It's usually proposed by alluding to wild animals and mentioning that they all eat a species specific diet. Why does every animal of the same species eat the same diet except humans?? Doesn't make any sense, does it???
This is one belief that is upheld which is used to strengthen the idea of a "perfect diet". If there's such a thing as a "perfect diet" then any problem that one encounters while doing the diet must be some problem of the dieter. It could be user-error, candida, parasites, bacteria overgrowth, or a multitude of unseen lurking maladies which are secretly plaguing the person. Whatever the problem is, it's either a user error or some previous condition which is blocking the shining truth of perfection from showing through.
One profound information resource that has enlightened me about a lot of health issues is the Track Your Plaque website (http://www.trackyourplaque.com/). I cannot recommend this blog enough. Using precise imaging techniques to physically scan levels of plaque in the circulatory system they can actually track the progression or decline of your plaque deposits. There's no better proof than the kind that you can witness with your own eyes.
So lets break down this paradigm shall we??
Apolipoprotein E (APOE) is a class of apolipoprotein found in the chylomicron and IDLs that binds to a specific receptor on liver cells and peripheral cells. It is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.[1] (Wiki.org).
Apolipoproteins are genetically determined factors which greatly influence the metabolism of fats.
As said by Dr. William Davis, 2) Apo E4–If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the “rescue.”
3) Apo E2 + Apo E4–It’s possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.
http://www.trackyourplaque.com/blog/2011/08/diet-one-size-does-not-fit-all.html
Variants in this gene can cause one person to have enormous success on this diet while others unpredictably get worse.
How dramatic can these variations be??
http://typ.trackyourplaque.com/report/Lipoproteins/Apoprotein_E_Diet.aspx
The gene for apo E3 is the most common; approximately 60% of people have two genes for apo E3, i.e., apo E 3/3. Apo E4 is the next most common, with 20% of Americans having one apo E4, while an additional 5% have two, i.e., apo E 4/4. Apo E2 is the least common, with 10% of Americans having one apo E2, only 1% having two, i.e., apo E 2/2. Also rare is apo E 2/4 (Mahley 2000).
The product of the apo E gene, apoprotein E (all types), is responsible for directing the fate of postprandial (after-eating) lipoproteins like chylomicrons, chylomicron remnants, and VLDL. Postprandial particles that contain apo E are recognized by the liver for uptake and processing. HDL also contains apo E, although it appears to not have as important as role as with postprandial lipoproteins.
Apo E2 closely resembles apo E3 except for 2 amino acids. That small difference causes it to bind weakly (1/100th the binding power of apo E3) to the liver receptor. This means that chylomicron remnants and VLDL—all the postprandial byproducts of your last meal—fail to be taken up by the liver when one or two apo E2 genes are present (Mahley 2000). It means that people with apo E2, especially E2/2, can accumulate postprandial lipoproteins, like chylomicrons, chylomicron remnants, and VLDL, often suggested by high triglyceride and low HDL levels. The expression of the high VLDL/triglyceride, low HDL pattern is especially marked when metabolic syndrome is present, i.e., central obesity and associated features. Despite the accumulation of postprandial lipoproteins, LDL measures like LDL particle number, apoprotein B, and even calculated LDL tend to be slightly lower (<10%) in people with one apo E2, more so (25%) in people with apo E2/2 (Schaefer 1994).
1/100th the binding power. Pretty dramatic yah???
Genetic variation plays in many other areas that affect personal consumption habits such as alcohol detoxification, caffeine detoxification, liver enzymes, lactase persistance, fructose malabsorption, and many many more.
If you still hold the belief that there's a single perfect diet across the species then here's the only piece of evidence you'll need to start to reconsider. These cardiologists are ahead of the game and the validity of these claims are tested time and time again in practice.
