Recommended Healthful

Part 1: Cardiovascular disease causes

The pharma generated view of plaque forming

Pathogens which cause the resposne are missing

For the evidence in support of infection in the artery walls,  for anevaluation of the cholesterol myth

  KEY POINTS:  Everything your doctor has learnt about CVD is a product of pharma-generated tobacco science.   What medical science has uncovered about CVD.  CVD is synonymous with atherosclerosis, a process where the artery walls are damaged by the accumulation of plaque (atheroma).  “An atheroma is an accumulation of degenerative material in the tunica intima (inner layer) of artery walls. The material consists of (mostly) macrophage cells,^[1][2] or debris, containing lipids (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue” Wiki.   The cause of the plaque formation is an inflammation response by white blood cells (macrophages) and LDL to the presence of pathogens within the tunica intima (layer just below the endothelium).  Yes, LDL has two functions, one of transport of cholesterol and triglycerides, the other in the immune system, it contains on its surface antibodies.  The role of pathogens was accepted more than a hundred years ago.[1]  The LDL and white blood cells are actively transported by the endothelia cells that line the artery was as a response to the pathogen.  If the immune system can destroy the pathogen then no puss like atheroma will form.  If not then the wall of the artery will expand due to the accumulation of plaque.  A number of factors can promote this process.  Since the endothelia cells act as a barrier to pathogens circulating in the blood, various chemicals which diminish the function of those cells increase the risk of infectious invasion.  Among those are reactive chemicals circulating in the blood, of which carbon monoxide and fructose are the most clinically significant.  Tobacco smoke and a high sugar diet are the major sources.  Fructose also contributes through a process in which it is converted to fat and stored in the liver, thereby resulting in metabolic dysfunction of which insulin resistance is one consequence.  Fatty liver is a result of the combination of sugar (fructose) and glucose mostly from starches-- both are consumed in excess by those eating a Western diet.  (CVD is nearly unknown among the elderly populations that eat a hunter-gatherer—paleo—diet.)  The effect of the Western diet upon the immune system also contributes, as does drug which compromise immune functions—see NASIDs.  Another causal factor is chronic infectious conditions such as gingivitis.  Pharma makes billions treating the fake causes and the consequences of CVD.    

 A cutting edge restatement of the above causes of cardiovascular disease (CVD) from a 2009 Journal article:  “Atherosclerosis is now recognised as a chronic inflammatory disease occurring within the artery wall and ultimately responsible for myocardial infarction, stroke and peripheral vascular disease. A crucial step in atherogenesis is the infiltration of monocytes[2] into the sub-endothelial space of large arteries where they differentiate into macrophages and become functionally active. Macrophage[3] accumulation within plaques is a hallmark of all stages of atherosclerosis, indeed recent studies have shown their presence has the potential to act as a non-invasive marker of disease activity and plaque stability.  Activated macrophages are major players in all stages of lesion development. They not only accumulate lipids but also express effector molecules that are pro-inflammatory, cytotoxic and chemotactic. Furthermore, they secrete enzymes that degrade extracellular matrix leading to plaque destabilisation and increased risk of rupture.  However, macrophages are heterogeneous and when appropriately activated they have the potential to drive tissue remodeling and ultimately vascular repair. Pharmacological modulation of macrophage activities therefore represents an important strategy for the prevention and treatment of atherosclerosis and other inflammatory diseases.”   So what is the main cause of the immune response?  “Glycation of LDL occurs chiefly due to the non-enzymatic reaction of fructose [glycation] and its metabolites with the free amino groups of lysine in which LDL is rich. There is generally more circulating glycated LDL than oxidatively modified LDL…. Both prevent LDL receptor-mediated uptake and promote macrophage scavenger receptor uptake. The recognition that LDL glycation is at least as important as oxidation in atherogenesis…”   The wrong causal model--that of cholesterol plugging up arteries--entails poor results.  The drug to lower cholesterol in LDL transport, statins, in the early clinical trials proved that lowering cholesterol had no effect upon the endpoint of death”.[4]  The later trials didn’t meet scientific standards.  Why does this false theory of high LDL, cholesterol, and triglycerides persist?  See appendix at bottom for a brief discussion and read Prof. Uffe Ravnskov’s book Ignore the Awkward!   It is one of the 2 best on the Cholesterol Myths, and it has a section on the real cause. 

Dietary cholesterol causes clogged arteries:  In 1913 Nikolai Anichkov (Russian) fed rabbits cholesterol and showed that it caused atherosclerosis (but rabbits are herbivores).  Propter and Gamble in marketing their hydrogenated vegetable oil, Crisco, latched on this experiment to promote the idea that vegetable fats don’t cause CVD.  Using bad science generated by the food industry, bad government ran with the myth that a high fat diet causes CVD, and added to it the cholesterol (see Part 2).  It was in an era of unrestricted use of the blood vessel clogging unnatural transfats—clogging because the body lacks an enzyme for its metabolism.  These transfats are still common because of pseudo government regulations.  Some European countries totally ban transfats (see Part 4).  Part 3 explains the greater role of carbohydrates especially fructose in obesity and CVD.  Part 4 goes into the fat myth and also reviews the evidences on the good and bad fats.   Part 5 is on diet and healthful choice.  Part 6 is on the diet vector in illnesses and dietary fixes.  And Part 8 deals with the second deadly specter, the obesity epidemic.  And there is a posting on the Atkins diet with JK’s improvement.  A search of the site using the internal Google search engine will uncover articles to answer most questions.   

So why doesn’t pharma market drugs to prevent AS?   Pharma in their business model has 3 principle reasons:  1) there are no drugs that remove the plaque which is inside the artery tunica intima.[5]  2) To promote drugs that would prevent or slow atherogenesis would reduce the sales of drugs to treat hypertension (HT), prevent blood clots, arrhythmia, and high TC[6].  The drugs that prevent AS also reduce the risk of developing those chronic conditions, and thus would lower pharma’s profits by 50% within a generation (see part 4). 3) There are 4 drugs which significantly lower the risk of developing AS, but estradiol and testosterone are off-patent drugs, and the other two are over-the-counter, 325 mg aspirin and CoQ10.  Moreover, these drugs as a group greatly reduce the risk of blood clots, cancer, Alzheimer’s disease, osteoporosis, acute ischemic events, HT  and other diseases.  Thus they do tobacco science to protect profits.  And it gets worse, since the best preventive treatment is a healthful diet.  Pharma treats TC with one of their 10 statins and HT with three from their over 120 drugs, which come in 7 categories based on method of action.   A patient who is in the high risk group for an ischemic event is also placed on an anticoagulant.  And if he has had a heart attack such person is likely to show on and EKG (electrocardiogram) an abnormal pattern, and is given an arrhythmia drug.  A protein pump inhibitor (PPI) is added ulcer prevention.  Typical drugs following a myocardial infarction (MI) averages $70,000 per year.   Moreover, over half of seniors age 65 to 74 are on statins, and 40% of men 55 to 64.  For women the number is a bit lower.  Pharma is very good at marketing. 

Understanding the role of atherosclerosis in the development of CVD is necessary for rational, evidence-based heart choices.  Atherosclerosis is caused by pathogens within the artery walls and the immune system’s response [See LDL illustraton, top].  This response results in the formation of unstable young plaque within the lumen of arteries which over a period of several years will become harden (stable plaque).  The unstable plaque which causes only a slight constriction at most of the artery causes over 80% of MIs (myocardial infarctions, heart attacks) & 85% of strokes.  (Retain this essential relationship.)  Thus even those without CVD are at risk for MI and stroke because they are very likely forming some young unstable plaque, the rate of which can vary according to a number of factors, the most important being diet, reactive chemical, chronic infections, and drugs.      

Understanding the role of damaged LDL in the development of AS:  LDL (see illustration above) consists of chains of fatty acids with about 6 apolipoproteins molecules.  They form a ball with about 1,500 cholesterol molecules in interior of the ball and 3,000 to 6,000 triglycerides (see illustration at top of page).  Fatty acids (including those in triglycerides) and cholesterol are not blood/water soluble.  Lipoprotein with attached acid end of the triglyceride form LDL which is water soluble. LDL is produced in the liver for transport of cholesterol and fatty acids to cells as needed throughout the body.  During that transport process in the blood and when taken up by the arteries, the LDL can become damage by superoxides and by glycation[7].   More important is the fact that LDL has on its surface antibodies which permit it to attach to pathogens and some of the toxins they produce.  This function has been known for a hundred years-- read Prof. Uffe Ravnskov’s book Ignore the Awkward! p 136-140.  “In the laboratory it has been shown that human LDL is able to inactivate more than 90% of most toxic bacterial products” supra. 138. This is but one of a number of confirmatory experiments on LDL’s immune-system function.  Multiple functions are the norm in animal biology.  Insulin for example has listed over a dozen functions--see Wikipedia .  This function fits in neatly:  the LDL is actively transported into the tunica media of the artery because of its immune system function.  It also explains why lymphocytes including the scavenger macrophages are in the tunica media.  Pharma’s claim simply doesn’t make sense that LDL would be in the tunica media in sufficient concentration in a tissue with a low rate of metabolism and thus low requirements for cholesterol and/or triglycerides.  Certain tissues of low activity are prone to infection, and given the autopsy evidence, the tunica media is one of them.   Given the presents of white blood cells, it must be in the immune function which accounts for the presence of LDL.  Pharma’s oxidation theory within the tunica media is counter the normal function for LDL.  And why in the tunica media instead of in the plasma where there are more reactive chemicals?  Pharma makes no mention of pathogens in the tunica media.  Rather they hold that the inflammatory response involving leucocytes is due to injury (See Braunwald Heart Disease 5^th Ed., 1113-1115).  There is no mention of pathogens by Braunwald, though there are 100s of journal articles on pathogens within the artery walls.   An excellent summary of the evidence is in The Great Cholesterol Con by Anthony Colpo, at 207-215.   There are two stories one Ptolemaic, the other Copernican; one complex and far-fetched, the other simple and within the norm of immune system function.   One ignores evidence of pathogens, the other doesn’t.       

Lack of association between hypercholesterolemia and CVD:  This association has been put forth as proof of that A causes B.  As stated earlier being a bystander does prove causation, and that the cause is reactive chemicals which overload the cleanup system or damage LDL by macrophages.  Thus according to pharma’s model those with more LDL would be have a higher rate of damage.  But there is a problem with this model, since the presents of LDL is through active transport into the tunica media, higher serum cholesterol would entail more than needed levels of LDL in the tunica media.  This is confirmed in numerous studies of those with high cholesterol as to the rate of atherosclerosis and the subsequent MI (myocardial infarctions, heart attacks).  Those with familial hypercholesterolemia (level due to a genetic defect that are at least double the level considered high) do not have significantly more heart attacks or die significantly sooner than those with normal level (at least in older studies before the use of statins).  One would expect a strong association, but studies only find a minor association, at most—see Uffe at.  The failure to find an association of elevated TC with MI is thoroughly described in the books by Uffe and Colpo supra.  I go over this evidence at and also. There are numerous books in addition to the two mentioned which expose this myth, just visit Amazon to find them, or watch the documentaries.     

Atheroma:  “The atheroma (accumulation & swelling in an artery wall) consists of LDL [see illustration], calcium, fibrous connective tissues, T-lymphocytes macrophages, and pathogens.  While in the early stages, based on gross appearance, have traditionally been  termed fatty streaks by pathologists, they are not  composed of fat cells (adipose cells), but are accumulations of  white blood cells, especially macrophages, that have taken up damaged low-density lipoprotein (LDL).  After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) the macrophages are called foam cells. When foam cells die, their contents are released, which attracts more macrophages.  Left out of this pharma tale is the fact that macrophages can be damaged by the toxins produced by bacteria—see and, possible including those which are found on the surface of LDL antigens.    

Coronary artery disease (CAD), hypertension & CVD, pharma’s version:  Atherosclerosis affects coronary arteries and thus the blood supply to the heart muscle. “Atherosclerosis is the most common type of heart disease and cause of heart attacks.  The disease is caused by plaque  building up along the inner walls of the arteries of the heart, which narrows the arteries and restricts blood flow to the heart. It is the leading cause of death worldwide.^[1]  After decades of progression, some of the  atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death,^[2] and the leading cause of death over the age of 20 years.^[3]   Most commonly, unstable young plaque ruptures and may lead to an acute myocardial infarction (AMI). Cholesterol is delivered into the vessel wall by cholesterol-containing low-density lipoprotein (LDL) particles. To attract and stimulate macrophages (a type of white cell), the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process” Wiki.   “The process is worsened if there is insufficient high-density lipoprotein (HDL).  The lipoprotein particles [HDL] remove cholesterol from tissues and carry it back to the liver.  When the macrophages [type of white blood cell] engulf a large amount of the oxidized cholesterol [as part of the disposal process] they are called foam cells because of appearance. In sufficient numbers they form the fatty streaks of the plaques of atheroma in the innermost layer of the artery wall.  A protective fibrous cap normally forms between the fatty deposits and the artery lining (the intima).  These capped fatty deposits (now called 'atheromas') produce enzymes that cause the artery to enlarge over time. Atheromas within the vessel wall are soft and fragile with little elasticity. Arteries constantly expand and contract with each heartbeat, i.e., the pulse. In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, as they progress, lead to a loss of elasticity and stiffening of the artery as a whole” Wiki.  Pathogens are not mentioned, nor is the young unstable plaque compared to a boil.  Pharma focuses on occluded vessels by mature plaque, upon elevated TC and HT. Hypertension thus is a trailing result not a cause of AS.  The higher risk of ischemic events (MI and ischemic strokes) that occurs with HT is a result of a statistically higher rate of atherogenesis & thus young plaque. [8]  To lower blood pressure does not significantly affect unstable plaque the cause of acute ischemic events.  Macrophages during their cleanup function weaken the protein matrix and thereby increase the risk for the young plaque will leak out of the lumen.  A person with HT is more likely to have a clot form at the point where the plug has limited the flow of blood.   HT contributes to the clotting process; but not to atherogenesis.  HT is mere a sign of atherogenesis, which causes ischemic events.  MIs often occur with normal blood pressure and normal TC.  AS, oxidative damage to LDL, and unstable young plaque are not treated by Pharma’s drugs, thus they stresses TC and HT to promote sales.   

Most atherosclerotic formations are the result of infections in the tunica media.  “Cytomegalovirus  (CMV) infection is also associated with cardiovascular diseases.^[13]  In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques.  The accumulation of calcium leads to a loss of elasticity and stiffening of the artery as a whole [one cause of hypertension] “ Wiki.  A number of chronic conditions are contributors to CVD:   women with rheumatoid arthritis have “double the risk of heart attacks when compared to women without it… An infection that starts in the gums, for example, can easily lead bacteria into the blood-stream that may find fertile ground in a weakened arterial wall and fan the fires of inflammation there” (Bowden 45).  Thus infection is a cause of AS.   Note how Wiki consistently fails to mention the presence of pathogens in the artery walls—a clear sign of pharma’s influence. 

The infection vector in the causes of AS consists of a direct involvement through infection within the artery lumen, and an indirect through chronic infection.  Among chronic infections, the Helicobacter pylori (the cause for over 80% of ulcers) increase the risk of MI by 75%.  “A number of acute and chronic infections including:  Chlamydophila   pneumoniae,  lupus erythematosus, influenza, and Porphyromonas gingivalis [gingivitis] among others have been linked to atherosclerosis and myocardial infarction” Wiki.   “Women with rheumatoid arthritis, a highly inflammatory condition that primarily affects the joints, wind up having double the risk of a heart attack…” (Bowden 45).  Within the artery lumen Cytomegalovirus, herpes virus and several other pathogens have been found upon examination during autopsy examinations.   The immune response of LDL is also documented:  “Antibodies to oxidized LDL (ox-LDL) and LDL-containing immune complexes (LDL-IC) have been reported to be associated with the presence or progression of arteriosclerosis” at.  “Antibody is a large, Y-shape protein produced by plasma cells that is used by the immune system to identify and neutralize pathogens such as bacteria and viruses” Wiki. These antibodies on LDL are further indication of their immune function.  Moreover long-term test for C-reactive protein (CPR) is a better predictor of ischemic events in men followed long-term than that of elevated LDL.  CPR is a marker for infection[9].  Further support is found in that NSAIDs down-regulate COX-2 prostaglandin and thereby increase acute ischemic events through inhibition of the immune system which is found to promote the atherogenic process--(aspirin is the only known COX2 inhibitor that doesn’t promote AS).[10]  Given the role of oxidative damage to LDL and the inflammation response, lowering LDL can at best have only a minor effect.  The current attempts to prevent the consequences of AS do not address its two major causes: damage to LDL and the subsequent immune response.  A review of the first 50 citation for “infection + atherosclerosis” found not one article published after 2003 on infection as a cause for atherosclerosis but for 3 on HIV.  A promising area of research is not being funded because of pharma and their friends.  Since pharma is driven to maximize profits, thus treating disease not preventing them.  They treat signs as though they are diseases and anything else that will up profits.  So how does pharma handle the evidence of the immune function of LDL?     

The oxidized LDL myth as cause of atherosclerosis:  Oxidized means a chemical reaction involving the sharing or transfer of electron.  Thus a toxin, virus, or bacteria bonding (attaching) counts as oxidized.  For pharma the cause of oxidized LDL caused by reactive chemical byproducts from metabolism and this occurs in the tunica media, where the plaque forms.   Then lymphocytes enter the tunica media, spot the oxidized LDL and signal for the specialized macrophages which then enter the tunica media, and devour the oxidized LDL.  Upon ingesting too many of these damaged LDL, the macrophages are converted to foam cells (swollen macrophages) which then undergo apoptosis (cell death).  The debris from the apoptosis which consists mostly of triglycerides and cholesterol from the ingested LDL, if sufficient, will form plaque, the foundation for the development of AS.[11]    Nice story, but unlikely.  Unlikely because 1) in a biologically inactive area (unless there is an infection and healing process), the tunica media, there is not a need for LDL.  LDL occurs in metabolically active areas where its contents of fats and cholesterol are used in cell building.  2) This area of low activity will not produce very many reactive byproducts of metabolism to attach to LDL and oxidize them.  Should not this plaque forming process according to pharma’s theory be most prevalent in areas of high metabolism?  3) It has not been shown that leucocytes start an inflammatory process because of a few oxidized LDL.  However leucocytes primary function is to respond to toxins, foreign matter, and pathogens.  LDL is a protein rap around cholesterol and fat molecules that travels to tissues as needed.  5) Polyunsaturated fats have been demonstrated to be subject to a process of oxidation by reactive chemicals, most of which come from products of metabolism; however, these oxidize fats do not cause an immune system response.  This is more evidence that oxidation is not the cause of the inflammatory response.  Note:  the problem with these rancid fats is that the body lacks enzymes for their disposal.  Their accumulation, like transfats, contributes to the atherogenic process.  6) It has not been shown that the macrophages would ingest oxidized LDL—unless they had on their surface antibodies with toxins or pathogens attached thereto.  7) Pharma then hypothesizes that our body makes antibodies which recognized oxidized LDL attach to it, and thereby causes the immune response.  However it is the LDL with immune complex that have occupied sites that are shown to be subject to digestion by macrophages, at.  “These results indicate that the binding of lipoprotein immune complexes to Fc receptors on monocytic cells activates a series of responses that could accelerate the initiation or progression of atherosclerosis” at.  Pharma’s story of AS being caused by reactive chemical attached to LDL is far-fetched:  it creates new process occurring in low metabolic area; and it ignores the volumes of articles on pathogens in atheroma.   Big pharma has frames the discussion of AS in a way that has researchers looking under the wrong bush. 

Lowering LDL is irrelevant:  Since the presence of LD in the tunica media involves active transport, lowering the serum level of LDL doesn’t impact the number of LDL actively transported by the epithelial cells.  Corollary having a high level of LDL doesn’t increase its presence in the tunica media, this explains the lack of association between level of cholesterol, LDL and coronary artery disease, and why drugs which lower them aren’t worth their side effects—see cholesterol myth. 

The evidence that LDL has an immune system function:  “In the laboratory it has been shown that human LDL inactivates more than 90% of most toxic bacterial products” Uffe supra at 138.  Lipoproteins in experiments inhibit endotoxins.[12]  “When Kenneth Feingold and his co-workers at the University of California in San Francisco reduced blood cholesterol in rates [thus also LDL] and gave them an injection of bacterial toxin, most of them died quickly, but if they injected purified human LDL beforehand they survived” Uffe Supra 138.  A similar mechanism in which lipoproteins neutralize E. coli, N. meningitides , and complete Gram-negative bacteria-- full.  “Thus, lipoproteins, in addition to playing a role in lipid transport, may have protective functions” Feingold 1995.  The LDL is homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL auto-antibodies are found in the Vasa Vasorum (blood vessels that nourish the tissue with in larger arteries).[13]  There is a large body of experimental evidence to confirm the immune function of LDL.  This function along with transporting the materials for building cell walls (cholesterol and triglycerides) explains why they are actively transported through the epithelial lining of artery walls; they are need for this function.  An intervention which interfered with this healing function is dangerous. 

What really causes atherosclerosis:   Pathogens living in the tunica media cause an immune response from both their physical presence as foreign matter and biotoxins which they release that cause cellular.  In response to their presence and the biotoxins the endothelial cells then actively transport LDL with antibodies on their surface for to attack the pathogens and absorb their toxin--see.  The endothelia cell also signal for leucocytes to fight the infection.  The leucocytes then signal for macrophages to assist.  The macrophages engulf pathogens, toxins, and the toxin laden LDL.[14]  An overload of toxins, pathogens, and toxin laden LDL results in apoptosis (program cell death) of the macrophage with the release of its contents.  This infection process if sufficiently vigorous will result in the formation of plaque, in much the same way a boil forms under the skin because of an immune response to bacterial activities.  In fact Uffe refers to this process as being similar to that of the formation of a boil.  “… the vulnerable [young] plaque is a pustule, a small boil” Uffe supra 138.  The results of NOT accepting pharma’s model for AS is tragic: doctors are prescribing and patients take drugs which do not affect the progression of atherosclerosis, and they undergo invasive procedures which do not reduce risk of acute events and deaths from CVD, while effective alternative are criticized based upon pharma’s tobacco science.   Moreover researchers are looking under the wrong bush.  A review of the first 50 citation for “infection + atherosclerosis” I found not one article published after 2003 on infection as a cause for atherosclerosis—I excluded the 3 which  were on HIV, because HIV is known to compromise the immune system.  A promising area of research is not being funded because of big pharma.    

Unstable plaque, the wild card:  unstable plaque is fresh, young plaque that forms within the lumen of an artery.  It doesn’t show up in an angiograms, because occlusion is under 20%.  Testing for infection is only moderately associated with the process.   The measure of C-reactive protein is only weakly associated with plaque formation, since such infections are often minor and temporary. Infections in the tunica media are nearly always without symptoms.  Macrophages in their cleanup healing role for young plaque “secrete cytokines and protease that weaken the fibrous cap, causing it to erode or rupture.  The newly exposed sub-endothelium and pro-coagulant factor precipitate platelet aggregation and local thrombus formation, sometimes leading to infarction [MI]” AHA, 2013.  The best way to reduce this risk for the formation of unstable, young plaque is to improve immune functions and overall health through a healthful diet, one that is similar to those of our poorer ancestors two centuries ago.  The effects of fatty liver, IR, fructose, refined carbs, unhealthful polyunsaturated and transfats, and carbon monoxide from cigarettes have cumulatively brought about atherosclerosis with its consequences and a host of other conditions.    

Some positive choices:  Everyone by the age of 40 has some young plaque, especially males. Women are protected by estradiol, this is why contra-pharma, post-menopausal women should take natural HRT for cardiovascular protection.[15]  Past attempts—1950s to 1980s--to find an estrogen analog for men have failed.[16]  The sex hormones, in their androgen effect, promote healing.  Estrogen, for example, has been shown “to promote the resorption of extras-cellular lipids [constituents of plaque] and reversal of endothelial dysfunction” AHA.  In addition it protects LDL from oxidative damage (see myth 12 above).  Testosterone also has been shown to be protective:  those elderly men whose level is the top 20% have a very significantly lower incidence of death from CVD.   However the most important risk reduction comes from a healthful diet and maintaining a healthy liver (see above myths 7 through 17).  There is a library of technical materials on diet at the rh website section including links to the best of documentaries and academic lectures on the topics discussed.   Remember that metabolic dysfunction caused by the Western diet is 80% reason for the difference is rates of CVD, cancer, Alzheimer’s disease, arthritis, osteoporosis, and a host of other conditions between us and those who eat a paleo-diet, or the peasant’s diet of Orientals and Europeans two centuries ago.