Section 3: Diabetes and Cholesterol: The invisible disease and the friendly enemy

Part 1: Article by Atomic Dog

Source: book named Open Heart by Jay Neugeboren. (He underwent cardiac surgery, a quadruple bypass, and researched this thoroughly) and Atomic Dog (www.t-nation.com )

More than a third of individuals who have heart attacks have normal cholesterol. If you look at all the studies, you’ll find no evidence that lowering cholesterol prolongs life. Disturbingly, there’s a consistent and mysterious increase in deaths from other causes when you reduce cholesterol. And, get this, once you drop cholesterol below 180 mg/dl, the death rate increases.

Yet, every two years, experts from around the world meet and decide that the normal and accepted cholesterol level is lower than it was at the last meeting–without having any solid evidence to back it up.

Why is it that in the 1950’s no one even cared about cholesterol? And suddenly, we were afraid of it? Were we any more informed about our bodies? Had we undergone overnight evolution? Or did money greedy companies around that world fool us into this?

By the early 1970’s, each biochemical step of the chain from dietary fat to cholesterol to heart disease had been mapped out, but the legitimacy of the claim as a whole is no proven. The closest they’ve come is through a study in 1991 funded by the US Surgeon’s Office. They determined that if Americans cut the amount of saturated fat they ingested, they could delay 42,000 deaths each year. What does that mean? Well, if a woman who might otherwise die on her 65^th birthday, after avoiding saturated fat her entire life time, might live an additional two weeks.

“Of course, two weeks is nothing to sneeze at, because it might allow her to live long enough to find out if the father of Brook’s baby is really Bobby on The Bold and the Beautiful.” (props to Atomic Dog on that one. Indeed this whole section is his)

So where does the cholesterol myth originate?

You probably need to look no further than the drug companies that manufacture cholesterol drugs. A recent study involving the cholesterol-lowering drug cholestryamine (Questran) and 1900 patients found that out of those taking the drug, only 30 had a fatal heart attack. And the number of those not taking the drug that had fatal heart attacks? Thirty-eight. Statistically, that means the cholestryamine, over a course of seven years, reduced the chances of having a fatal heart attack by less than half a percent. However, the drug company interpreting the tests found it preferable to say that cholestryamine reduced the chances of dying from a heart attack by 25%. Sure, 8 fewer deaths out of a total of 38 patient is indeed 25%.

As they say, there are lies…and then there are statistics.

But even if cholesterol does lead to severe blockages, these blockages cause at most three out every ten heart attacks. While doctors almost across the board used to believe that heart attacks were caused by a build up of plaque that would eventually rupture and cause blockages, that isn’t necessarily the case anymore.

So what does cause heart attacks? It seems that if you combine all “known” (although the original article is chock full of information, I think it’s a little outdated, in that it still believes in the low fat diets of today) risk factors such as high fat diets, cholesterol, smoking, high blood pressure, markers for inflammation, and diabetes, they explain only half the risk of developing atherosclerosis.

The answer most often given to explain this conundrum is that it’s likely genetic, which, according to Dr. Rich Helfant, a cardiologist and friend of Jay Neugeboren, is another way of saying "We don’t know why these things happen."

Some researchers think that these inexplicable cases of heart disease have to do with fetal environment and research seems to confirm their belief: babies with a larger head circumference and a higher birth weight have less chance of developing heart problems during middle age. Furthermore, babies who weigh less than 18 pounds at a year old have a middle-age death rate that’s almost three times higher than those individuals who weighed more than 27 pounds at a year.

Still, there’s got to be more to it than that.

Then there’s the problem of diagnosis. "Put a patient with even the slightest set of maladies in front of five doctors, and you might get five different diagnoses, five different prognoses, and five different recommendations for treatment," explains Dr. Helfant.

A 1997 study involving 453 recent medical school graduates found that more than 20 percent of the time, the grads couldn’t identify common heart problems with a stethoscope. While that might not sound that bad given that the lay public probably considers the stethoscope archaic, this simple tool can be incredibly valuable in diagnosing heart problems.

While we seem to hold more technical diagnostic tools in high regard, the truth is much different. Neugeboren cites a British study that found that 75 percent of information leading to a correct diagnosis comes from detailed patient history; 10 percent comes from physical exam; 5 percent comes from routine tests; 5 percent comes from invasive tests; and 5 percent of the time no answers are found.

But perhaps, in one way, this epidemic lack of diagnostic success mentioned above isn’t as dire as it sounds because clinical trials that evaluate ways of treating heart disease are inconclusive. No, diagnostic ineptitude is dire in another way because whether a doctor recommends bypass surgery, angioplasty, drug therapy, or beating-heart surgery, the results are usually the same. The sobering fact is that even if a patient receives what the consensus considers to be optimal care and treatment, there’s less than a 50 percent chance that the patient will live longer than he or she would have without the treatment!

Even common lab tests are woefully inaccurate. Consider the common blood test for cholesterol. Helfant explains that if you send a blood sample to two different labs, there’s a strong possibility that you’ll get two different results. As an experiment, Helfant had the same lab repeat his cholesterol test on the same blood sample. The first time, the machine indicated that his total cholesterol was 152. The same sample tested a 176 mg/dl a few minutes later, a discrepancy of 17%

"If I had had a 17 percent rise, say from 200 to 234, 34 points above what’s considered to be normal, and I’d been seeing all those ads about cholesterol and heart disease, I might have gone on a cholesterol medication for the rest of my life, and who knows what the side effects would be for me down the road since we have no long-term studies of what these medications will do to us," said Helfant.

Neugeboren sums up this worrisome fact by writing, "The troubling news is that when a test is performed more often, the result is both fewer missed cases and more false positive results."

What do all these false positives and missed diagnoses mean? Well, according to Dr. Stephen Oesterle, director of interventional cardiology at Massachusetts General Hospital, over 50 percent of angioplasty performed each year in the US is unnecessary. That translates to over a hundred thousand needless and risky procedures every year. The other side of the coin is that some patients who really needed treatment are sometimes misdiagnosed and end up dying on a cold sidewalk somewhere.

Could there be something more at work in regards to some of these unnecessary procedures, something more sinister than simple ineptitude?

According to the January 2002 issue of The Journal of the American Medical Association, 9 out of 10 medical experts who make recommendations concerning the treatment of diseases like heart disease have financial ties to the pharmaceutical industry. Furthermore, these ties are rarely, if ever, disclosed.

Similarly, many cardiologists and cardiac surgeons own stock in companies that make cardiac stents, surgical instruments, catheters, and drugs. All too often they’re also involved in the clinical trials that examine the efficacy of these products.

So where does that leave us? Doctors for the most part can’t agree on what causes heart disease. Sure, there are some statistical probabilities that point to the wisdom of lowering blood pressure and cholesterol, but they don’t mean squat if you’re one of the 50 percent of men or 63 percent of women who die from heart attacks while not exhibiting any symptoms or strong risk factors. Similarly, the "correct" treatment is often based on widely varying opinion, outdated science, and even corruption and greed.

The only thing that doctors and scientists seem to agree on regarding heart disease is that it’s a disease of inflammation. What’s common to just about everyone who dies of a heart attack is a large collection of the white blood cells known as macrophages. These macrophages collect around fatty deposits and they secrete enzymes that digest protein. As you well know, the insides of blood vessels are made of proteins and in trying to eliminate the fatty deposits, the blood vessels are eaten away, made thinner, made more susceptible to rupture.

What surprised researchers, though, was that they found these macrophages in the arteries of vessels that had not ruptured–in presumably healthy arteries. This indicated that the inflammation was systemic and not localized. This may be why aspirin–which reduces inflammation–seems to be so valuable in thwarting heart disease. It might also explain why some statins seem to work—-not because they lower cholesterol–but because they have an anti-inflammatory effect.

No doubt, if you’ve read this far, I’ve pierced the veil of cardiac invulnerability you might have once had. You thought your exercise regimen, along with your low-saturated fat diet and admirable blood pressure had bulletproofed you against a heart attack.

Unfortunately, it’s just not so. So what are we left with? The troubling knowledge that we could keel over at any minute, the anticipated embarrassment of having died from something so common as heart disease?

"Geez, I always thought the son of a bitch was healthy. Just goes to show you all that exercise was for nothing."

I don’t have too much comfort to give. All I can recommend is that, if you’re ever faced with the prospect of cardiac disease, is that you find a doctor who listens carefully to your symptoms lest you be misdiagnosed with heartburn and sent on your way. I’d also recommend a second or third opinion from big-city, high-paid docs, even if some are corrupt.

As far as nutritional advice, I have to believe that avoiding saturated fats and trans fatty acids is still sound advice for everyone, but more than that, and given that heart disease seems to be a inflammatory disease, I’d recommend 80 mg. of aspirin a day (if you’re not at risk for hemorrhagic stroke), and 6 to 10 grams of fish oil a day, from wild sources (farm-raised fish have different fatty acid profiles).

Through my readings, both in the context of heart disease and nutrition in general, I think that fish oil is going to be the magic bullet against heart disease. I have to believe that. It’s a slender thread to hang my hopes on, but it’s better than nothing.

The above in italics is something that you can listen to if you want. But I believe I’ve made my point when I said fat actually stops the heart diseases, after all it never had anything to do with the heart diseases in the first place and messing with our diets has only compounded it. As for the advice with aspirin, whilst yes it helps, I find that messing with our bodies with drugs isn’t the best thing to do. I’m sure cavemen asked around for aspirin to ease heart conditions. Stupid.

Part 2: Saturated Fats and Cholesterol: The Raw Deal

Saturated fats don’t do anything in the way of heart disease. The levels in the blood should be roughly a 1:2 ration of HDL and LDL. (High density lipoprotein and low density lipoprotein respectively.) Because all those who die of heart disease seem to have Extremely high levels of LDL, LDL has been blamed for deaths. In other words the finger seems to point at LDL and this has become something of a “bad” fat now. However, nothing could be further from the truth.

Both fats have their own functions. I won’t go through them here, but suffice to say they both are important.

Excluding saturated fats will not reverse these deaths. Saturated fats and cholesterol will enter the bloodstream and be broken down with bile. If not, then it will be in the blood attached to its HDL. Whilst we may not think so at the moment, but saturated fats are extremely important to the body, in fact even a part of the small intestine produces it in small quantities for emergencies. Such is its importance and here we are swearing off meat and other fatty things in the claim that its harmful to our health. Anyways, back to the human body, when we drop low in HDL, our body produces in the liver LDL. Ironically, as our bodies have always had a moderately high fat diet, the body has no controlling mechanism for this and we spiral out of control and BOOM atherosclerosis.

So my opinion. It’s conjecture but its physiologically sound and a certain Dr. Harris also supports this view. Cholesterol and saturated fats are just imaginary enemies to our bodies when in fact they are our allies against the flab and bad health.

Population Studies of cholesterol and saturated fats

This is truly where we find the battle lines of international companies and the health of individuals. Suppressed information and other things that wouldn’t be amiss in a conspiracy movie abound in this section. (Warning: Not suitable if you believe every conspiracy theory and/or you are gay. Not suitable for children under 15 or for people who enjoyed Matrix: reloaded for that matter. May contain nuts.) All saturated fats have been blamed for many years as a cause of increased serum cholesterol levels, which supposedly leads to heart disease. But studies done on traditional tropical populations that consume large amounts of coconut oil (almost 100% Saturated BABY!) show just the opposite. One of the best ways to study the affects of coconut oil on human nutrition is to look at tropical populations that get most of their caloric intake from the saturated fat of coconut oil. Logic would dictate that if the saturated fat/cholesterol theory of heart disease and obesity were correct, those populations with the highest consumption of saturated fats would be the most overweight and have the highest rates of heart disease. Such is not the case.

According to a maverick female scientist Dr. Mary Enig who seems to have devoted her life to that most exciting of fruits; the Coconut, there is a study published in 1981 in which the populations of two South Pacific islands were examined over a period of time starting in the 1960s, before western foods were prevalent in the diets of either culture. The study was designed to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. Coconuts were practically a staple in the diets, with up to 60% of their caloric intake coming from the saturated fat of coconut oil. The study found very healthy people who were relatively free from the modern diseases of western cultures, including obesity and heart disease. Their conclusion: "Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations."

Another study was done on the Indian subcontinent comparing traditional cooking oils with modern oils in relation to prevalence of atherosclerotic heart disease and Type-II diabetes. Their conclusion: "In contrast to earlier epidemiologic studies showing a low prevalence of atherosclerotic heart disease (AHD) and Type-II dependent diabetes mellitus (Type-II DM) in the Indian subcontinent, over the recent years, there has been an alarming increase in the prevalence of these diseases in Indians--both abroad and at home, attributable to increased dietary fat intake. Replacing the traditional cooking fats condemned to be atherogenic, with refined vegetable oils promoted as 'heart-friendly' because of their polyunsaturated fatty acid (PUFA) content did: (absolutely JACKSHIT! to save our sub continental friends. The original content wasn’t like that. You see my point of course). Current data on dietary fats indicate that it is not just the presence of PUFA, but the type of PUFA that is important--a high PUFA n-6 content and high n-6/n-3 ratio in dietary fats being atherogenic and diabetogenic. The newer 'heart-friendly' oils like sunflower or safflower oils possess this undesirable PUFA content and there are numerous research data now available to indicate that the sole use or excess intake of these newer vegetable oils are actually detrimental to health and switching to a combination of different types of fats, including the traditional cooking fats like ghee, coconut oil and mustard oil, would actually reduce the risk of dyslipidaemias, AHD and Type-II DM."

Oh MAN! Not convinced? Here’s another slice of your “low cholesterol” ass on a plate courtesy of “see appendix for sources”.

When measurements of serum cholesterol (cholesterol levels in the blood) were first done, only the total of both HDL ("good cholesterol") and LDL ("bad cholesterol") were read. Now that testing has become more sophisticated, researchers look more at the balance of these two types of cholesterol. They note whether a substance raises cholesterol levels of HDL or LDL levels. In some cases, certain foods lower total cholesterol, but only by lowering “good” HDL cholesterol while at the same time actually raising levels of the “bad” LDL cholesterol. I’ll explain a little more about why “good” and “bad” makes this a very dangerous area of interest.

Faulty Science

In a lecture given in Viet Nam in 1996, our friend Dr. Mary Enig, she of the rebellious nature and hilarious coconuts, stated that “The problems for coconut oil started four decades ago when researchers fed animals hydrogenated coconut oil that was purposely altered to make it completely devoid of any essential fatty acids. The animals fed the hydrogenated coconut oil (as the only fat source) naturally became essential fatty acid deficient; their serum cholesterol increased. Diets that cause an essential fatty acid deficiency always produce an increase in serum cholesterol levels as well as in increase in the atherosclerotic indices. The same effect has also been seen when other highly hydrogenated oils such as cottonseed, soybean or corn oils have been fed; so it is clearly a function of the hydrogenated products, either because the oil is essential fatty acid (EFA) deficient or because of transfatty acids.”

Here we go again with coconut oil, you must understand that coconut oil is one of the few oils that is super saturated and just happens to be a staple in many tropical diets. What about studies where animals were fed unprocessed coconut oil? Enig, of the coconuts, wrote: "Host mark et al (1980) compared the effects of diets containing 10% coconut oil and 10% sunflower oil on lipoprotein distribution in male Wistar rats. Coconut oil feeding produced significantly lower levels (p=0.05) of pre-beta lipoproteins (VLDL) and significantly higher (p=<0.01) alpha-lipoproteins (HDL) relative to sunflower feeding.” She also cited a study by Awad (1981) on Wistar rats fed a diet of either 14% (natural) coconut oil or 14% safflower oil. She stated: “Total tissue cholesterol accumulation for animals on the safflower diet was six times greater than for animals fed the [anhydrated] coconut oil. A conclusion that can be drawn from some of the animal research is that feeding hydrated coconut oil devoid of essential fatty acids (EFA) potentate the formation of atherosclerosis markers. It is of note that animals fed regular coconut oil have less cholesterol deposited in their livers and other parts of their bodies.”

Enough of the coconuts.

Do Saturated Fats Clog Arteries?

Blamed for "clogging arteries" and leading to heart disease I’m sure that it’s proverbially “sad”. However to brighten up its proverbial “day” an examination of the research and science behind saturated fats leads one to a vastly different conclusion, suggesting that the attacks against saturated fats have been primarily political and economical, and not scientific nor ethical for that matter.

First of all, saturated fats are essential to our health. They comprise about 50% of our cell membranes (the phosphor lipids from biology), and some proportion of saturated fats are found in all fats and oils, whether seed based or animal based.

The anti-saturated fat campaign launched by the U.S. has resulted in the whole of the western nations eating less saturated fat. However, despite this, U.S. is one of the fattest countries in the world, if not the most. Australia in recent years has over taken it in terms of ratio. Looks like the bronzed surfer of the olden/golden days are long gone, replaced by the proverbial “horizontally challenged”. Many are now questioning the "wisdom" behind the low-fat nutritional advice that has dominated the popular media. Finally David H.Y. Tang’s proverbial “justice” to the rescue. I have been angry my friends…like “an old man trying to send soup back at a deli”.  

Does research support the claim that saturated fats raise cholesterol levels and clog arteries? No a thousand times no!!! This "lipid theory" of heart disease, which blames high cholesterol levels as causing heart disease, is seriously being questioned by researchers and doctors well at least the ones into coconuts and not into money. Malcolm Kendrick M.D., Dr. Mary Enig PhD of the coconuts., Uffe Ravnskov M.D., PhD, George Mann M.D., Sc.D, and many other top researchers have written extensively on the flaws of the “cholesterol theory” of heart disease. You can add to that list “Edward Kim” if you want to after I become a world famous magician. Although I must admit, most of the “conventional” medical convention seems to have a dislike for everything like this; they hate new age fools for their narrow minded opinions. Wonder if hypocrite means anything to those pompous bastards. Well, sure as hell doesn’t mean anything to those New Age hippies.

As to the research on "clogged arteries", a study was done at the Wynn Institute for Metabolic Research, London, examining the composition of human aortic plaques. This study found that the "artery clogging fats" in those who died from heart disease were composed of 26% saturated fat: the rest (74%) were polyunsaturated fatty acids, such as those found in vegetable oils commonly consumed in today's modern societies. Their conclusion: "No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favoring increased intake of polyunsaturated fatty acids should be reconsidered."

Not convinced? You stubborn bastard! Time to bust out the justice of myself with references from Robert Harris.

In all animals, there are two sources of cholesterol, humans not an exception. The sources are the liver, and of course the diet. Cholesterol derived from the diet enters the bloodstream and becomes immediately attached to high-density lipoprotein (HDL). HDL is body produced and is the active carrier protein that transports the cholesterol into the tissue cells where it undertakes its jobs. This cholesterol is referred to as HDL-cholesterol (HDL-C). So important is cholesterol derived from the diet (the sole source of HDL-C) that the wall of the small intestine (through which the dietary cholesterol passes on its way to the bloodstream) is able to produce small quantities of the HDL-cholesterol as a back-up if the level of dietary cholesterol drops too drastically. (This goes against the theory that we are herbivorous by nature. There is no cholesterol found in any plant material as it is animal derived.

The other major source of serum cholesterol, and by far the most prolific, is the liver. The liver produces a lot of cholesterol, but about 85% of that is converted into cholic acid, a bile salt, and deposited in the gall bladder. This cholesterol doesn’t/cannot/will not/and/or never will enter the bloodstream and hence shouldn’t be brought up in a discussion about elevated serum blood cholesterol. (For some reason it does…Poor Bastards.) The remaining 15% of liver cholesterol is tagged with the carrier low-density lipoprotein (LDL) to form LDL-cholesterol (LDL-C) and then released into the bloodstream.

Under normal conditions there should be a little over one-third HDL-C and a little under two-thirds LDL-C in the bloodstream. Together they should register around 195mg percent, or 4.8 milimoles per liter of blood, depending on the evaluation process used.

The body has two cholesterol monitoring and control devices. The first is the bile salt, cholic acid, which renders fat into a pre-digestible form. As there is a limit as to how much cholic acid the body can produce and use at any one time, this exerts a level of control over fat and cholesterol absorption into the bloodstream. Fat and cholesterol not emulsified by cholic acid is passed off in the feces. The second control device is the liver that constantly monitors the level of HDL-C in the bloodstream. If the level of HDL-C drops sufficiently the liver will increase its production of LDL-C to make up the shortfall. Ironically, the liver does not monitor the level of LDL-C in the bloodstream, simply because our bodies have adapted over the past two million years to consuming a moderately high level of dietary fat.

If the roles of HDL-C and LDL-C were interchangeable, the now low HDL-C and high LDL-C levels would not be a problem, but they are not. Although they share some roles, HDL-C and LDL-C have a number of specific roles to play. Therefore, a diet deficient in saturated fat will drastically lower HDL-C levels and the liver will keep on over-producing LDL-C, much of which cannot be used by the body. This results in an overall increase in serum cholesterol levels with a very low HDL-C component and a very high LDL-C component.

“HDL-C has become known as the good cholesterol while LDL-C has been branded as being bad cholesterol.” Nothing could be further from the truth says Dr. Robert Harris with an all but visible shaking of his head. “Both HDL-C and LDL-C are important”, I concur wholeheartedly, but in our search for a better answer, we have missed the obvious solution. So let’s eat like we used to.

Part 3: Diabetes, the silent epidemic

A rare disease 50 years ago, the incidence of diagnosed cases of diabetes mellitus (DM) has reached an alarming level. In 1997 the World Health Organization issued a report that predicts the number of diagnosed cases of DM will rise from 125 million in 1995 to an estimated 300 million in 2025.

There are two divisions of diabetes. There is the genetic and the one that we get during life. Genetic diabetes is not contrary to popular belief, something we are born with. It merely means we are more predisposed to develop it in our natural life.

In 1990 the estimated global death rate from DM was 572,000 and was ranked as the 16th leading cause of death in the world. Over the next 20 years the annual global death rate from DM is expected to pass the 1,000,000 mark. In reality, the annual death rate is much higher as many deaths are attributed to the associated conditions of heart, kidney and liver failure, and not to the real cause.

“In Australia, a country with a population of just 20 million, there are over 900,000 diagnosed DM sufferers. This number is expected to reach 1.5 million by the year 2010. There are 51.4 million DM suffers in Asia; 18.5 million in Europe; 16 million in the United States;12.6 million in Latin America; 6.6 million in the former USSR; 5.3 million in Africa and almost 1 million in Oceania.” (WHO statistics)

About 200,000 people currently die annually in the United States from DM, a number equal to 35% of the world total of DM deaths. African Americans suffer DM at a rate 1.7 times that of white Americans. Latinos suffer at a rate double that of other whites, while native Americans and native Australians suffer at a rate 2.5 times that of whites. Whilst we cannot really explain what is causing this, “maybe natives were never equipped to deal with this disease?”, but all ethnic people who suffer extremely high levels of diabetes through its population have high carbohydrate diets. Similarly Australian ethnic groups also suffer similar discrepancies in their diabetic sufferers and other dietary diseases.

The current scientific trend is to blame immune and genetic reactions, but the evidence does not support this. While the overall percentage of sufferers of early age onset DM has remained relatively unchanged, there has been an explosion in diagnosed cases of late onset DM. Until recently the etiology of early age onset could usually be linked to inherited and genetic traits, but that is all changing. People as young as 13 years are now being diagnosed with what was traditionally thought to be late age onset, so once again the scientific community going to have to again move the goal posts to accommodate this change. “If the condition doesn't fit…change the rules.” A somewhat understandably heated Dr. Harris pants.

There are many sub-categories of DM. In addition to the common Type I and Type II classifications, DM falls into a number of minor categories including malnutrition; gestational (pregnancy); impaired glucose tolerance; fragile and borderline diabetes. Other causes include pancreatic damage; hormonal imbalance and the adverse reaction of some drugs and medication. But the leading cause in my opinion has to be excess carbohydrate consumption in my earnest opinion. Many leading doctors are now beginning to see the light, possibly because their vision was impaired by all the dollar signs they’ve been seeing.

We all know that insulin is produced in direct response to the amount of carbohydrate consumed. However, as we have stopped eating the moderately high amount of fat we used to eat on the grounds that it’s “healthier”, we eat obscene amounts of carbohydrates. However, because we have evolved to eat moderately low amounts of carbohydrates, our beta cells that create the insulin stop functioning properly. The cells were never equipped to handle the huge workload. The cells will CAESE to operate. Not stop and start after a bit of rehabilitation, this is STOP until you die…which is not really true either because being dead won’t better your situation much less coerce your beta cells to create insulin once more. What this means is this: Instant Diabetes.

“The first step to reducing the incidence of DM is the removal of the cause. If every person living on this planet reduced his/her consumption of carbohydrate to a tolerable level, we could nip this epidemic in the bud. The second line of defense is management, and here the battle lines are drawn.

The multinational drug companies that produce synthetic insulin do not want to see an end to this epidemic. Nor do the scientists who benefit from their research dollars. If a better way to control DM is found (such as stem cell therapy, that is currently proving to be a failure) that will be acceptable, provided there is still money to be made.” Once again we see the echoed sentiment that companies tend to see us like guinea pigs. The companies tend to place “Profit” before “Human life”, and “Ethical” next to “Technically”, things not seen except in “Kill by Contract” and “sternly abridged dictionary” respectively.

The current medical management protocol is propagating rather than diminishing the incidence of DM. Frequent meals high in carbohydrate, followed by frequent and often large doses of insulin, “guarantees disaster 100% life-time (also sternly abridged) money back guarantee”. Because most of the carbohydrate consumed is converted into unwanted body fat, DM has been linked to obesity. While the two conditions are the product of a single cause, they are in fact not related diseases. DM sufferers are now being urged to equate their insulin dosage at a ratio of two units of insulin per 2lb/1kg of total bodyweight (total body weight is the number you see on a scale...live body weight is a percentage found from skin caliper tests and then you times it by total body weight to find that fat percentage. The live muscle/body weight is the total body weight minus the fat weight). Now we have a situation where the patient gets fatter by the day, the insulin dosage rises accordingly and the need for additional carbohydrate to absorb the insulin also increases. “Where does it end?”

What about a cure and a management protocol that costs nothing and simply relies on dietary modification? Such an assertion will be strongly opposed by the scientific community, but in the majority of cases of diagnosed DM that is all that is required.

So where have we gone wrong? Instead of searching for answers because of the problem of eating too much fat, most scientists don’t want to entertain the idea that they were wrong in the first place. Nobody should blame them either, it was a decision made without prior knowledge or hindsight to exclude fat from diet. But, a good scientist should be a humble scientist. Instead of analyzing different substances like synthetic insulin and the effects of L-cartinine on fat metabolisation, we should search for a more profound natural way of going back. Go back to the original diet. Original and the best.

Diabetes - the Unnecessary Epidemic by Dr Robert Harris is a must read for every person. By simply adopting this balanced approach to eating we can collectively save millions of lives and billions of dollars and put a virtual end to this dreadful disease. (I even based a lot of my breakfast ideas on his work. Anyone sheepish enough to place a Ph. D next to his name has got to be onto something! Plus he’s a fellow martial artist…)

What a shitload of long crap that was. Okay…let’s move onto something less scientific shall we?

"Are we humans really committed herbivores?"

"As I've said, 'A man can't survive on instant ramen alone!'!"