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THE FATAL FLAW THAT SUNK THE TITANIC

The R.M.S. Titanic was the world’s largest man-made, mobile object when the ship was commissioned in 1912. Everyone knows the Titanic hit an iceberg in the North Atlantic and sank within 2 hours and 40 minutes. It was the highest-profile marine disaster of all time, and most people still blame the accident on the iceberg. What few people know is the real root cause—the fatal flaw that sunk the Titanic and killed over 1,500 people.

There were two official inquiries into the Titanic’s sinking. Both concluded the iceberg was the issue (without the iceberg, there was no problem), although the investigation processes considered many contributing factors—natural, mechanical, and human. There were errors found in the Titanic’s design, production, navigation, communication, and especially in the motivation of its builder, the White Star Line. While fingers were pointed, no blame was attached, and the only real outcome of the Titanic inquiries was adopting the International Convention for the Safety of Life at Sea (SOLAS) that still governs marine safety today.

The Titanic accident investigations used the best resources of the time, however the inquiries were conducted long before the wreckage was found, a forensic analysis was applied, and computer-generated recreation was available. Today, we have a clear picture of exactly how the Titanic disaster took place from a mechanical perspective but finding the root cause has remained buried as deep as its bow in the muddy bottom. It shouldn’t be, because the fatal flaw—the root cause—of what really sunk the Titanic is clearly obvious when analyzed objectively.

Both official inquiries into the Titanic sinking called sworn testimony of the surviving crew members, passengers, rescuers, builders, and marine regulators. They used an adversarial approach that was common for investigations at the time. That involved formulating a conclusion—the iceberg—then calling selective evidence and presenting in a way that supported the iceberg findings.

One investigation by the U.S. Senate concluded the accident was an Act of God—the iceberg was a natural feature and shouldn’t have been there under normal conditions. The second investigation by the British Wreck Commissioner agreed with the natural cause conclusion but qualified it with a statement, “What was a mistake in the case of the Titanic would, without a doubt, be negligence in any similar case in the future.” In other words, “In hindsight, it shouldn’t have happened and we’re not going to tolerate it again.”

Both twentieth-century investigations concluded that when the Titanic collided with the iceberg, a gigantic gash was ripped in its hull allowing massive water ingress and compromising the ship’s buoyancy. At the root of the accident, they found the cause to be simply the iceberg.

They were wrong. They failed to identify the real cause of the Titanic tragedy.

Today’s professional accident investigators take a different approach to fact finding. They take a “Root Cause Approach” to accident investigation and the industry leaders in Root Cause Analysis or Cause Mapping are the front-line company Think Reliability.

Think Reliability developed a root cause analysis of the Titanic sinking that’s outlined in an instructional video and a detailed event flow chart that identifies over 100 points of contributing factors. They’re excellent presentations but even Think Reliability missed a few contributors and did not categorically identify the one fatal flaw that caused the deaths of so many innocent people.

In getting to the root cause and finding the fatal flaw, it’s necessary to look at the stages of how the Titanic came to be and then determine exactly what caused it to go down.

History of the Titanic

The Royal Mail Ship Titanic was one of three sister vessels planned by the British ocean liner company, White Star Line. The Olympic was commissioned in 1910 and already in operation when the Titanic was under construction. A third ship, the Britannic, was in planning.

The Titanic’s construction was under an extremely tight timeline. Politics were at work, as was economics. Transcontinental ocean travel was rapidly expanding and the once-dominated British control on this lucrative industry was being threatened by German built and operated liners. In protective reaction, the British Government decided to subsidize White Star’s competitor, the Cunard Line. This left White Star resorting to private funding to compete and it came from American financier, J.P. Morgan, who put tremendous pressure on White Star to perform.

Harland & Wolff shipbuilders in Belfast, Ireland, built the Titanic. She was 883 feet long, stood 175 feet to the top of the funnels from the waterline and weighed 46,329 tons in water displacement. Her keel was laid in March 1909, and was set to sea trials on April 2, 1912. Eight days later, on April 10, 1912, the Titanic disembarked Southampton, England on her maiden voyage destined for New York City. Officially, 2165 passengers and crew were on board, but this figure is not accurate due to no-shows, an inaccurate crew count, and additional passengers who were taken on in Ireland as well as inevitable stowaways.

Some of the world’s most influential and wealthy people were on the Titanic which included the ship’s designer, Thomas Andrews, as well as the head of White Star Line, Bruce Ismay. It was beyond a voyage—it was a cultural event and a chance for White Star to regain its place in international shipping by proving the fastest and most luxurious way to sail between Europe and America. A lot was riding on the Titanic’s success.

The Iceberg Collision

The route Titanic took to New York had been traveled for several hundred years. It was the standard passageway for international liners and the main shipping lane between Europe and North America. The Titanic’s master, Captain Edward Smith, was a thirty-two-year White Star Line veteran and was chosen to command the Titanic due to his experience in international navigation, specifically this plot.

On the evening of April 14, 1912, the weather was perfect. It was clear, cold, and the sea was flat calm however, visibility was limited to ¼ mile due to there being a new moon and the only illumination was from starlight.

At 11:35 p.m., the Titanic approached a point 375 nautical miles south-southeast of Newfoundland where the cold Labrador current from the north met the warmer Gulf current from the south. This location was well known for being the edge of pack ice and was notorious for icebergs which calf or break-off from their parent shelf.

Captain Smith had inspected the bridge at approximately 9:30 p.m. According to testimony from the surviving helmsman, Captain Smith discussed the potential of icebergs although none were yet seen. Smith directed the helmsman to maintain course and to raise him if conditions changed. The captain left the bridge, retiring to his quarters. He was no longer involved in mastering the ship until after the collision.

Testimony from the Titanic’s helmsman, Robert Hitchens who was at the wheel during the iceberg collision, records that the Titanic was at 75 propeller revolutions per minute which calculated to 22.5 nautical miles per hour, just short of its maximum design speed of 80 revolutions or 24 knots. The helmsman also testified the Titanic was actually speeding up when it struck the iceberg as it was White Star chairman and managing director, Bruce Ismay’s, intention to run the rest of the route to New York at full speed, arrive early, and prove the Titanic’s superior performance. Ismay survived the disaster and testified at the inquiries that this speed increase was approved by Captain Smith and the helmsman was operating under his captain’s direction.

The Titanic was built long before radar became the main nighttime navigational aid. The watch depended on a crew member in the forward crow’s-nest who stared through the dark for obstacles. Other ships were not a concern as they were brightly lit and the only threat to the Titanic was an iceberg.

From the dim, Titanic’s watchman saw the shape of an iceberg materialize. It was estimated at ten times the Titanic’s size above water, which equates to a total mass of one hundred Titanics. The watchman alerted the bridge that an iceberg was at the front right, or starboard side, and to alter course.

Testimony shows that confusion may have caused a mistake being made in relaying a course change from the bridge to the steerage located at the ship’s stern. It appears the rudder might have been swung in the wrong direction and they accidently turned into the iceberg. It’s reported that when the helmsman realized the error, he ordered all engines in full reverse. Screw and rudder ships cannot steer in reverse. They can only back up in a straight line, but it was too late.

Stopping the Titanic was impossible. It was speeding ahead far too fast to brake within a ¼ mile, which is 440 yards. Without a speed reduction, covering 440 yards at 22.5 nautical miles per hour would take 36 seconds. Testimony from the inquiries recorded that during the eight-day sea trials, the Titanic was tested from full-ahead at 22 knots to full-stop. This took 3 minutes and 15 seconds and the deceleration covered 850 yards.

The Titanic sideswiped the iceberg on its starboard front, exchanging a phenomenal amount of energy. It immediately began taking on water that filled the ship’s six forward hull compartments. Water cascaded over the tops of the bulkheads in a domino effect and, as the weight of the water pulled the bow down, more water ingressed. This caused the stern to rise above the waterline. With the rear third of the ship losing buoyancy and the weight from her propellers being in the air, the stress on the ship’s midpoint caused a fracture. The ship split in two and quickly sank to the bottom. It was 2:20 a.m. on April 15, 1912—two hours and twenty minutes after the iceberg collision.

Warning and Life Saving Attempts

Captain Smith came to the bridge shortly after the collision. Again, survivor testimony is conflicting, and Smith did not live to give his version of what took place in mustering the crew and passengers for safe abandonment.

Without any doubt, there was complete confusion—some said utter chaos—in abandoning ship. The voyage had been so hastily pushed that the crew had no specific training or conducted any drills in lifesaving on the Titanic, being unfamiliar with the lifeboats and their davit lowering mechanisms.

Compounding this was a decision by White Star management to equip the Titanic with only half the necessary lifeboats to handle the number of people onboard. The reasons are long established. White Star felt a full complement of lifeboats would give the ship an unattractive, cluttered look. They also clearly had a false confidence the lifeboats would never be needed.

It’s well documented that many lifeboats discharged from the Titanic weren’t filled to capacity. Partly at fault was a “women and children first” mentality, but the primary reason is that no one person took charge of the operation. Testimony is clear that Captain Smith was involved during the lifeboat discharges but there’s no record of what charge he actually took. Some accounts tell of the captain remaining on the bridge and going down with the ship, as the old mariner’s line goes.

Another well-documented issue was the failure of the ocean liner Californian to come to Titanic’s rescue. The Californian was within visual view of the Titanic. In fact, the crew of the Californian had sent the Titanic repeated messages warning of icebergs and the Californian had stopped for the night because of limited visibility and high risk of iceberg collision. These messages were improperly addressed and were never relayed to the bridge of the Titanic.

Further, the crew of the Californian had seen Titanic’s distress flares, but the Californian’s Captain refused to respond. This was a major issue brought up at both official inquiries and a reasonable explanation from Californian’s Captain was never resolved.

Eventually, the ocean liner Carpathia responded. It, too, sent the Titanic iceberg warnings before the collision. The inquiries drilled down into the message relay flaws. They discovered the wireless operators on board the Titanic weren’t crewmembers nor directed by White Star. They were employees of the Marconi Telegraph Company privately contracted in a for-profit role to deliver all messages to and from the Titanic. In the few hours before the iceberg collision, the Titanic was within range of an on-shore relay station, and this gave them a short window to pass high-priority messages for wealthy passengers. Navigation warning messages to the Titanic were given low or no priority.

Hearing testimony recorded that shortly after dark, as early as 7:00 p.m., the Titanic was sent at least five iceberg warnings. There’s no record these were passed on to the ship’s bridge nor the captain. The Marconi operator aboard the Titanic survived to testify there’d been a severe backlog of paying customer messages and he was being “interrupted” by incoming navigational alerts. The warnings were set aside as they were not addressed “MSG” which means “Master Service Gram”. By policy, MSG messages required the captain’s personal action whereas non-marked messages were delivered when time permitted.

Finding the Titanic — Design and Damage

Although the Titanic was the largest ship of its time, there was nothing technologically new about its design, materials, or method of construction. The hull was built of large steel plates, some as large as 6 feet by 30 feet and between 1 and 1 ½ inches thick. The technology at the time was to rivet the sections together where today, modern ships are welded at their seams.

Riveting a ship’s seams was an entire trade on its own—almost an art. There were two types of rivets used on the Titanic. Rivets in the mid-section of the hull, where stresses from lateral wave forces were greatest, were made of steel and triple-riveted while those in the bow and stern were composed of cheaper iron. The bow and the stern endured less force when under normal operation and only required double riveting by design. Further, with the mid-section of the Titanic being straight and flat, these rivets were installed with hydraulic presses where the curved plates at the ship’s ends had to be hand riveted. That involved setting rivets in place while white hot and hand-hammering them closed.

Anyone who’s watched the movie Titanic knows the ship was designed with sixteen “watertight” compartments, separated by fifteen bulkheads that had doors which could be shut off in the event the hull was compromised anywhere along these sections. The “watertight” design only applied below or at the waterline, leaving the entire hull open above the top of these bulkheads.

The bulkheads were the fatal design cause of the Titanic’s sinking, but they weren’t the root cause of the disaster.

The ship’s architect, Thomas Andrews, was aware that flooding of more than four compartments would create a “mathematical certainty” that the bulkheads would overflow and cause the ship to sink. Testimony records that Andrews informed Captain Smith of this right after he realized the extent of flooding. This triggered the abandon ship order.

Over the years following the sinking and before the Titanic’s wreckage was discovered, most historians and naval experts assumed the ship suffered a continuous gash in the hull below the waterline and across all six compartments. There was one dissenter, though, who surmised it only took a small amount of opening in each compartment to let in 34,000 tons of water and that was enough to compromise the ship.

Edward Wilding was a naval architect and co-designer of the Titanic who testified at the American inquiry. He calculated that as little as 12 square feet of opening in the hull would have been enough to let in that much water in the amount of time the Titanic remained afloat. Wilding stated his opinion that there was not a long gash, rather it was a “series of steps of comparatively short length, an aggregate of small holes” that were punctured in the hull. Wilding went as far to speculate that the force of the collision probably caused rivets to “pop or let go” and it was “leaks at the ruptured seams” that let in seawater.

In September 1985, the Titanic’s wreckage was found by a deep-sea expedition led by Dr. Bob Ballard. It was in 12,500 feet of water and its debris field covered 2,000 yards. Her hull was in two separate main pieces with her bow nosed into 35 feet of muddy bottom. Since then, many dives have been made on the Titanic including one which used a ground penetrating sonar that mapped the section of the bow that was under the mud.

The sonar readings clearly showed six separate openings in the forward six hull compartments. They were narrow, horizontal slits in various spots, not at all-in-one continuous line like the gash theory held. The sonar map was analyzed by naval architects at Bedford & Hackett who calculated the total area exposed by the slits was 12.6 square feet—almost the exact figure proposed by Edward Wilding in 1912.

The architects also stated the rivets were clearly at fault and they’d failed from the impact. The rivets either sheared off on the outer heads or simply fractured and were released by the impact’s force. Immediately, many experts questioned why only a few rivets in a few seemingly random places failed and not most all along the area of impact.

In one of the dives, a large piece of the Titanic’s forward hull was recovered. This led to a forensic study on the plate steel and rivet composition by metallurgists Jennifer McCarty and Tim Foecke which they documented in their book What Really Sank the Titanic. Drs. McCarty and Foecke established many of the Titanic’s iron rivets had an unacceptable amount of slag in their chemical makeup, contrary to what the ship’s design specified. The metallurgists concluded when the inferior, weak rivets were exposed in below-zero Fahrenheit water temperature on the night of the sinking, they were brittle and shattered from the collision force.

The metallurgists went further in their investigation. They found during the rush to complete the Titanic on time, the builders purposely resorted to inferior metal than specified by the designers. The builders were also faced with a critical shortage of skilled riveting labor. This led to a compounded error of inferior rivets being installed by inferior tradesmen that likely explains the randomness of failed areas.

Today, the failed rivet theory stands as the most logical explanation for the mechanical cause of the Titanic disaster, but this still doesn’t get at the root cause of the tragedy.

At the core of Root Cause Analysis is the question “Why?”. This form of accident investigation forces the question “Why did this happen?” to be asked over and over until you cannot ask anymore “Whys?”. In Titanic’s case, this path leads to answering the root cause—the fatal flaw in why over 1,500 innocent people lost their lives.

The two official investigations back in 1912 started with a conclusion—the Titanic hit an iceberg and sank. They made somewhat of an attempt to answer why that happened without attaching too much blame. The result was not so much as getting to the root cause but to try and make some good come from the disaster and ensure there was less chance of it happening again.

That is a good thing and, to repeat, it led to improving world marine safety through SOLAS. But that still doesn’t get to identifying the fatal flaw in what really sank the Titanic.

Think Reliability identified five root causes of the Titanic disaster:

1. Iceberg warnings were ignored.

2. The iceberg wasn’t seen until too late.

3. The Titanic was traveling too fast for visual conditions and couldn’t avoid colliding with the iceberg.

4. The rivets failed, compromising the hull’s integrity and letting in enough water to exceed the design buoyancy.

5. Insufficient lifesaving procedures and equipment were in place.

While these five reasons are the prime contributors to why the accident and tremendous loss of life happened, they still don’t arrive at the true, single root cause—the fatal flaw that sunk the Titanic.

Finding the fatal flaw requires answering ‘Why” to each of these five points.

1. Why were the iceberg warnings ignored?

The answer is a systematic failure of communication operating on the Titanic. There was ample reason to suspect icebergs might be in the Titanic’s path. Any competent captain would be aware of hazards like this and would liaise with other ships along the route for warning information. Navigational communication was not a priority under Captain Edward Smith’s command.

2. Why was the iceberg not seen until too late?

There’s another simple answer here. Night visibility was poor as there was limited light. Testimony from the surviving crewmembers consistently estimated the visibility range to be no more than ¼ mile. Eyesight, combined with compass readings, were the only forms of navigation in 1912. The Titanic was going too fast for the crew to react because Captain Smith allowed his ship to exceed a safe speed for navigation conditions.

3. Why was the Titanic traveling too fast for navigation conditions?

Without question, Captain Smith was under pressure from Bruce Ismay to bring the Titanic into New York earlier than scheduled. While this would never have set a speed record for the route, it certainly would reflect positively on the White Star Line and its business futures. Captain Smith succumbed to unreasonable pressure and allowed his ship to be operated unsafely.

4. Why did the rivets fail?

While Captain Smith had no input into the construction of the Titanic, he certainly knew its design limits. The Titanic was built as an ocean liner, not a battleship or an icebreaker. Captain Smith knew how dangerous an iceberg collision could be, yet he still risked his ship being operated in unsafe conditions.

5. Why were there insufficient lifesaving equipment and procedures in place?

The fault began with White Star’s failure to provide the proper number of lifeboats as well as rushing the Titanic into service before the crew was properly trained in drills and equipment operation. Captain Smith was aware of this. Despite, he allowed the Titanic to sail unprepared.

At the root of each of question lies irresponsibility of the Titanic’s captain. It’s long held in marine law that a ship’s captain is ultimately responsible for the safety of the vessel, the crew, and the passengers.

Captain Smith had full authority over every stage in the Titanic’s disaster and he failed on each point. Clearly, Captain Edward Smith is the fatal flaw that sunk the Titanic.

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Note: Writer Garry Rodgers holds a 60 Ton Transport Canada Marine Captain Certification which includes accredited training in Ship Design & Stability, Navigation, Communication, SOLAS, and Marine Emergency Duties. Garry is also formally trained in Think Reliability Root Cause Mapping.

IS AMANDA KNOX REALLY INNOCENT OF MURDERING MEREDITH KERCHER?

The Amanda Knox story captured worldwide attention during the years she passed through the Italian legal system and was convicted—twice—of complicity in murdering her college roommate, Meredith Kercher. Ultimately, Knox was exonerated of the murder charges but convicted of criminal slander based on coerced statements she made while under initial and unlawful police interrogation. Now, the international spotlight is again upon Knox with a retrial underway after her slander charge was overthrown by Italy’s highest court. All this circles back to many still questioning if Amanda Knox really is innocent of murdering Meredith Kercher.

There’s a lot of internet information on the Amanda Knox murder case. Some of it’s factual. Much is sensational tabloid junk about “Foxy Knoxy”—the “Ice Lady”—disseminated by socially dysfunctional trolls operating from surplus metal sea-cans converted into dwellings via an extension cord hooked to one bare light bulb. To find out the truth, it’s necessary to first look at the overall facts and then examine how the Italian legal system handled the case through a dragged-out, eight-year-long process.

Meredith Kercher

In 2007, Amanda Knox was a 20-year-old student from Seattle, Washington. She moved to Perugia in central Italy (slightly north of Rome) to further her journalism studies as Perugia was well-known for outstanding universities and educational opportunities—a popular place for foreign students. Here, Knox met a British exchange student, 21-year-old Meredith Kercher, and they shared a ground-floor, four-bedroom apartment with two other young ladies.

Quickly, Knox became romantically involved with a young Italian man, Raffaele Sollecito, and Kercher did the same with Giacomo Silenzi. At the time, Knox also worked part-time in a nightclub run by Patrick Lumumba. It was this pentagon of five that the Italian prosecutors would present as a sex game gone wrong that resulted in Meredith Kercher’s death.

On the evening of November 1, 2007, Knox, Sollecito, Silenzi, and Kercher socialized with others at Sollecito’s apartment near to where the ladies roomed. Present was a man named Rudy Guede who was invited by one of the group members but who was unknown to Knox and Kercher. Around 9 pm, Kercher excused herself from the gathering and walked back to her residence alone. Bit by bit, the gathering broke up leaving Knox and Sollecito to overnight there together.

At midday on November 2, Knox repeatedly tried to phone Meredith Kercher. She got no answer and became concerned, so Knox and Sollecito went to the co-habitation and found Kercher’s bedroom door locked. Knox tapped on the door and called out, but Kercher didn’t answer. Then Knox and Sollecito noticed some bloodstains, including a bloody footprint, in the bathroom.

Being alarmed, Knox called her mother in America who directed Knox to call the Italian police. She did so. However, there was a significant delay which was advanced as part of the prosecution’s later case against Knox and was supported by a timeline presented through cell phone records.

The first attending police officers were not homicide detectives. They were an Italian version of postal inspectors crossed with communication fraud investigators. There hadn’t been a murder in Perugia in over twenty years, so it was a considerable time before “competent” scene processors and trained murder cops arrived. Naturally, the scene was contaminated, and the ensuing DNA evidence used in convicting Amanda Knox of murdering Meredith Kercher was compromised.

What the scene processing showed was Kercher had been attacked, raped, and had her throat cut in her bedroom. Her official cause of death was exsanguination (bleeding out) after being injured with a sharp-edged weapon. Kercher’s bedroom window was open, and the investigators deduced that to mean that a break-in had been staged with the real killer setting the crime up to appear that a stranger was involved.

Police initially treated Amanda Knox as a witness. She was questioned on different occasions, but the homicide investigators slowly formulated a theory that Knox was lying to protect the actual murderer. They also developed a motive theory that Kercher was killed because she refused to take part in a multi-person sexual trist. An orgy.

On November 6, the Italian homicide detectives again brought Knox in for questioning. This time it turned into a full-on, hard-core interrogation that lasted hours. This is a complex and controversial part of the Amanda Knox story and precise details—at least as precise as possible because the authorities did not audio or video record it (rather they elicited a written confession from Knox)—can be read on the website amandaknoxcase.com under The Interrogation of Amanda Knox.

In Amanda Knox’s written confession, she states to have been present while her nightclub boss, Patrick Lumbumba, raped and murdered Meredith Kercher. Knox did not supply any motive or any details which only an involved person would know. Lumbuba was arrested on the strength of Knox’s statement and it was shortly proven, beyond all doubt, that Lumbumba had an air-tight alibi and he was flat-out innocent. (This “accusation’ against Lumbumba is what led to her criminal slander conviction which is once again, in 2024, before the Italian courts. A verdict in set for June 5th.)

Rudy Guede

Amanda Knox was held in custody while the prosecution put an indictable case together. Meanwhile, the scene forensic evidence identified a DNA profile from semen on Kercher’s body. They conclusively linked it to Rudy Guede who had been at the social gathering on the evening when Kercher was last seen alive. Guede was arrested in Germany where he confessed and indicated that Amanda Knox had nothing to do with Kercher’s murder.

By now, the Italian legal system had a freight train rolling along the justice track. Instead of applying the brakes, the police, prosecutors, and judges threw more coal on the fire and kept on persecuting Amanda Knox. This was due to the archaic inquisitional system Italy was trying to gentrify into a western adversarial legal framework.

The common US-style evidence rules didn’t apply in the Italian arena. Despite Amanda Knox being hardline interrogated for hours without legal representation, being informed of her rights, denied food, water, and toilet facilities, slapped around, and breaking down in the middle of the night, the Italian court accepted Knox’s coerced confession as solid evidence that had to be admitted under their law structure. It didn’t matter that the prosecution’s perceived motive—some kinky sex game—had no factual basis, and it didn’t matter that Knox’s boyfriend, Raffaele Sollecito, provided Knox with her air-tight alibi. No, the Italian legal machine went right on persecuting Amanda Knox.

Knox stood trial through the summer and fall of 2009. Her case received massive public attention and the British tabloids sensationalized it like nothing ever seen. This was now the day of the emerging internet where chatrooms and social media made a spectacle of the trial and a massive mess of Amanda Knox’s life.

Amanda Knox was convicted of Meredith Kercher’s murder on December 4, 2009. She was sentenced to 26 years in jail. She appealed and had her murder conviction overturned on October 3, 2011, now having served nearly two years in an Italian prison.

In March of 2013, Italy’s Court of Cassation ordered a new trial and on January 30, 2014, she was once again convicted for killing Meredith Kercher. By now, Amanda Knox was back in America and was not returned to Italy during her new appeal. On March 27, 2015, Italy’s highest court again overturned her conviction, and her legal persecution was over.

Any rational person asks, “How could this miscarriage of justice possibly happen?” The answer is as complicated as the Amanda Knox story, if that’s possible to fully tell. It’s a murky mix of systematic incompetence and utter lack of regard for the truth. In the high court’s final ruling, the judge cited “sensational failures”, “glaring errors”, “investigative amnesia”, “guilty and culpable omissions”, “ignorance of expert forensic testimony that demonstrated contamination of evidence”, “outright falsification of forensic evidence”, and “a case without any foundation”.

The horrific Amanda Knox wrongful conviction story is best told by Amanda, herself. In a past interview with The Atlantic titled Who Owns Amanda Knox? , Amanda says:

Does my name belong to me? Does my face? What about my life? My story? Why is my name used to refer to events I had no hand in? I return to these questions again and again because others continue to profit off my identity, and my trauma, without my consent. Most recently, there is the film Stillwater, directed by Tom McCarthy and starring Matt Damon and Abigail Breslin, which was, in McCarthy’s words, “directly inspired by the Amanda Knox saga.” How did we get here?

In the fall of 2007, a British student named Meredith Kercher was studying abroad in Perugia, Italy. She moved into a little cottage with three roommates—two Italian law interns, and an American girl. Less than two months into her stay, a young man named Rudy Guede, an immigrant from the Ivory Coast, broke into the apartment and found Meredith alone. Guede had a history of breaking and entering. A week prior, he had been arrested in Milan while burglarizing a nursery school, and was found carrying a 16-inch knife. He was released.

A week later, he raped Meredith and stabbed her in the throat, killing her. In the process, he left his DNA in Meredith’s body and throughout the crime scene. He left his fingerprints and footprints in her blood. He fled to Germany immediately afterward, and later admitted to being at the scene.

I am the American girl in that story, and if the Italian authorities had been more competent, I would have been nothing more than a footnote in a tragic story. But as in many wrongful convictions, the authorities formed a theory before the forensic evidence came in, and when that evidence indicated a sole perpetrator, Guede, ego and reputation led them to contort their theory to maintain that I was still somehow involved. Guede was quietly convicted for participating in the murder in a separate fast-track trial, and then I became the main event for eight long years.

While I was on trial for the murder of Meredith Kercher, from 2007 to 2015, the prosecution and the media crafted a story, and a doppelgänger version of me, onto which people could affix all their uncertainties, fears, and moral judgments. People liked that story: the psychotic man-eater, the dirty ice queen, Foxy Knoxy. A jury convicted my doppelgänger and sentenced her to 26 years in prison.

But the guards couldn’t handcuff that invented person. They couldn’t escort that fiction into a cell. That was me, the real me, who returned to that windowless prison van, to those high cement walls topped with barbed wire, to those cold, echoing hallways and barred windows, to that all-consuming loneliness.

Ten years ago, at the age of 24, I was acquitted, and I tumbled into a kind of purgatory. I left one cell and immediately entered another: the quiet of my childhood bedroom. Outside, the telephoto lenses were fixed on my closed blinds. Prison had given me an appreciation for all the freedoms I’d taken for granted. Freedom showed me how many I still lacked.

As I walked back into the free world, I knew that my doppelgänger was there alongside me. I knew that everyone I would ever meet from then on would have already met, and judged, her. I had been acquitted in a court of law, but sentenced to life by the court of public opinion as, if not a killer, then at least a slut, or a nutcase, or a tabloid celebrity. Why doesn’t she just go away already? Her 15 minutes are over.

In freedom, I had become a pariah. Looking for work, going back to school, buying tampons at the pharmacy, everywhere I went I met people who already thought they knew who I was, what I’d done or not done, and what I deserved. I was threatened with abduction and torture in broad daylight; I was threatened with having Meredith’s name carved into my body. Strangers sent me lingerie and bizarre love letters.

All over the world, people believed they knew me, a warped assumption that turned me into a monster to some and a saint to others. I felt like I was always standing behind that cardboard cutout, Foxy Knoxy, saying, Hey, back here, the real me! Even most of the strangers who offered kindness and support didn’t truly see me. They loved her.

It’s hard to make friends, to date, to be a regular person when everyone you meet has a preconceived notion of who you really are, whether positive or negative. I could have chosen to hide out, to change my name, to dye my hair, and hope no one recognized me ever again. Instead, I decided to embrace the world that had dehumanized me, and all those who turned me into a product.

From the moment I was arrested, my name and face and trauma became a source of profit for news organizations, filmmakers, and other artists, scrupulous and unscrupulous. The most intimate details of my life, from my sexual history to my thoughts of death and suicide in prison, were taken from my private diary and leaked to journalists. Those journalists turned my darkest fears into fodder for hundreds of articles, thousands of blog posts, and millions of hot takes.

People speculated about my mental state and sexuality, they diagnosed me from afar, they used my predicament as a metaphor, they made TV movies about me, based characters in legal shows on me, and the worst of them took every opportunity they could, while I was in prison and while I’ve been out, to shame me for something I didn’t do, to shame me for living while Meredith is dead, to shame me for being in the very headlines they write, for being in the photographs they take without my consent.

The hypocrisy and the cruelty are maddening. And yet, being under that microscope has given me insight into how wrong a media narrative can be, how easy it is for all of us to consume other people’s lives as if they were mere content to fill up our Twitter feeds.

This focus on me led many to complain that Meredith Kercher had been forgotten. But whom did they blame for that? Not the Italian authorities. Not the press. Somehow it was my fault that the police and media focused on me at Meredith’s expense. The result of this is that 14 years later, my name is the name associated with this tragic series of events I had no control over.

Meredith’s name is often left out, as is Rudy Guede’s. When he was released from prison in late 2020, the New York Post headline read: “Man Who Killed Amanda Knox’s Roommate Freed on Community Service.” My name is the only name that shouldn’t be in that headline.

I never asked to become a public person. The Italian authorities and global media made that choice for me. And when I was acquitted and freed, the media and the public wouldn’t allow me to become a private citizen again.

I have not been allowed to return to the relative anonymity I had before Perugia. I have no choice but to accept the fact that I live in a world where my life, and my reputation, are freely available for distortion by a voracious content mill.

———

There is no doubt—no doubt whatsoever—that Amanda Knox really is innocent of murdering Meredith Kercher. She’s a true victim. A victim of a horrific crime. A victim of an abominable justice system. A victim of disgusting tabloids. And a victim of soulless trolls.

Footnote: Today, Amanda Knox is 36 years old and a mother of two. She hosts a successful podcast titled Labyrinths: Getting Lost with Amanda Knox with the themes of injustice and wrongful conviction. Amanda is a professional journalist, author, and activist. She recently signed with Hulu for a 12-part series based on her life story. One of the film’s co-producers is Monica Lewinsky.

WHAT REALLY KILLED ROBIN WILLIAMS

On August 11, 2014, entertainment genius Robin Williams took his own life inside his Paradise Cay, California home near San Francisco. The coroner initially ruled that Williams, age 63, died by suicide—asphyxia by hanging antecedent to, or caused by, clinical depression. However, when the final autopsy results were in, an entirely different picture played out. Robin Williams was in the advanced stage of a somewhat common, but almost always undiagnosed, brain disease called Lewy Body Dementia or LBD.

As Williams’ window, Susan Schneider Williams who now represents the Lewy Body Dementia Association, stated, “The disease was a terrorist in my husband’s head. Any way you look at it, the presence of Lewy bodies in his brain took his life. Depression was only a symptom. Unfortunately, we as a culture don’t have the vocabulary to discuss brain disease in the way we do about depression. Depression is only a side effect of LBD—it’s rooted in neurology. His brain was literally falling apart, and not one thing could be done about it.”

Lewy Body is a strange term. We’ll examine where that name came from, what exactly LBD is, what causes it, and how this always-fatal disease can be managed in its three progressive stages: early, mid, and late. But first, let’s have a brief look at this remarkable man’s achievements. Perhaps “remarkable” isn’t a powerful enough word for Robin Williams.

Robin McLaurin Williams was born on July 21, 1951, into an average American family. But from an early age, there was nothing average about him. He showed a God-given gift for improvision comedy and acting. By the early 1970s, Williams was in high demand as a San Francisco-based stand-up comedian, and he went on to be one of the funniest funnies of all time.

Few can forget many of Robin Williams’ outstanding character roles. He got his television start in Mork & Mindy and went on to film. Popeye. Hook. Good Will Hunting. Dead Poets Society. Good Morning Vietnam. The World According to Garp. World’s Greatest Dad. Night at the Museum. The Birdcage. Moscow on the Hudson. Jumanji. And, of course, Mrs. Doubtfire.

Williams also did voice-overs in Aladdin, Robots, and Happy Feet. He won numerous awards—six Golden Globes, five Grammys, two Primetime Emmys, two Screen Actors Guilds, and an Oscar for Best Supporting Actor. As well, Williams won the Cecille B. DeMille award in 2005.

Robin Williams had his struggles through life, though. He was addicted to cocaine and alcohol which set him into fitful mood swings. He was in and out of rehab for years. However, by 2010 he was stable and substance free, except for therapeutic prescriptions issues to combat what was thought to be clinical depression.

It was not. Robin Williams had an undiagnosed brain disorder. A disease that was only discovered after his death and was verified by brain sectioning at his autopsy. What was suspected to be Alzheimer’s or Parkinson’s in the last year of his life turned out to be Lewy’s Body Dementia—a condition under the general dementia umbrella and an extremely deadly disease.

You’re likely wondering what this weird name is and what it entails. Rather than me paraphrasing the information, let’s go to the best source available. No, not Wikipedia or ChatGPT.  It’s the website of the Lewy Body Dementia Association, and here’s what it says:

Lewy body dementia (LBD) is the 2nd most common type of progressive dementia after Alzheimer’s disease. The name comes from a discovery by Dr. Friedrich Lewy in the early 1900s of abnormal bodies or deposits of alpha-synuclein proteins in areas of the brain that can only be verified through an autopsy. These bodies alter the production of dopamine and acetylcholine that are vital neural transmitters.

LBD is not a rare disease. It affects more than a million people in the United States alone. Because LBD symptoms may closely resemble other, more commonly known disorders like Alzheimer’s and Parkinson’s disease, it is widely under-diagnosed.

LBD is an umbrella term for two related diagnoses:

  • A person with dementia with Lewy bodies will develop dementia and other LBD symptoms, one of which may be changes in movement, like a tremor (parkinsonism).
  • With the other form of LBD, people will present first with changes in movement, leading to a Parkinson’s disease diagnosis; over time many will develop dementia years later. This is diagnosed as Parkinson’s disease dementia.

As time passes, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms. The earliest symptoms of dementia with Lewy bodies and Parkinson’s disease dementia are different, but both are due to the same underlying biological changes in the brain.

LBD is a multi-system disease and usually requires a comprehensive treatment approach with a collaborative team of physicians and other health care professionals like occupational, physical, or speech therapists. Early diagnosis and treatment may extend your quality of life and independence. Many people with LBD enjoy significant lifestyle improvement with a comprehensive treatment approach, and some may even experience little change from year to year.

For a more in-depth explanation of Lewy Body Dementia disease, here’s a trip to the medical research department at Johns Hopkins University:

Lewy Body Disease (LBD) is a complex and often misunderstood neurodegenerative disorder that affects millions of individuals worldwide. Characterized by the accumulation of abnormal protein deposits called Lewy bodies in the brain, LBD poses significant challenges to both patients and caregivers. In this article, we delve into the neurological aspects of LBD, exploring its development, detection, effects on the human body, and its associated symptoms.

Development of Lewy Body Disease

Lewy Body Disease primarily affects older adults, typically manifesting after the age of 50. While the exact cause of LBD remains unknown, researchers believe that a combination of genetic, environmental, and lifestyle factors may contribute to its development. Genetic mutations, particularly in genes associated with the production and clearance of alpha-synuclein protein, have been implicated in some cases of familial LBD. However, most cases of LBD occur sporadically without a clear genetic link.

Neurological Pathology

At the core of LBD pathology is the abnormal accumulation of alpha-synuclein protein, forming Lewy bodies within neurons. These protein aggregates disrupt normal cellular function and communication within the brain, leading to widespread neurodegeneration. Areas of the brain particularly affected by Lewy bodies include the substantia nigra, which plays a crucial role in movement control, and the cerebral cortex, responsible for cognitive functions.

Detection and Diagnosis

Diagnosing LBD can be challenging due to its overlapping symptoms with other neurodegenerative disorders such as Parkinson’s disease and Alzheimer’s disease. A comprehensive medical history, neurological examination, and a battery of neuropsychological tests are often employed to assess cognitive function, motor abilities, and psychiatric symptoms.

Brain imaging techniques, such as MRI and PET scans, may reveal characteristic patterns of brain atrophy and dysfunction associated with LBD. Additionally, a definitive diagnosis of LBD can only be made post-mortem through the examination of brain tissue for the presence of Lewy bodies.

Effects on the Human Body

Lewy Body Disease has profound effects on both motor and non-motor functions, significantly impacting quality of life. Motor symptoms include bradykinesia (slowed movements), rigidity, tremors, and gait disturbances resembling those seen in Parkinson’s disease. Non-motor symptoms encompass cognitive impairment, hallucinations, fluctuations in attention and alertness, sleep disturbances, autonomic dysfunction (such as orthostatic hypotension and urinary incontinence), and psychiatric manifestations like depression and anxiety.

Treatment and Management

While there is no cure for Lewy Body Disease, various treatment strategies aim to alleviate symptoms and improve patients’ quality of life. Medications targeting dopamine levels in the brain, such as levodopa, may help alleviate motor symptoms. Cholinesterase inhibitors, commonly used in Alzheimer’s disease, may improve cognitive function and psychiatric symptoms in some LBD patients. Multidisciplinary approaches involving physical therapy, occupational therapy, speech therapy, and psychological support are essential for managing the diverse array of symptoms associated with LBD.

Takeaway

Lewy Body Disease presents a complex clinical picture characterized by the interplay of motor, cognitive, and psychiatric symptoms. Understanding its neurological underpinnings is crucial for early detection, accurate diagnosis, and effective management of the disease. Ongoing research efforts aimed at unraveling the molecular mechanisms underlying LBD pathogenesis hold promise for the development of targeted therapies that can ultimately improve outcomes for individuals living with this challenging condition.

I’ll jump back to the Lewy Body Dementia Association for the diagnostic symptoms of the disease.

Motor Symptoms

  • Bradykinesia (slowed movements)
  • Rigidity (stiffness)
  • Tremors (usually less prominent than in Parkinson’s disease)
  • Gait disturbances (shuffling gait, balance problems)

Cognitive Symptoms

  • Fluctuating attention and alertness
  • Memory loss
  • Executive dysfunction (problems with planning, organizing, and problem-solving)
  • Visuospatial difficulties (problems with spatial awareness and perception)

Psychiatric Symptoms

  • Hallucinations (visual hallucinations are particularly common)
  • Delusions (often related to the hallucinations)
  • Depression
  • Anxiety
  • Apathy
  • Irritability or aggression
  • Sleep disturbances (REM sleep behavior disorder, vivid dreams, acting out dreams)

Autonomic Dysfunction

  • Orthostatic hypotension (drop in blood pressure upon standing)
  • Urinary incontinence or urgency
  • Constipation
  • Erectile dysfunction (in men)

Other Symptoms

  • REM sleep behavior disorder (acting out dreams physically)
  • Sensitivity to neuroleptic medications (may worsen symptoms)
  • Changes in sense of smell
  • Difficulty swallowing (dysphagia)

Note that not all individuals with LBD will experience all of these symptoms, and the severity and combination of symptoms can vary widely from person to person. Additionally, symptoms may fluctuate over time, with periods of relative stability interspersed with episodes of worsening symptoms. Early recognition and management of these symptoms are crucial for improving the quality of life for individuals living with LBD.

Detecting and verifying Lewy Body Disease (LBD) involves a comprehensive approach that combines clinical evaluation, neurological assessments, and diagnostic tests. Here’s a breakdown of the steps involved in the detection and verification process.

Clinical Evaluation

  • A thorough medical history is obtained from the patient and their caregivers, focusing on the onset and progression of symptoms.
  • A neurological examination is conducted to assess motor function, cognitive abilities, and psychiatric symptoms. This may include assessing gait, muscle tone, reflexes, coordination, memory, attention, and mood.
  • Careful observation of symptom patterns, including fluctuations in cognition and alertness, visual hallucinations, and motor symptoms resembling Parkinson’s disease.

Diagnostic Criteria

  • LBD is diagnosed based on established clinical criteria, such as the consensus criteria proposed by the DLB Consortium or the McKeith criteria.
  • These criteria outline the characteristic features and diagnostic markers of LBD, including cognitive fluctuations, visual hallucinations, Parkinsonism, and rapid eye movement (REM) sleep behavior disorder.
  • Criteria may also specify supportive features, such as neuroimaging findings and autonomic dysfunction, which further support the diagnosis of LBD.

Neuropsychological Assessment

  • Neuropsychological tests are administered to evaluate cognitive function, including memory, attention, executive function, and visuospatial abilities.
  • These tests help quantify cognitive impairment and track changes over time.

Neuroimaging Studies

  • Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans may be performed to assess brain structure and function.
  • MRI may reveal patterns of cortical atrophy and changes in brain volume associated with LBD.
  • PET imaging with radiotracers targeting dopamine transporters or amyloid plaques can provide additional evidence supporting the diagnosis and differentiate LBD from other neurodegenerative disorders like Alzheimer’s disease.

Cerebrospinal Fluid Analysis

  • Lumbar puncture may be performed to analyze cerebrospinal fluid (CSF) biomarkers associated with LBD, such as levels of alpha-synuclein protein and markers of neuroinflammation.
  • While not routinely performed, CSF analysis can provide supplementary information to support the diagnosis of LBD in some cases.

Genetic Testing

  • Genetic testing may be considered in cases of familial LBD or when there is a strong family history of neurodegenerative diseases.
  • However, genetic testing is not typically performed as part of routine diagnostic evaluation for sporadic LBD.

Multidisciplinary Evaluation

  • A multidisciplinary team approach involving neurologists, neuropsychologists, geriatricians, psychiatrists, and other healthcare professionals is often utilized to ensure a comprehensive assessment and accurate diagnosis of LBD.
  • Verification of LBD relies on the integration of clinical findings, diagnostic tests, and adherence to established diagnostic criteria.
  • Given the complexity and variability of LBD presentation, accurate diagnosis and ongoing monitoring are essential for effective management and supportive care.

Treatment Options

  • LBD is a multi-system disease and typically requires a comprehensive treatment approach, meaning a team of physicians from different specialties, who collaborate to provide optimum treatment of each symptom without worsening other LBD symptoms.  ​
  • A comprehensive treatment plan may involve medications, physical, occupational, speech or other types of therapy, and counseling.

Medications

  • There are many treatments that can help with the symptoms; all medications prescribed for LBD are approved by the Food and Drug Administration to treat symptoms in other diseases, like Alzheimer’s disease and Parkinson’s disease.
  • These medications can offer symptomatic benefits for cognitive, movement, sleep, mood and behavioral changes in LBD.
  • There are not yet any medications that slow or stop the progression of LBD.

Cognitive Symptoms

  • Medications called cholinesterase inhibitors are considered the standard treatment for cognitive symptoms in LBD.
  • These medications were developed to treat Alzheimer’s disease. However, some researchers believe that people with LBD may be even more responsive to these types of medications than those with Alzheimer’s.
  • These drugs sometimes help control behavior problems and hallucinations as well.
  • Another medication that may be helpful is memantine (Namenda).

Movement Symptoms

  • Movement symptoms may be treated with a Parkinson’s medication called carbidopa/levodopa (Sinemet), but if the symptoms are mild, it may be best to not treat them in order to avoid potential medication side effects.

Visual Hallucinations

  • If the hallucinations are not disruptive, they may not need to be treated. However, if they are frightening or create challenging behavioral changes, a physician may recommend treatment.
  • Cholinesterase inhibitors are sometimes effective in treating hallucinations and other psychiatric symptoms of LBD. In addition, newer ‘atypical’ antipsychotic medications may be tried.
  • Most LBD experts prefer quetiapine or clozapine when treatment is necessary for safety or quality of life concerns.
  • Caution is required to find the lowest effective dose in this situation.
  • A newer medication, pimavanserin, was approved to treat psychosis in Parkinson’s disease; results from another clinical trial of this medication in people with dementia and psychosis are pending.
  • While older ‘traditional’ antipsychotic medications such as thorazine and haloperidol are commonly prescribed for Alzheimer’s patients with disruptive behavior, these medications may cause severe side effects in those with LBD.
  • For this reason, older traditional antipsychotic medications like haloperidol should be avoided.

WARNING: Up to 50% of LBD patients treated with any antipsychotic medication may have a severe reaction, such as worsening confusion, heavy sedation, and increased or possibly irreversible parkinsonism. If severe fever or muscle rigidity occurs, contact your doctor immediately; you may have a potentially life-threatening condition that is treated by stopping the medication.

REM Sleep Behavior Disorder (RBD)

  • RBD can be quite responsive to treatment, so your physician may recommend a medication like melatonin and/or clonazepam.

Medication Side Effects

  • Speak with your doctor about possible side effects.
  • The following drugs may cause sedation, motor impairment, or confusion:
  • Benzodiazepines, tranquilizers like diazepam and lorazepam
  • Anticholinergics (antispasmodics), such as oxybutynin and glycopyrrolate
  • Older antidepressants
  • Certain over-the-counter medications, including diphenhydramine and dimenhydrinate.
  • Some medications, like anticholinergics, amantadine, and dopamine agonists, which help relieve parkinsonian symptoms, might increase confusion, delusions, or hallucinations.

Surgery and Anesthesia

  • Be sure to meet with your anesthesiologist in advance of any surgery to discuss medication sensitivities and risks unique to LBD.
  • People with LBD often respond to certain anesthetics and surgery with acute states of confusion or delirium and may have a sudden significant drop in functional abilities, which may or may not be permanent.
  • Possible alternatives to general anesthesia include a spinal or regional block. These methods are less likely to result in postoperative confusion.
  • If you are told to stop taking all medications prior to surgery, consult with your doctor to develop a plan for careful withdrawal.

Other Types of Treatments

  • Lifestyle interventions include eating a healthy diet, exercising, and remaining socially active.
  • Physical therapy includes cardiovascular, strengthening and flexibility exercises, as well as gait training.
  • Speech therapy may improve low voice volume, poor enunciation, muscular strength, and swallowing difficulties.
  • Occupational therapy helps maintain skills and promotes functional ability and independence.
  • Music and aromatherapy may reduce anxiety and improve mood.
  • Individual and family psychotherapy may be useful for learning strategies to manage emotional and behavioral symptoms and to help make plans that address individual and family concerns about the future.
  • Support groups may be helpful for caregivers and persons with LBD to identify practical solutions to day-to-day frustrations and to obtain emotional support from others.

—   —   —

This might be a lot of cut & pasted material—some maybe repetitive—however I think it’s important to be aware of Lewy Body Dementia.

So far, LBD is incurable but somewhat manageable if detected early-on. Our population is aging. Today’s demographics represent an ever-increasing older population, and the numbers are that many of our folks and friends around us, including ourselves, will develop some form of a degenerative brain disorder like LBD which is what really killed Robin Williams.