These doctors seem to think that anything that puts sugar into the blood is bad, and not just bad, but more like the worst thing one can possibly do. A doctor that Dr. Mercola favors most highly is Dr. Ron Rosedale who claims that there is no need for dietary carbohydrate at all, that the body can make all the glucose it needs from protein, and that's the best way to get it. He really thinks it's best not to consume any carbohydrate. It is the most extreme carbo-phobia I have ever come across.
But, I won't expound further about their ideas, not when I'm paying the freight. You can look them up online if you want to. I'm here to refute them and to point out the things that they are not saying. A lie by omission is just as big as an outright lie.
Of course, it is true that when you eat a food that is sweet or starchy that it adds sugar to the blood. But, your body doesn't just look the other way when that happens; it deals with it. Your body has a steady-state, an equilibrium for blood sugar, just as it has an equilibrium for potassium, sodium, and many other things. Piling sugar into the blood is definitely a disturbance of homeostasis, and your body responds to it. But, "disturbance" may be too strong a word because we are talking about a very normal, natural, everyday happening.
As soon as sugar starts entering your blood, your body starts sending it to the liver, where much of it is stored as glycogen. To give you an idea how much can be stored, the weight of the liver can rise by about 10% from a single meal due to glycogen storage. And if you are healthy and physically-fit, the process is very efficient. That stored glycogen becomes a steady source of glucose for the body between meals as your liver slowly releases it into the bloodstream to maintain a constant level of blood glucose. Think of it like a thermostat.
How efficient is the process? It depends on how healthy you are. If your liver is healthy, it can store a lot of sugar and quickly. But, if it's diseased, say with fatty degeneration, then then the process is impaired. But that would not be the fault of carbohydrates. Or, if it's knarly and fibrotic from cirrhosis, glycogen synthesis and storage will also be impaired, but again, that would not be the fault of carbohydrates. And regarding the ability of muscles to make and store glycogen, it depends on how large the muscles are and how fit they are. The larger the muscle is, the more glycogen it stores. That is not to say that you need muscles as large as Arnold Schwartzenegger's. But, reasonably well-developed muscles are definitely a plus when it comes to sugar storage. And the more fit you are, the more accustomed you are to physical exertion, the more avidly your muscles store that glycogen. Therefore, if you have a healthy liver and strong, well-developed muscles, your tolerance for carbohydrates should be very substantial. You should be able to eat a lot of carbohydrate with only a modest and temporary rise in blood glucose.
So, the question becomes: does a diet based on fat and protein, with practically no carbohydrates, result in healthier blood sugar levels than a diet high in unrefined carbs? It might seem like a no brainer that a low-carb or no-carb diet would be better in that respect, but don't be so sure. Dr. Mercola provided no clinical data about it, only fearmongering. And what about Dr. Kempner at the Rice House at Duke University? For decades, he put diabetics on a diet of rice and fruit to correct their diabetic condition, and he often got them off medication. How did that happen? Well, they dropped so much weight, and I mean fat-weight, that their insulin resistance went away, and so did their diabetes.
So, besides having a healthy liver and fit muscles, the other thing that fosters tight blood sugar control is leanness. Having low body fat is necessary to keep insulin sensitivity sharp. When there is lots of body fat, then insulin resistance sets in, which means that glucose can't enter liver and muscle cells to be stored as glycogen. It's like the body is so overloaded with the fuel known as fat that it resists havng the fuel known as glycogen stored. So, there has to be leanness for the body to sanction the whole process. Diets high in unrefined carbs, meaning whole natural starches and intact whole fruits, support and encourage leanness. And that's why high-carb diets can actually help to improve blood sugar control.
But, let's get back to the question of which diet actually works better in terms of glucose tolerance. First note that in order to make the comparison fairly, you would have to compare diets that were calorically equal. Obviously, if you had a low-carb meal that consisted of leafy green salad, cooked non-starchy vegetables, and a very small amount of meat or fish, it would likely raise the blood sugar a lot less than eating a whole pot-ful of beans and rice. The best approach would be to serve the same amount of salad and non-starchy vegetable to both parties, and then feed one the animal food and the other the equivalent in calories in, say, beans and rice. Who would win that contest? I think the plant fare would win, and I can tell you that attempts to remove carbohydrate from the diets of diabetics and just serve them protein and fat to control blood sugar have FAILED MISERABLY. Why? First, realize that just as the body can easily store glucose as glycogen, thereby removing it from the blood, the body can also very easily convert amino acids and the glycerol portion of fat into glucose, thereby adding sugar to the blood. So, if there are excess calories from protein and fat coming in, those excess calories can easily be converted into sugar. That process is known as gluconeogenesis.
And, you can't just look at the immediate effect on blood sugar; you have to look at the long term effects. It is widely known that high-protein/high fat/low carb diets do not support physical and athletic activity very well. The number of elite athletes who avoid carbohydrates, to the extent that Dr. Mercola and Dr. Rosedale recommend, is virtually zero. I just finished reading the biography of Lance Armstrong, winner of 7 Tour de France bicycle races, and I learned that before and during races, he loaded up on carbs: pasta, potatoes, rice, etc. Name me one top-tier elite endurance athlete who lives on salad and meat? You can't. There aren't any. That's because the body runs on carbs.
So, what I am getting at is that it's not just the food you are putting in- it's the activity you are putting out. And diets high in unrefined carbs support that output VERY WELL.
I am taking the liberty of posting the newsletter of another doctor, Dr. Uffe Ravnskov, of Sweden, whom I am happy to say is an acquaintance of mine, although I have never met him in person. Dr. Ravnskov is probably the foremost and most highly respected cholesterol skeptic in the world today.
He shows in the article that the most recent testing of high-dose cholesterol-lowering statin drugs was a complete failure. And he also reveals the conflicts of interest that existed. I find it appalling.
Parts of it are very technical, but you can gloss over the technical parts and still grasp what he is saying.
It is a long article, so I will just turn it over to Dr. Ravnskov- with my thanks.
November 2011 Newsletter of Dr. Uffe Ravnskov
The New England Journal of Medicine recently published the results of the SATURN trial. It was designed to study the effect of atorvastatin (Lipitor) vs. rosuvastatin (Crestor) on the volume of atheroma in a coronary artery. It was hoped that the volume would be reduced, demonstrating that high dose statins can decrease the burden of atherosclerosis.
Initially 1578 patients were selected for the trial, but after a run-in period of 2 weeks where they were treated with half-maximal doses of either atorvastatin or rosuvastatin, 193 patients were excluded. The rest were treated either with 80 mg atorvastatin or 40 mg rosuvastatin. After 2 years of treatment a further 346 patients had disappeared.
Before and after the trial the patients underwent intravascular ultrasonography to measure the lumen diameter and the total diameter of a coronary artery. Subtracting the lumen area from the total area of the artery is thought to reflect the total atheroma volume, (represented as the percentage atheroma volume). The primary endpoint was to measure the reduction in percent atheroma volume
After the treatment the lumen had increased on average by 0.99 % in the atorvastatin group, and by 1.22 % in the rosuvastatin group, and the per cent atheroma volume (eg. the area of the arterial wall) had decreased by 1.1 % and 1.3 % respectively.
There was also a secondary end-point. However, I must admit that I did not understand what it meant, and if anyone does, please explain it to me. Here is what the authors wrote:
“A secondary efficacy end point, normalized total atheroma volume (TAV), was calculated as follows:
TAVnormalized = ? (EEMarea ? lumenarea) x median no. of
no. of images in pullback images in cohort
For TAV, the summation of the EEM area minus the lumen area is performed first. This value is divided by the number of images in the pullback and then multiplied by the median number of images in the cohort. The average plaque area in the pullback was multiplied by the median number of images analyzed in the entire cohort to compensate for differences in segment length between subjects. The efficacy end point of change in normalized TAV was calculated as the TAV at 104 weeks minus the TAV at baseline. Regression was defined as a decrease in PAV or TAV from baseline.”
Anyway, the critical measure was the difference between the inner and outer area of the artery. Unfortunately, there is no evidence that the figure from this calculation reflects atheroma volume. For example, vascular dilation will increase the inner diameter, without having any effect on the thickness of the arterial wall. But this would result in an apparent decrease in atheroma volume. To further understand what I mean, read the following section from my book Fat and Cholesterol are GOOD for You!
The anguish of angiography
Let us still have in mind, that a change of the coronary diameter is nothing but a surrogate outcome. It is assumed that a widening of a coronary vessel on an X-ray means less atherosclerosis and thus a better chance to avoid a heart attack, but this is only an assumption.
Artery walls are surrounded by smooth muscle cells. When such cells contract, the artery narrows. When they relax, it widens. Various factors may stimulate the smooth muscle cells of the coronary arteries. Most important, mental stress, anxiety, exposure to cold, and even a sustained handgrip may lead to contraction. The latter effect was studied six years earlier by Dr. Greg Brown, the same Dr. Brown who led the angiographic trial mentioned above (1). He found that a handgrip sustained for a few minutes was followed by a 35 per cent decrease of the vessel diameter.
Consider that the changes seen in the trials were only a few per cent on average. What do you think you would do yourself if somebody were to put a long catheter all the way from your groin up to your heart and into your coronary vessels? If you are not a stuntman or an astronaut I think that you probably would have gripped the nurse's hand or something else very tightly.
Also, drugs which relax the coronary vessels, and which are used by almost all coronary patients, may have disturbed the study. In the trial Dr. Brown and his coworkers were aware of that problem. The use of such drugs was "duplicated as exactly as possible." This can't have been too easy because the level of any drug in the blood depends on a large number of factors, which are difficult to standardize. And Dr. Brown and his colleagues didn't write anything about duplicating possible handgrips or anxious feelings because such duplication is, of course, impossible. So, any factor which may influence the state of the smooth muscle cells in the coronary vessels may have influenced the vessel diameter much more than the possible appearance or disappearance of a tiny amount of cholesterol.
There are more uncertainties. Dr. Seymor Glagov and his colleagues from University of Chicago studied the hearts of 136 deceased individuals and found that when vessels become sclerotic, they widen to compensate for the narrowing brought about by the deposition of cholesterol in their walls. In fact, this widening overcompensates for the deposition until the cholesterol deposits occupy about 40 per cent of the area beneath the muscle wall. Only thereafter does the vessel become steadily narrower. In other words, an increase of vessel diameter may be due to disappearance of cholesterol in a highly sclerotic vessel, but also to a compensatory widening during the first stages of cholesterol deposition. How could the trial directors know whether the increase of vessel diameter was due to a disappearance of deposited cholesterol, or to a compensatory widening due to an appearance of deposited cholesterol or due to less anxiety at the second angiography?
In short, the degree of arterial dilation is a massive and uncontrolled variable in the SATURN study. This problem could have been solved if the investigators had included a placebo group (a group of patients who unknowingly received an ineffective pill). However, “It was not considered ethically possible to measure disease progression in placebo-treated patients”, as they wrote.
There were other major problems with this study. The issue of drug related adverse events is extremely important. This was virtually dismissed within the paper. “Both agents had acceptable side-effect profiles”.
Can this be true. A more detailed review of adverse events reveals that “new proteinuria”, defined as an excretion of more than twice the amount of protein in the urine during the follow-up, in 1.7 and 3.8 %, respectively in the two groups. An increase in proteinuria is a measure of progressive damage to the kidneys. This trial only lasted two years, so we don´t know what would have happened in the longer term.
Equally it was stated that less than two per cent had laboratory signs of liver damage. However, liver damage was only recorded if the laboratory signs were at least three times higher than the upper limit of the normal range. And whilst less than two per cent had muscular damage, this was only reported if the laboratory signs were at least five times higher than the upper limit of the normal value. What do you think will happen with the liver and muscles of patients whose laboratory signs were “only” twice or four times higher, respectively?
In the end a further 22 % of the patients had disappeared. The reasons were said to be preference of patient (7.7% and 7.8 %), adverse effects (7% and 6.5 %), loss to follow-up (1.3% and 2.9 %) and noncompliance (2.3% and 1.9 %). What they meant with “preference of patient” I don´t know, but I am confident that “non-compliance” and perhaps also “loss to follow-up” represent those who could not tolerate the medication. Thus, whilst the authors claimed that ‘both agents had acceptable side effect profiles,’ the reality is that 12% could not tolerate these agents at the start of the study, and another 23 % dropped out – most likely to due to intolerable adverse events.
My summary of the SATURN study would be that it used a primary end point that has never been properly validated, and can be affected by a host of confounding variables e.g. stress . This variability could only have been controlled for by including a placebo arm, which was not done. Therefore, the result is rendered meaningless.
More importantly, it would appear that the burden of adverse events from using high doses of statin drugs is unacceptably high. It is likely that more than a third of patients will be unable to tolerate 80 mg Atrovastatin, or 40 mg of Simvastatin. All of this suffering in order to have an uncertain effect on a surrogate end-point, which may or may not mean anything.
Finally, I should mention that the study was supported by AstraZeneca, and most of the results were in favour of their drug rosuvastatin, although most of the differences were not statistically significant. I shall leave you with a list of the authors´ conflicts of interest:
Dr. Nichollsreports receiving consulting fees from Roche, Esperion, Merck, Omthera, Sanofi-Aventis, and Boehringer Ingelheim, serving as an unpaid consultant for Abbott, Pfizer, LipoScience, Novo Nordisk, AtheroNova, and CSL Behring, receiving grant support from Eli Lilly, AstraZeneca, Novartis, Anthera, LipoScience, Roche, and Resverlogix and lecture fees from AstraZeneca and Roche; Dr. Ballantyne, receiving grant support from Abbott, Astra-Zeneca, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Kowa, Merck, Novartis, Roche, Sanofi-Synthelabo, and Takeda, consulting fees and honoraria from Abbott, Adnexus, Amarin, Amylin, AstraZeneca, Bristol-Myers Squibb, Esperion, Genentech, GlaxoSmithKline, Idera, Kowa, Merck, Novartis, Omthera, Resverlogix, Roche, Sanofi-Synthelabo, and Takeda and lecture fees from Abbott, AstraZeneca, GlaxoSmithKline, and Merck; Dr. Barter, holding an advisory board position for AstraZeneca, Merck, Roche, CSL Behring, and Pfizer, receiving grant support from Merck, consulting fees from CSL Behring, and lecture fees from AstraZeneca, Kowa, Merck, Pfizer, and Roche; Dr. Chapman, receiving grant support from Merck and Kowa, consulting fees from Merck and Pfizer, and lectures fees from Merck and Kowa; Dr. Erbel, receiving grant support from the Heinz Nixdorf Foundation and the German Research Foundation and support for travel, accommodations, or meeting expenses from Biotronik, Sanofi, and Novartis; Dr. Libby, serving as an unpaid consultant for Novartis, Johnson & Johnson, Amgen, and Roche, serving in unpaid leadership roles for clinical trials sponsored by AstraZeneca, GlaxoSmithKline, Novartis, Pfizer, Pronova, and Sigma Tau, and having previously received royalties from Roche for the patent on CD40L in cardiovascular risk stratification; Dr. Raichlen, being an employee of and owning stock in AstraZeneca; and Dr. Nissen, receiving consulting fees from Eli Lilly, grant funding from AstraZeneca, Pfizer, Novartis, Karo Bio, Novo Nordisk, Takeda, Resverlogix, and Omthera, and support for travel, accommodations, or meeting expenses from Novo Nordisk, Takeda, Karo Bio, Eli Lilly, Pfizer, Novartis, and Amgen. No other potential conflict of interest relevant to this article was reported.
It is a sad fact that this report has been accepted for publication in The New England Journal of Medicine considered the leading medical journal in the world Either the editors and referees did not do their jobs, are not qualified for their tasks, or they have been blinded by Mammon.
There are more miserable news. Recently an expert panel appointed by the National Heart, Lung and Blood Institute and endorsed by the American Academy of Pediatrics has published new guidelines according to which every child in the United States should be tested for high cholesterol between ages nine and 11 so steps can be taken to prevent heart disease later on.
Such crazy thoughts have been aired several times in the past. In a letter to The Lancet (published on January 1, 2000; a good start of the new millennium). I tried to explain why this is a most dangerous idea, but obviously the letter made no impact.
How can an expert panel produce such malicious recommendations, you may ask. Because they are paid by the industry, of course. Read for instance Larry Hustens report or the one from the non-profit organisation Integrity in Science
I’m sure that everyone has heard that the world’s most beloved old curmudgeon died last week, Andy Rooney. It almost seems that Andy Rooney was born to be old. I’ve seen pictures of him as a young man, but it’s strange to see them because his public identity, his celebrity, was based entirely on his being old. And as old curmudgeons go, I think he was clever and cute. But, my favorite master of acerbic wit will always be H.L.Mencken. Mencken died in 1956, which was within my lifetime, but before my awareness. But, I became aware of him years later, and as crotchety, grouchy, old contrarians go, Mencken is still tops in my book. He tackled subjects Andy Rooney wouldn’t touch.
But, Rooney lived long, to 92, which is pretty old. And he was quite a bit overweight, which doesn’t usually accompany great age. And, I’m sure he was a conventional eater, which is never very promising. And he was, obviously, not a fitness buff. So, he was very lucky indeed to live so long.
But, it sounds like his luck ran out at the end. He was old, but he didn’t have any terminal illness that we know of. He did his last stint on television just a couple of weeks before he died, and he seemed fine. Yet, he soon died and unexpectedly after what was called a “minor surgery.” So, what happened?
As I see it, there are essentially two ways to die, (not counting trauma): You can die suddenly and quickly of a catastrophic event, such as a heart attack or stroke, OR, you can die slowly and haltingly of a protracted illness, such as cancer or diabetes. Clearly, Andy Rooney did not die the latter way because if he had, they would have said so. In fact, they said the opposite, that he did not have any such dire problems. And if he had suddenly had a heart attack or stroke, I’m sure they also would have said so, as they often do. So, what does that leave?
It leaves iatrogenic death. They did say that there were “major complications” from the “minor surgery” that he underwent. They aren’t providing any details. But, what are the possibilities?
It could have been a drug reaction. I have to assume that he received general anesthesia, and that involves taking many drugs simultaneously and sequentially. And they are, of course, drugs that affect not only consciousness, but also heart action, respiration, blood pressure, etc. In a 92 year old man, that’s dicey. It’s always dicey. A very popular anesthetic in use today is propofol- the drug that allegedly killed Michael Jackson.
I do not know what Andy Rooney’s problem was. But, what I do know is that he was nowhere near dying before that surgery, and now he’s dead. I think the lesson is that if you are very old, you do not submit to general anesthesia unless you absolutely have to.
Another possible cause of his death was severe infection- either as a consequence of the surgery or just from being in the hospital. Infection is always a major risk in the very elderly. And if he developed a severe infection and they gave him strong antibiotics, he could have died from that, as Christopher Reeves did.
Were blood thinners involved? I don’t know, but if for any reason he was taking blood thinners before the surgery, it could have had a catastrophic effect.
I could continue to speculate, but I think the point has been made: there is plenty that can go wrong from operating on the elderly. And the doctors aren't talking; they’re not saying anything except that he had “major complications” which makes it even more eerie. Is it a matter of family privacy or a matter of damage control for the doctors and the medical industry? I certainly don’t know, but what I do know is that if I’m lucky enough to make it to my 90s, I am going to leave well enough alone. Hey, I’m in my 60s, and I already feel that way.
This coming Tuesday, November 22, will be the 48th anniversary of the murder of President Kennedy. I hope that a lot will be said and written about it. And to the Occupy folks in Dallas, I really think they should move their occupation over to Dealey Plaza. Occupy Dealey Plaza because what happened in Dealey Plaza in 1963 has more to do with all that is wrong in America today than anything that ever happened on Wall Street.
I have been a student of the JFK assassination for a long time, and I have read a lot of books about it, most recently JFK: Analysis of a Shooting by Orlando Martin, who looked at it from his perspective as an expert on ballistics and firearms. Another was Head Shot: The Science Behind the JFK Assassination by G. Paul Chambers, who looked at it from his perspective as a physicist.
But now, to commemorate the assassination, I want to look at the Zapruder film from my perspective – as a chiropractor.
Note that there is a lot controversy, even among conspiracy theorists, about the proper interpretation of the Zapruder film. And, some analyses delve into very minute and arcane elements of it. But, I intend to skip the minutia and just look at the broad, basic elements of it. I mean the things that stand out to the naked eye upon one viewing. They really tell you all that you need to know to draw valid conclusions.
There is a convenient dividing point in the Zapruder film: the Stemmons freeway sign, which temporarily puts the limousine out of view. Before the limousine passes behind that sign, President Kennedy is waving and smiling at the crowd, and it appears that all is well. So, let’s assume it is. And then, as soon as the limo emerges from behind the sign, his hands go up to his neck, and he is obviously in distress, and it is from having been shot. That’s very clear. There is no other reason why his hands would go up like that. Something happened to his neck, and that something is that he got shot. It’s not like he was snacking and starting choking on some food. Nobody is suggesting that. Everybody, on all sides of the debate, agrees that he is reacting to having been shot. To put a number on it, we are talking about frame 225 in the Zapruder film.
It will be helpful if you go to http://assassinationresearch.com/zfilm/ and bookmark it. It has every frame of the Zapruder film as stills. So go to that page and click on the box that says 225, and you’ll see Kennedy’s hands starting to go up. That is the first visible sign of his reaction to having been shot. You will notice also that Jackie is looking directly at him. She must have been aware that something was wrong.
Now continue viewing the successive stills, say, through 235. What you see is that he continues raising his hands up, and not just his hands, but also his arms. His elbows are out, so really, he is raising and lifting his entire upper extremity, on both sides. A lot of muscles have to be working in order to do that. Notice also that he is not leaning backward against the seatback. He is sitting upright and unsupported, or I should say, self-supported. If anything, he is leaning slightly forward. Whether his jacket is touching the back of the seat at all, I really can’t tell, but what I can tell from his overall inclination, is that he is supporting his own weight. He is, as we say, "standing on his sit-bones" which refers to the ischial tuberosities. He is supporting his own weight against gravity. He is not leaning against anything.
And in that series from 225 to 235, look at his "head/neck relationship." It’s good. Posturally speaking, it’s very good. There are millions, and perhaps billions, of people who don’t have that good a head/neck relationship even when they haven’t been struck by a bullet. What I am referring to is the balance, symmetry, and coordination between his head and his neck, and it’s very good.
Realize that the head does not sit squarely on the neck like a pumpkin on a pole. It doesn’t just plop there like a heavy weight compressing the spine. There is a very small pivot point between the head and neck (the atlanto-occipital junction) and two-thirds of the weight of the head is forward of that small articulation, and only one-third is behind it. So, with optimal functioning, there is a natural forward inclination of the head in relation to the neck. And, it’s very important because it takes the weight of the head off the spine, allowing the neck to lengthen, and it also fosters mobility. Through proper muscular balance, the head is suspended – freely – in front of the neck in a fluid, mobile, and coordinated way. That is what is called a good head/neck relationship, and that is what you see in Kennedy.
But, many people have a faulty head/neck relationship, and it because, over time, they become contracted and shortened and tightened, and they habitually pull their head back and lock it onto the neck – effectively freezing the whole mechanism. But again, Kennedy was doing very well in that respect – even in the midst of everything that was happening to him. Through it all, he was maintaining excellent head/neck coordination.
Now, how does that relate to the official story? Well, the official story is that Kennedy was shot in the back of the neck with a big, fat, high-powered bullet that went coursing through his neck from back to front, exiting his body right below his Adam’s apple, and turning his body into a veritable donut. Keep in mind that having your body traversed by a bullet is always a dangerous thing, but some places are more dangerous than others, depending on what’s there. The neck is a very bad place for it to happen. Obviously, a bullet going through your head or your heart would be worse because that would kill you instantly. But, the neck is probably the third worst place for it to happen. And that’s because of what’s there. You’ve got the spinal cord there. And considering how central the shot was, I don’t see how it could have missed the spinal cord.
The bullet, allegedly, exited the front of his neck right in the center – dead center. And it, allegedly, (according to Arlen Specter and Gerald Ford) entered the back of his neck a little to the right of center. There is controversy about that, and there is solid evidence, including photographic evidence, that the back entry wound was much lower. But for now, we are going with the official story, which is that the bullet entered the back of his neck and exited the front of his neck.
So, it was a very central course, and we know what is in the center of the neck: the spinal cord. And the course must have been central because if it had been lateral, there are major blood vessels there, the carotid arteries and the jugular veins, and if any of them had been hit, he would have lost blood pressure to his brain and collapsed right away from circulatory failure. There is no way he would have remained sitting and supporting his weight – never mind with above-average postural balance and neuromuscular integrity. No, his major blood vessels were definitely not ruptured, which means that the bullet would have had to have gone down the middle and cut through the spinal cord.
So, with such an injury, how was he able to continue to sit there? We all know what happened to Christopher Reeve when he fell off a horse and broke his neck and severed his spinal cord. He immediately, instantly lost consciousness, and he would have died very soon thereafter if not for rapid and heroic medical and surgical intervention.
And let’s consider that such a bullet would also have demolished Kennedy’s voice box. Nellie Connally, the wife of Governor Connally, who was riding with her husband in the jump seat in front of the Kennedys, told the Warren Commission that after being shot, JFK said "My God! I’m hit!" Could he have said that if he was injured in the way reported?
Keep in mind that the fatal head shot didn’t come until much later: Zapruder frame 313. You can see it plain as day: a big red explosion at his right temple. But, from 225 to 312, Kennedy goes on sitting there and supporting his weight and staying in rather good postural balance. He leans towards Jackie some, but hey, he was hurting, and she was his wife. That’s what people do when they’re hurt; they seek comfort from someone they know. And he is also leaning more forward; you could say that he is slumping some. But still, his head/neck relationship isn’t bad. There is still good continuity there. His head is leading, and his body is following, which is how it should be. No way has this guy had a bullet pass clear through his neck. No way, no how, no chance. It isn’t even debatable.
I’ll tell you what: if there is a pathologist or neurologist or any other kind of qualified doctor who wants to make the case that Kennedy’s actions and responses, what we can see on the Zapruder film, particularly his neuromuscular responses and his postural performance, after being shot are consistent with having had a 6.5 mm full-metal jacketed, military round traverse his neck from back to front, I’ll post it on my website. That I would like to read.
Remember that when Arlen Specter came up with the Single Bullet Theory, the public had not yet seen the Zapruder film. And, there was no intention of making it public. But, it eventually came out, and the first television showing was in 1975. But, that was twelve years after the assassination. Would they have ever tried to claim the single bullet theory if the Zapruder film had been widely shown immediately? I don’t see how. Until the fatal head shot which blew his brains out, Kennedy looks too good. He functions too well. His body, his whole organism, is working too well. Nothing was cut between his head and his neck. All the channels of communication were working. That’s obvious. He would have been incapacitated, but he wasn’t.
Have you any idea how ridiculous, how totally ludicrous and whacky it is to suggest that Kennedy could go on sitting there, breathing, talking, supporting his weight, maintaining his balance, his blood pressure, his muscle control, and even his posture, with a bullet hole tunneled through his neck from back to front? It is insane.
But now, let’s look at Connally because he was part of the Single Bullet Theory as well. Supposedly, the bullet that exited Kennedy’s neck impacted Connally and went right through his rib cage and out his chest, and at the speed it was travelling, it would have been virtually simultaneous. We should see Connally reacting at the same moment as Kennedy.
Go back to Zapruder 225. Kennedy is raising his hands, so he has been hit, and Connally is turning a little to the right. Connally said that he turned to the right not because he was hit but because he had heard the sound of gunfire which seemed to come from behind his right shoulder. So, he turned to check it out, and that’s all that was going on with him at the time. That’s what he claimed, and that’s how it appears.
The bullet that went through Connally was a powerful blast. Consider that after traversing him, it, allegedly, still had enough energy left to strike his wrist and demolish his radius, which is a thick, heavy bone, a veritable club. So, we would expect a force like that to impact him in a big and noticeable way.
So for Connally, we are looking for two things: a reaction in his face, and a reaction of his body.
As I view 225 to 235, Connally turns to his right and then turns back to center, but there is no sign of any disturbance in him. In his face, he doesn’t seem to be acting out, but I admit that I can’t see his face that well. So, I have to rely primarily on the movement of his body, and there is nothing irregular about it. There is nothing startling. There is no break. He does not seem to have been impacted by anything.
But then, there is a break. But, first note that he is holding the blue Stetson hat the whole time. Would a man who was already blasted through his chest on the right side continue to hold his hat in his right hand?
Now compare 234 to 236. I am skipping 235 just for the sake of clarity, but you can look at that too if you want. But, what you see in 236 is that Connally is suddenly twisting to the right; his left shoulder is pinched, raised; his right shoulder is depressed. He is turning to the right, and he is also laterally bending to the right. He is getting gnarled up. This is happening very fast. Each frame of the Zapruder film covers just 1/18 of a second, but the frames start changing distinctly from one frame to the next after that.
I downloaded frame 236 and then enlarged it. And when you do that, you can see that there is also a change in the countenance of Connally’s face. His mouth is open; he looks startled. Posturally, this is a man who is under extreme tension. He is really a mess posturally at this point. The balance, the equilibrium in his shoulders is completely lost. He looks agitated, discombobulated, flurried. It is in stark contrast to the preceding frames.
From that point on, he is moving rapidly. Each succeeding frame, 237, 238, 239, show him continuing to turn and twist. He keeps turning until he is facing the car door. He has turned 90 degrees by this point. And clearly, he is preoccupied with himself; he is not focused on Kennedy. By 255, he has passed the horizontal axis, and he may be able to see Kennedy. And it looks like has his left hand on top of the door, helping to support himself. He keeps turning around, and by 271, he appears to be looking at Kennedy. And, he looks at Kennedy for a good long while. Click through it frame by frame and you’ll see.
But, about 290, Connally starts turning back around from whence he came. And at the same time, he starts leaning backwards, like he’s having trouble sitting up. It’s like he is falling into his wife, and he is falling into his wife. Take a close look at the frames after 290. He is falling into Nellie with a pained look on his face. That’s another break. To me, that indicates when a separate bullet impacted his wrist.
By 300, he is leaning back into her markedly, and his mouth is wide open. And if you can’t see it clearly, you can tell that his mouth is open by the tractioning of his cheeks. At this point, he is totally absorbed with what is happening to himself and not to Kennedy. Frame 304 is a very clear shot. You can see that his mouth is open. He is in pain. He is probably audibly moaning and crying. Nellie is pulling him in close. At this point, Connally seems more incapacitated than Kennedy.
Then, the head shot hits Kennedy at exactly frame 313 with a big explosion at his right temple, and he goes back and to the left – not just his head, but his whole body. And he goes limp. He is totally out of it. And from then on, in the still frames, Connally and his wife are very much blurred, and I suspect it’s because the limo speeded away. Many reported that prior to the head shot, the limousine slowed to a crawl. Some said it came to a complete stop. But after the fatal head shot, it accelerated immediately and rapidly. It looks like Connally and his wife are ducking down as best they can. Then there is a long sequence involving Jackie’s trek across the limo and the Secret Service agent going to her aid, which put the Connallys completely out of view. And after that, the limo is speeding away so rapidly and at great enough distance that there is no discerning anything about the Connallys.
So, what do we make of all this? First, note that Connally’s chief thoracic surgeon, Dr. Robert Shaw, said that it was mostly likely frame 236 in which Connally first reacted to being hit. Here is his exact testimony from the Warren Report:
Mr. SPECTER – Dr. Shaw, have you had an opportunity today here in the Commission building to view the movies which we referred to as the Zapruder movies and the slides taken from these movies?
Dr. SHAW – Yes.
Mr. SPECTER – And what, if any, light did those movies shed on your evaluation and opinions on this matter with respect to the wounds of the Governor?
Dr. SHAW – Well, my main interest was to try to place the time that the Governor was struck by the bullet which inflicted the wound in his chest. This meant trying to carefully examine the position of the Governor's body in the car so that it would fall in line with what we knew the trajectory must be for this bullet coming from the point where it has been indicated it did come from. And in trying to place this actual frame that these frames are numbered when the Governor was hit, my opinion was that it was frame number, let's see, I think it was No. 36.
Mr. SPECTER – You mean, 236?
Dr. SHAW – Yes, 236, give or take a frame or two. 235, 236, 237.
What’s my take? Well, I couldn’t agree with him more. 236 is where the break occurs. That is where Connally first reacts, facially and posturally, and it is a very sudden break.
So, if Dr. Shaw is right, that Connally did not react until 236, whereas Kennedy was clearly reacting already by 225, it is a definite disconnect. We really don’t know when Kennedy began to react because he was concealed by the freeway sign until 225. But, he was definitely reacting as he emerged from behind the sign at 225.
So, that means that there is no way on God’s green Earth that Kennedy and Connally were reacting to the same bullet – not at the speed it would have been travelling. For all practical purposes, it would have been instantaneous. That interval between 225 and 236 is proof-positive that they were hit at separate times by separate bullets.
What does this mean for the current status of the Kennedy assassination? It means that we are living in a bizarro world. Kevin Costner was right; we are through the Looking Glass. Black is white; up is down; in is out. The official story has become so ludicrous, whacky, and incredible, and the evidence against it has become so indomitable and overwhelming, that it borders on insanity to continue believing it. The Kennedy assassination has become the elephant in the room, the emperor with no clothes. And I predict that as time passes, the mainstream media will withdraw completely from defending it. They will only speak about it in general terms. They will get psychologists to address the sociology, that is, the patho-sociology, of the JFK truth movement – as they do with the 9/11 truth movement. But, they are not going to sit down and debate particulars with the likes of Mark Lane, Jim Marrs, Orlando Martin, James Douglass, Phillip Nelson, Paul Champers or other Kennedy researchers. "Shut up, and believe what you’re told." That, in essence, will be all they’ll have to say.
A reader asked me about prescription blood thinners, such as Plavix. When I think of such powerful blood thinners, I think of the former Prime Minister of Israel, Arial Sharon. He is in a permanent vegetative state since 2006 from having been given a strong blood thinner (not Plavix) which caused a massive hemorrhagic stroke. It is amazing that he is still alive, although one has to assume that he doesn’t really have a life, and the most merciful thing might be to let him pass on. At the time, his doctors gave him a potent blood thinner because previously he had had a small ischemic stroke, and they were trying desperately to prevent another one. Keep in mind that Israel has one of the most advanced medical systems in the world, and he was the leader of the country, so unquestionably, he was getting the best medical care that money can buy. Still, this catastrophe happened to him.
And there have been similar catastrophes with Plavix. Right now, there are many class-action and independent lawsuits against the maker of Plavix- Bristol Meyers Squibb. There are quite a few lawyers who specialize in Plavix litigations. Here is one: http://www.plavixlawsuit.com. Gastrointestinal bleeding, other internal hemorrhaging, heart attacks, strokes and more have been linked to Plavix. It is going to take years for these cases to wind their way through the courts, and in the meantime, new cases will arise because Plavix is still widely prescribed (it is one of the bestselling drugs in the world) and more people will be similarly affected. So, this is now the normal landscape for pharmaceutical drugs of this kind: lots of prescriptions, lots of catastrophes, lots of lawsuits, lots of judgments and settlements, but still a lot of profit, and so it just keeps going and going and going.
And, I had a minor emergency with one of my patients relating to blood thinning. Be aware that just about everything you put in your body has a net influence as either pro-coagulant or anti-coagulant, including the foods you eat. For instance, green vegetables are high in Vitamin K1, which is a pro-coagulant. However, green vegetables are also high in natural salicylates, which are aspirin-like compounds, and the net effect of green vegetables is to have a blood-thinning effect. Well, a young Iranian woman came to my health retreat to lose weight. She had a congenital liver disorder which posed a danger of blood clots, so doctors had her on Wayfarin (also known as Coumadin) permanently. Coumadin is much weaker than Plavix, but it’s stronger than aspirin. I didn’t tamper with it. I just put her on a high fruit and vegetable, plant-based diet. The result was that in short order, she started bleeding. You could see the hemorrhaging underneath her skin. We rushed her to the ER, and her doctor in California was contacted. They gave her a shot of Vitamin K, and they had her temporarily discontinue the Coumadin. Slowly, the hemorrhaging receded, and when it was gone, the doctor had her resume taking a lower dose of Coumadin. In her case, the blood-thinning effect of the unrefined plant diet was added to that of the drug, and it was too much.
Plavix is much higher risk than Coumadin, and they use it in high-risk cases. Basically, it knocks out every platelet in your body. But, those platelets are there for a reason, and it isn’t to sabotage you. On the contrary, they are there to protect you. I realize that a patient may be at high-risk from his condition, but he will also be at high-risk from taking Plavix. So, it is truly a devil’s gambit.
Obviously, the goal should be to never let oneself to get into such a dire state that such a stark choice becomes a reality.
Still, it is a fair question to ask: what would I do if I faced such a choice? I will answer that, but first I want to emphasize that I am only speaking for myself. I do not pose this as advice to anyone else. I am not speaking generally about what others should do. My advice to others is to work with a doctor whom they can trust- and hopefully one who is broadly educated and not just a pharmaceutical shill. But, I think I know myself well enough to realize that I would never be comfortable taking a drug like Plavix, and I don’t think I would ever do it. I would take my chances going without it. But, it doesn’t mean that I would do nothing. Here is what I would do if I thought I was at risk for having a deadly or catastrophic clot:
First, I would certainly be willing to take natural blood thinners, such as Vitamin E, fish oil, and turmeric. I already take those things as part of my daily program, but, I would increase the doses if I thought I was at risk for a clot. And I would be open to taking aspirin. And, I am sure I would consult with physician friends of mine, such as Dr. Joel Fuhrman and Dr. Ward Dean. I have already discussed this matter with Dr. Dean- although not concerning myself- and he told me that using natural blood thinners and other nutritional and lifestyle measures, that the only blood-thinning drug he ever has to resort to, even in advanced cases, is aspirin. He never prescribes Plavix or the likes of Plavix. That is heartening to know.
And, I would be very diligent about my food, casting aside anything suspect. And I would also consider fasting, which has its own blood-thinning effect.
But, I have no expectation of facing such a predicament. I am confident that the actions I am taking now to safeguard my health will keep me far removed from having blood clots. The idea is to never get anywhere near that territory.