات التسوق وأجهزة الصراف الآلي لا تسبب العدوى، فقط اغسل يديك، وعش حياتك كالمعتاد.

6. إن C19 ليست عدوى غذائية، تترافق مع قطرات من العدوى مثل الانفلونزا، لا يوجد خطر واضح لانتقال C19 عن طريق طلب الطعام.

7. يمكن أن تفقد حاسة الشم مع الكثير من الحساسية والالتهابات الفيروسية، هذه ليست دائما أعراض تدل على إصابة بفيروس C19.

8. بمجرد أن تكون في المنزل لا تحتاج إلى تغيير ملابسك على وجه السرعة والاستحمام، الطهارة فضيلة، ولكن هوس الخوف ليس كذلك!

9. فيروس C19 لا يعلق في الهواء. هذه عدوى تنفسية تتطلب اتصالًا وثيقًا.

10. الهواء نظيف يمكنك المشي في الحدائق (فقط حافظ على مسافة الحماية المناسبة).

11. يكفي استخدام الصابون العادي ضد C19 ، وليس الصابون المضاد للبكتيريا.

12. لا داعي للقلق بشأن طلبات الطعام الخاصة بك، ولكن يمكنك تسخينها في الميكروويف، إذا كنت ترغب في ذلك.

13. فرصة إحضار C19 إلى المنزل مع أحذيتك غير صحيحة. أنا أعمل ضد الفيروسات منذُ 20 عامًا – فالعدوى لا تنتشر بهذه الطريقة!

14. لا يمكنك القضاء على الفيروس بأخذ الخل وعصير قصب السكر والزنجبيل! هذه لرفع مستوى الحصانة وليست علاجا.

15. ارتداء الكمامة لفترات طويلة يتعارض مع مستويات التنفس والأكسجين. ارتديه فقط في الأماكن المزدحمة.

16. ارتداء القفازات هو أيضا فكرة سيئة. يمكن أن يتراكم الفيروس في القفاز وينتقل بسهولة إذا لمست وجهك. الأفضل أن تغسل يديك بانتظام.

17- المناعة تضعف إلى حد كبير من خلال البقاء دائماً في بيئة معقمة. حتى إذا كنت تأكل أطعمة تعزز المناعة ،

يرجى الخروج من منزلك بانتظام إلى أي حديقة / شاطئ، فالمناعة تزيد من خلال التعرض للأمراض، وليس عن طريق الجلوس في المنزل وتناول الأطعمة المقلية / الحارة / والسكريات.

The right to end your terminally miserable life out of constant pains?

Feasting on Gore (Written in 1999)

1.   X-rays don’t hurt: no pain.

Chemo is different: You lose your mane.

Cancer, hospital appointment, hospital confinement, terminal.

Convicted criminal, prison, delayed execution, terminus.

2.   Dressed in apron, back naked, abandoned, and forgotten;

Robbed of your money, robbed of dignity, and robbed of life.

A case study you are, for all to learn from experiments.

The more cases the better the knowledge.

3.   You lived; lived enough.

Let others learn and live, a while longer.

The “right to live folks” need to hang the Kevorkian’s,

Every single one of them:

Those who aid the terminally ill to die with his own choice.

4.   Pain, constant pains, no end in sight, no cure.

Wait till the healthy, spineless soul of the “right to live” maniacs

Needs a Kevorkian,

But will be surrounded with pale faces feasting on gore.

5.   I have the power to predict the end.  I know the odds:

You either die instantly or you live,

In the mind of all you know,

half-man. Abandoned.

6.   You may listen to the pillars of moral characters,

You may nod to the Talking Heads:  They talk well.

I have decided on my destiny.

It shall be quick.

Drug Research Contracts: Keeping Pharmaceutical companies out of reach from procsecution?

An article published in the NYT in November 29, 2004

“Of the 12 studies for (the church of Pfizer), all 5 of the reports claiming positive results, meaning the drug worked without worrisome side effects, that were submitted for possible regulatory approval were published.

The 7 other studies were inconclusive or negative, which can mean that the drug failed to work or that the test failed because of its design.

(Two of the studies were never submitted to the Food and Drug Administration to support an application for the drug’s approval.)”

“In her Zoloft study, Dr. Wagner acknowledged that she had received “research support” over the years from several drug manufacturers including Pfizer, which paid $80,000 to the Galveston center in connection with the Zoloft test.

But she did not state that she also received sizable payments from the company for work she did related to the study.”

Dr. Karen Dineen Wagner of the University of Texas Medical Branch at Galveston Published in November 29, 2004 under “Contracts Keep Drug Research Out of Reach”

(Page 3 of 5)

Dr. Wagner, vice chairwoman of the department of psychiatry and behavioral sciences at the Galveston center, declined to be interviewed for this article but did reply to some questions in writing. Officials of the Galveston center insisted that the industry money she received did not affect her work.

A Researcher’s Role

It was hardly surprising that many manufacturers of popular antidepressants already approved for use in adults would turn to an established researcher like Dr. Wagner to test them in young patients.

In the late 1990’s, she was one of a small number of researchers with experience in testing drugs intended to treat children with problems like attention deficit disorder and bipolar disorder.

Over the last decade, Dr. Wagner has led or worked on some 20 studies published in medical journals, and the government has financed some of her work.

She has also attracted a large number of including those aimed at testing whether antidepressants approved for use in adults were safe and effective in children and adolescents.

Dr. Wagner’s role varied in 12 industry-sponsored trials in which antidepressants were tested against placebos for depression or other problems. On three of them, including a Zoloft trial, she was a lead investigator, working with company researchers to plan, analyze and write results up for publication.

On the others, her duties were limited to overseeing test patients at her clinic.

Of the 12 studies, all five of the reports claiming positive results, meaning the drug worked without worrisome side effects, that were submitted for possible regulatory approval were published. The seven other studies were inconclusive or negative, which can mean that the drug failed to work or that the test failed because of its design. (Two of them were never submitted to the Food and Drug Administration to support an application for the drug’s approval.)

Because many of the antidepressant studies were unpublished, many doctors never heard about the results.

Their findings were typically disclosed in limited settings, like talks at meetings of medical specialists or on a poster displayed in a room with dozens of other posters, which is a typical way of disseminating research results at professional conferences.

Several researchers who worked on the pediatric antidepressant trials said that in many cases they had little incentive to submit ambiguous or failed trials to medical journals because they thought the papers would be rejected by journal editors.

One of those researchers, Dr. Neal Ryan, a professor of psychiatry at the University of Pittsburgh, said there has typically been little publishing interest in studies with inconclusive findings or those that failed to work because of study design, a type sometimes referred to as a negative study.

“No one gets famous from publishing negative studies,” Dr. Ryan said.

In response to a question, Dr. Wagner wrote that in all the cases where she was the lead investigator, test results had been or would soon be published or presented at medical meetings.

It was her study of Zoloft for childhood depression, financed by Pfizer, that attracted the most attention and criticism. Results were published last summer in The Journal of the American Medical Association as the debate on pediatric antidepressant use was rising; the study concluded that the drug effectively treated depression.

The finding received widespread publicity in newspapers, including The New York Times.

“This study is both clinically and statistically significant,” Dr. Wagner said last year. “The medication was effective.”

But some academic researchers said that the difference in improvement that the study found between young depressed patients taking Zoloft and similar patients who received a placebo – 10 percentage points – was not substantial.

Asked about complaints about the trial, Dr. Wagner referred to a statement in The Journal of the American Medical Association in which she responded last year to critical letters.

In that statement, Dr. Wagner said she believed that the 10 percentage point difference was “clinically meaningful.”

A Possible Conflict (of interest?)

In her Zoloft study, Dr. Wagner acknowledged that she had received “research support” over the years from several drug manufacturers including Pfizer, which paid $80,000 to the Galveston center in connection with the Zoloft test. But she did not state that she also received sizable payments from the company for work she did related to the study.

Note: Dr. Karen Dineen Wagner participated in more than a dozen industry-financed pediatric trials of antidepressants and other types of drugs from 1998 to 2001.

Continued <<Previous | 1 | 2 | 3 | 4 | 5 | Next>>

Environmental management practices in the Lebanese pharmaceutical industries

187(3):4290. doi: 10.1007/s10661-015-4290-3. Epub 2015 Feb 12.

Implementation strategies and challenges.

Author information

  • 1Department of Environmental Health, Faculty of Health Sciences, American University of Beirut, P.O. Box 11-0236, Riad el Solh, Beirut, 1107 2020, Lebanon,


This research attempts to provide an understanding of the Lebanese pharmaceutical industries’ environmental management strategies, priorities, and perceptions as well as drivers, barriers, and incentives regarding the implementation of the voluntary ISO 14001 Environmental Management System.

Accordingly, a semistructured in-depth interview was conducted with the pharmaceutical industries.

The findings revealed a significant lack of knowledge about the standard among the industries.

The main perceived drivers for adopting the ISO 14001 are improving the companies’ image and overcoming international trade.

The main perceived barriers for acquiring the standard are the lack of government support and the fact that ISO 14001 is not being legally required or enforced by the government.

Results revealed that adopting the ISO 14001 standard is not perceived as a priority for the Lebanese pharmaceutical industries. Although the cost of certification was not considered as a barrier for the implementation of ISO 14001, the majority of the pharmaceutical industries are neither interested nor willing to adopt the Standard if they are not exposed to any regulatory pressure or external demand.

They are more concerned with quality and safety issues with the most adopted international standard among the industries being the ISO 9001 quality management system.

This study highlights the aspect that financial barriers are not always the hurdles for implementing environmental management strategies in developing countries and underscores the need for regulatory frameworks and enforcement.

[PubMed – in process]
Investment in Medicine for virility and augmentation of breast:
5 times that of Alzheimer?
Drauzio Varella, Brazil Nobel laureate for medicine, said:
Currently, 5 times more are invested in Medicine for virility and augmentation of breast than on Alzheimer.
Within a few years, we will end up with a whole bunch of elder people with big breasts and rigid penis, and they will have no idea what they are for, and what they used them for…
La phrase qui tue !!!!....

Are making mistakes that essential?

“You show me a successful complex system, and I will show you a system that has evolved through trial and error.” (Mostly?)

God complex.  Almost all professionals in all disciplines believes he is absolutely certain in his convictions

Economics writer Tim Harford studies complex systems — and finds a surprising link among the successful ones: they were built through trial and error. In this sparkling talk from TEDGlobal 2011, he asks us to embrace our randomness and start making better mistakes

Tim Harford. Economist, journalist and broadcaster. His writings reveal the economic ideas behind everyday experiences. Full bio

Speech on July 2011

It’s the Second World War. A German prison camp. And this man, Archie Cochrane, is a prisoner of war and a doctor, and he has a problem. The problem is that the men under his care are suffering from an excruciating and debilitating condition that Archie doesn’t really understand. The symptoms are this horrible swelling up of fluids under the skin.

But he doesn’t know whether it’s an infection, whether it’s to do with malnutrition. He doesn’t know how to cure it.

And he’s operating in a hostile environment. And people do terrible things in wars.

The German camp guards, they’ve got bored. They’ve taken to just firing into the prison camp at random for fun. On one particular occasion, one of the guards threw a grenade into the prisoners’ lavatory while it was full of prisoners. He said he heard suspicious laughter.

And Archie Cochrane, as the camp doctor, was one of the first men in to clear up the mess. And one more thing: Archie was suffering from this illness himself.

1:23 So the situation seemed pretty desperate.  Archie Cochrane was a resourceful person. He’d already smuggled vitamin C into the camp, and now he managed to get hold of supplies of marmite (marmalade?)on the black market.

Some of you will be wondering what marmite is. Marmite is a breakfast spread beloved of the British. It looks like crude oil. It tastes zesty. And importantly, it’s a rich source of vitamin B12. So Archie splits the men under his care as best he can into two equal groups.

He gives half of them vitamin C. He gives half of them vitamin B12. He very carefully and meticulously notes his results in an exercise book. And after just a few days, it becomes clear that whatever is causing this illness, marmite is the cure (lack of vitamin B12. But this is No trial and error. It is an experiment designed to find the cause of the ailment)|By Tim Harford

So Cochrane then goes to the Germans who are running the prison camp. Now you’ve got to imagine at the moment — forget this photo, imagine this guy with this long ginger beard and this shock of red hair. He hasn’t been able to shave — a sort of Billy Connolly figure.

Cochrane starts ranting at these Germans in this Scottish accent — in fluent German, by the way, but in a Scottish accent — and explains to them how German culture was the culture that gave Schiller and Goethe to the world. And he can’t understand how this barbarism can be tolerated, and he vents his frustrations.

And then he goes back to his quarters, breaks down and weeps because he’s convinced that the situation is hopeless. But a young German doctor picks up Archie Cochrane’s exercise book and says to his colleagues, “This evidence is incontrovertible. If we don’t supply vitamins to the prisoners, it’s a war crime.” And the next morning, supplies of vitamin B12 are delivered to the camp, and the prisoners begin to recover.

I’m not telling you this story because I think Archie Cochrane is a dude, although Archie Cochrane is a dude. I’m not even telling you the story because I think we should be running more carefully controlled randomized trials in all aspects of public policy, although I think that would also be completely awesome.

I’m telling you this story because Archie Cochrane, all his life, fought against a terrible affliction, and he realized it was debilitating to individuals and it was corrosive to societies. And he had a name for it. He called it the God complex.

I can describe the symptoms of the God complex very easily. So the symptoms of the complex are, no matter how complicated the problem, you have an absolutely overwhelming belief that you are infallibly right in your solution.

Archie was a doctor, so he hung around with doctors a lot. And doctors suffer from the God complex a lot.

I’m an economist, I’m not a doctor, but I see the God complex around me all the time in my fellow economists.

I see it in our business leaders. I see it in the politicians we vote for — people who, in the face of an incredibly complicated world, are nevertheless absolutely convinced that they understand the way that the world works.

with the future billions that we’ve been hearing about, the world is simply far too complex to understand in that way.

 let me give you an example. Imagine for a moment that, instead of Tim Harford in front of you, there was Hans Rosling presenting his graphs. You know Hans: the Mick Jagger of TED. (Laughter) And he’d be showing you these amazing statistics, these amazing animations. And they are brilliant; it’s wonderful work.

But a typical Hans Rosling graph: think for a moment, not what it shows, but think instead about what it leaves out. So it’ll show you GDP per capita, population, longevity, that’s about it. So three pieces of data for each country — three pieces of data. Three pieces of data is nothing. I mean, have a look at this graph.

This is produced by the physicist Cesar Hidalgo. He’s at MIT. Now you won’t be able to understand a word of it, but this is what it looks like. Cesar has trolled the database of over 5,000 different products, and he’s used techniques of network analysis to interrogate this database and to graph relationships between the different products. And it’s wonderful, wonderful work.

You show all these interconnections, all these interrelations. And I think it’ll be profoundly useful in understanding how it is that economies grow. Brilliant work. Cesar and I tried to write a piece for The New York Times Magazine explaining how this works. And what we learned is Cesar’s work is far too good to explain in The New York Times Magazine.  (Explaining meta data analysis of various experiments that have Not much common ground in the designs)

Five thousand products — that’s still nothing. Five thousand products — imagine counting every product category in Cesar Hidalgo’s data. Imagine you had one second per product category. In about the length of this session, you would have counted all 5,000. Now imagine doing the same thing for every different type of product on sale in Walmart. There are 100,000 there.

It would take you all day. Now imagine trying to count every different specific product and service on sale in a major economy such as Tokyo, London or New York. It’s even more difficult in Edinburgh because you have to count all the whisky and the tartan. If you wanted to count every product and service on offer in New York — there are 10 billion of them it would take you 317 years.

This is how complex the economy we’ve created is. And I’m just counting toasters here. I’m not trying to solve the Middle East problem. The complexity here is unbelievable. And just a piece of context — the societies in which our brains evolved had about 300 products and services. You could count them in five minutes.

So this is the complexity of the world that surrounds us. This perhaps is why we find the God complex so tempting. We tend to retreat and say, “We can draw a picture, we can post some graphs, we get it, we understand how this works.” And we don’t. We never do.

 I’m not trying to deliver a nihilistic message here. I’m not trying to say we can’t solve complicated problems in a complicated world. We clearly can. But the way we solve them is with humility — to abandon the God complex and to actually use a problem-solving technique that works. And we have a problem-solving technique that works. Now you show me a successful complex system, and I will show you a system that has evolved through trial and error.

Here’s an example. This baby was produced through trial and error. I realize that’s an ambiguous statement. Maybe I should clarify it. This baby is a human body: it evolved. What is evolution? Over millions of years, variation and selection, variation and selection — trial and error, trial and error. And it’s not just biological systems that produce miracles through trial and error. You could use it in an industrial context.

 let’s say you wanted to make detergent. Let’s say you’re Unilever and you want to make detergent in a factory near Liverpool. How do you do it? Well you have this great big tank full of liquid detergent. You pump it at a high pressure through a nozzle. You create a spray of detergent. Then the spray dries. It turns into powder. It falls to the floor. You scoop it up. You put it in cardboard boxes. You sell it at a supermarket. You make lots of money.

How do you design that nozzle? It turns out to be very important. Now if you ascribe to the God complex, what you do is you find yourself a little God. You find yourself a mathematician; you find yourself a physicist — somebody who understands the dynamics of this fluid. And he will, or she will, calculate the optimal design of the nozzle. Now Unilever did this and it didn’t work — too complicated. Even this problem, too complicated.

But the geneticist Professor Steve Jones describes how Unilever actually did solve this problem — trial and error, variation and selection. You take a nozzle and you create 10 random variations on the nozzle. You try out all 10; you keep the one that works best. You create 10 variations on that one. You try out all 10. You keep the one that works best. You try out 10 variations on that one. You see how this works, right?

And after 45 generations, you have this incredible nozzle. It looks a bit like a chess piece — functions absolutely brilliantly. We have no idea why it works, no idea at all. And the moment you step back from the God complex — let’s just try to have a bunch of stuff; let’s have a systematic way of determining what’s working and what’s not — you can solve your problem.

 this process of trial and error is actually far more common in successful institutions than we care to recognize. And we’ve heard a lot about how economies function. The U.S. economy is still the world’s greatest economy. How did it become the world’s greatest economy?

I could give you all kinds of facts and figures about the U.S. economy, but I think the most salient one is this: 10% of American businesses disappear every year (No shame in taking risks and going bankrupt). That is a huge failure rate. It’s far higher than the failure rate of, say, Americans.

Ten percent of Americans don’t disappear every year. Which leads us to conclude American businesses fail faster than Americans, and therefore American businesses are evolving faster than Americans. And eventually, they’ll have evolved to such a high peak of perfection that they will make us all their pets — (Laughter) if, of course, they haven’t already done so.

I sometimes wonder. But it’s this process of trial and error that explains this great divergence, this incredible performance of Western economies. It didn’t come because you put some incredibly smart person in charge. It’s come through trial and error.

I’ve been sort of banging on about this for the last couple of months, and people sometimes say to me, “Well Tim, it’s kind of obvious. Obviously trial and error is very important. Obviously experimentation is very important. Now why are you just wandering around saying this obvious thing?”

So I say, okay, fine. You think it’s obvious? I will admit it’s obvious when schools start teaching children that there are some problems that don’t have a correct answer. Stop giving them lists of questions every single one of which has an answer.

And there’s an authority figure in the corner behind the teacher’s desk who knows all the answers. And if you can’t find the answers, you must be lazy or stupid. When schools stop doing that all the time, I will admit that, yes, it’s obvious that trial and error is a good thing.

When a politician stands up campaigning for elected office and says, “I want to fix our health system. I want to fix our education system. I have no idea how to do it. I have half a dozen ideas. We’re going to test them out. They’ll probably all fail. Then we’ll test some other ideas out. We’ll find some that work. We’ll build on those. We’ll get rid of the ones that don’t.” — when a politician campaigns on that platform, and more importantly, when voters like you and me are willing to vote for that kind of politician, then I will admit that it is obvious that trial and error works.

Until then, I’m going to keep banging on about trial and error and why we should abandon the God complex. Because it’s so hard to admit our own fallibility. It’s so uncomfortable. And Archie Cochrane understood this as well as anybody. There’s this one trial he ran many years after World War II. He wanted to test out the question of, where is it that patients should recover from heart attacks?

Should they recover in a specialized cardiac unit in hospital, or should they recover at home? All the cardiac doctors tried to shut him down. They had the God complex in spades. They knew that their hospitals were the right place for patients, and they knew it was very unethical to run any kind of trial or experiment.

Nevertheless, Archie managed to get permission to do this. He ran his trial. And after the trial had been running for a little while, he gathered together all his colleagues around his table, and he said, “Well, gentlemen, we have some preliminary results. They’re not statistically significant. But we have something. And it turns out that you’re right and I’m wrong. It is dangerous for patients to recover from heart attacks at home. They should be in hospital.”

And there’s this uproar, and all the doctors start pounding the table and saying, “We always said you were unethical, Archie. You’re killing people with your clinical trials. You need to shut it down now. Shut it down at once.” And there’s this huge hubbub.

Archie lets it die down. And then he says, “Well that’s very interesting, gentlemen, because when I gave you the table of results, I swapped the two columns around. It turns out your hospitals are killing people, and they should be at home. Would you like to close down the trial now, or should we wait until we have robust results?” Tumbleweed rolls through the meeting room.

Cochrane would do that kind of thing. And the reason he would do that kind of thing is because he understood it feels so much better to stand there and say, “Here in my own little world, I am a god, I understand everything. I do not want to have my opinions challenged. I do not want to have my conclusions tested.”

It feels so much more comfortable simply to lay down the law. Cochrane understood that uncertainty, that fallibility, that being challenged, they hurt. And you sometimes need to be shocked out of that. Now I’m not going to pretend that this is easy. It isn’t easy. It’s incredibly painful.

16:21 And since I started talking about this subject and researching this subject, I’ve been really haunted by something a Japanese mathematician said on the subject. So shortly after the war, this young man, Yutaka Taniyama, developed this amazing conjecture called the Taniyama-Shimura Conjecture.

It turned out to be absolutely instrumental many decades later in proving Fermat’s Last Theorem. In fact, it turns out it’s equivalent to proving Fermat’s Last Theorem. You prove one, you prove the other. But it was always a conjecture.

Taniyama tried and tried and tried and he could never prove that it was true. And shortly before his 30th birthday in 1958, Yutaka Taniyama killed himself. His friend, Goro Shimura — who worked on the mathematics with him — many decades later, reflected on Taniyama’s life. He said, “He was not a very careful person as a mathematician. He made a lot of mistakes. But he made mistakes in a good direction. I tried to emulate him, but I realized it is very difficult to make good mistakes.”


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.


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.


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.


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:



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




August 2020

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