Local Foods Local Health: The Keys to Sustainable Health

weightloss10

In the past years, I have come to understand the adjective, macrobiotic, to mean longevity. A truly macrobiotic approach is a longevity approach which was applied throughout the world to promote daily health and wellbeing. The challenge, today, is to adapt the practices and principles that were learned from eastern teachers to varying local environments and modern conditions.

Local foods are a good place to start. Traditional cuisines are based on local foods. A traditional Japanese saying, Shin Do Fu Ji, is universally true. Body and soil are one. To become sustainably healthy, it is important to shift our food choices to foods that grow locally. This means that diets will be more seasonal and more uniquely suited and varying for each specific environment. The power of the nutrition and energy from local foods is incredible.

In addition to eating locally, it is important to sort out the truths and myths of what it means to stay healthy.  Falsehoods exist about many health issues. Weight is on the top of the list. Healthy natural eating is really the key to creating a healthy weight. There is convincing evidence that skinny is not healthy for all and that no one should restrict themselves of calories by dieting.  Diet creates too many unintended consequences. Instead, the focus should be on a healthy diet and lifestyle. There are many surprising truths that are being uncovered about weight and health. Many of these findings contradict what we have commonly accepted (Why BMI Is a Big Fat Scam in Mother Jones Sept./Oct. 2014).

Popular nutritional approaches are another area where myths abound. Many diets that are recommended today are nutritionally poor. Traditional macrobiotic or longevity eating  around the globe was always nutritionally rich with an abundance of nutrients.  For optimal health, the best choice is nutritional wealth over nutritional poverty.

In order to create sustainable health, it is important to know when we are out of balance. Over the years, as a health teacher and counselor, I’ve put lots of time into research, thinking, observations and practice of health assessment or diagnosis. I found that I had to expand upon oriental diagnosis methods that I had learned to include Indian and Chinese diagnostic systems and modern biology. Through this synergy, I find it is possible to help people understand and re-balance weaknesses in their organs.  As this method becomes more known, it will be a great tool for modern people to guide their health as the traditional systems did in the past.

Traditional macrobiotic healing systems in Asia and around the world looked upon food as energy. The traditional explanations of the energetics of food are sometimes hard to fathom by modern people. A practical way to see food as energy is important to create lasting health.  Seeing food as energy can make sense of how the different nutritional components in food affect us and when certain nutrients and foods are needed.

FFF-Grass_Fed_Meat1

With the knowledge of combined food energetics and nutrition, mental and emotional health can be improved. Common and many serious sicknesses can be self-healed.

Sustainable macrobiotic healing includes an understanding of the influences of not only diet, but our thinking, lifestyle and the influence of the society that we live in. With knowledge of the energetic effects, all natural tools are available as remedies. With so many supplements, herbs, drinks, juices, aromas and treatments, it can be hard to sort out the wheat from the chaff. Practical energetics can help us find what is truly helpful for health and healing while at the same time emphasizing what we can do in our daily life to stay healthy and well.

*This article was written by John Kozinski. He has been a pioneer natural health teacher, author, and researcher since 1976. Education and diagnostic techniques are rooted in his clinical experience with 40,000+ students and clients. John resigned in 2013 from the Kushi Institute faculty after 27 years. To address catastrophic illness that developed in those following restrictive natural diets John reveals in a new training program his clinical experience and research into what was really working and why for people following popular diets. This education gives teachers, health practitioners, and students new skills to help evaluate and treat a wide variety of health conditions both naturally and complementary to medical treatments. www.macrobiotic.com

What causes heart attacks? (Part two)

heart

In a previous article in this journal (“What Causes Heart Attacks,” Fall 2007) I presented the case that the spectrum of heart disease, which includes angina, unstable angina, and myocardial infarction (heart attack), is better understood from the perspective of events happening in the myocardium (heart) as opposed to events happening in the coronary arteries (the arteries that supply the heart).

As we all know, the conventional view holds that the central event of heart disease occurs in the arteries, with the buildup of blockage called plaque. In this follow-up article I will go into more detail about the conventional theory and why it is largely misleading; then I will describe the precise and well documented events that do lead to MIs (myocardial infarctions or heart attacks).

This understanding is crucial because during the last fifty years the pursuit of the coronary artery theory has cost this nation billions of dollars in unnecessary surgical costs, billions in medications that cause as much harm as any positive benefits, and, most seriously, has led many to adopt a lowfat diet, which only worsens the problem. Newer twists on this theory only serve to further obscure the real cause. In contrast, by understanding the real patho-physiological events behind the evolution of MIs, we will be led to a proper nourishing traditional style of eating, the use of the safe and inexpensive heart tonic called g-strophanthin, and, most importantly, we will be forced to look at how heart disease is a true manifestation of the stresses of modern civilized life on the core of the human being.

To overcome the epidemic of heart disease we literally need a new medical paradigm, a new economic system, a new ecological consciousness; in short, a new way of life. The coronary theory misses all of this, just as it misinterprets the actual pathological events.

In writing this article, I am indebted to the work of Dr. Knut Sroka and his website heartattacknew.com. For all interested in this important subject I recommend reading the entire website and watching the video on the website. The video shows how the collateral circulation nourishes the heart even with a severe blockage of a coronary artery.

For health professionals and researchers, your understanding of this subject is incomplete without reading and studying two articles reprinted in full on the website. The first is by G. Baroldi, “The Etiopathologies of Coronary Heart Disease: A Heretical Theory Based on Morphology,” and the second by K. Sroka, “On the Genesis of Myocardial Ischemia.”

REBUTTAL OF CONVENTIONAL THEORY

Until recently I believed, along with the majority of physicians, that most MIs were caused by the progressive blockage caused by plaque buildup in the four major coronary arteries leading to the heart. These plaques were thought to be composed of cholesterol that built up in the arterial lumen (inside of the vessel), which eventually cut off the blood supply to a certain area of the heart, resulting in oxygen deficiency in that area, causing first pain (angina), then progressing to ischemia (heart attack). The simple solution was to unblock the stenosis (the blockages) with either an angioplasty or stent, or, if that was not possible, then by bypassing this area with coronary bypass grafting (CABG). Simple problem, simple solution.

The problems with this approach became apparent to me in several ways. The first emerged in a story related by the head of cardiology during a northern California heart symposium at which I was a speaker. He told us that during his residency he was part of a trial conducted in rural Alabama on black men. In this trial, they did angiograms (injecting dye into the coronary arteries to detect blockages) on all the men with chest pains. For the ones who had a single artery blocked, they did no interventions, only noting which part of the heart would have a subsequent heart attack if one occurred. Of course, they all predicted it would be in the part of the heart supplied by that particular coronary artery. Then they waited.

Eventually many did return and did have MIs, but to the researchers’ surprise less than ten percent had a heart attack in the area of the heart supplied by the original blocked artery. This means, of course, that had they performed the usual angioplasty, stent, or bypass on that artery, the patient would have received no benefit.

The second occurrence that helped change my mind was the publication in 2003 of a large study conducted by the Mayo Clinic on the efficacy of bypass surgeries, stents, and angioplasty.1 The study concluded that bypass surgery does relieve symptoms (chest pain); that bypass surgery does not prevent further heart attacks; and that only high-risk patients benefit from bypass surgery with regard to a better chance of survival.

In other words, the gold standard for treating arterial blockages provides at best only minimal benefits.

If you watch the video on www.heartattacknew.com and go to the FAQ called “The Riddle’s Solution,” it becomes clear why this is so. Large stable blockages, that is, sites that are over 90 percent blocked, in almost all cases compensate for the blockage by developing collateral blood vessels.

In fact, the view that the four coronary arteries supply all the blood to the heart is completely wrong. Starting soon after birth, the normal heart develops an extensive network of small blood vessels called collateral vessels that eventually compensate for the interruption of flow in any one (or more) of the major vessels. As Sroka correctly points out in the video posted at heartattacknew.com, coronary angiograms fail to show the collateral circulation; furthermore the procedure creates spasms in the coronary arteries through the injection of heavy dye under high pressure. Thus, coronary angiograms are notoriously inaccurate at assessing the amount of stenosis in the vessels as well as the true blood flow in the heart.

To this day, most of the bypasses, stents, and angioplasties are performed on minimally symptomatic patients who show a greater than 90 percent blockage in one or more coronary arteries. These arteries are almost always fully collateralized; it is not the surgery that restores blood flow, because the body has already done its own bypass. If tests found a major coronary artery 90 percent blocked, with only 10 percent flow “squeezing through the bottleneck,” how could you possibly still be alive if you did not have collateral blood vessels?

And are we really to believe that the decisive thing that will cause the eventual MI is when the stenosis goes from 93 percent to 98 percent? This is an insignificant difference, and the premise that this small increase will cause a heart attack is completely nonsensical. Yet this is what most of the procedures are meant to accomplish, to unblock the stenosis, which as the video on heartattacknew.com shows, does not actually improve blood flow. It is no wonder that in study after study these procedures fail to provide any significant benefit to the patients.

For these reasons, conventional cardiology is abandoning the stable plaque model in favor of a different model for the etiology of MIs, one that, as it turns out, is equally invalid.

MEET THE UNSTABLE PLAQUE

We can now all agree that the entire focus of cardiology on the stable, progressing calcified plaque—the thing we bypassed and stented for years, the thing we do CT scans of arteries for, the thing they told us is created from cholesterol buildup in arteries, the thing “alternative cardiology” like the Ornish program focused on eliminating—all this is not so important after all.

Don’t worry, though, say the “experts,” we know it must be the arteries, so let’s introduce another concept—drum roll—that of unstable or friable plaque. This insidious scoundrel can attack at any time in any person, even when there is no large blockage. That’s because these soft, “foamy” plaques can, under certain situations (we don’t know which situations), rapidly evolve and abruptly close off the involved artery, creating an oxygen deficit downstream, with subsequent angina and then ischemia. These soft plaques are thought to be the result of a combination of inflammatory “buildup” and LDL-cholesterol, the exact two components that are targeted by statin drugs. Therefore, since unstable plaque can come loose at any time, everyone should be on statin drugs to prevent this unfortunate occurrence. Some advocates have even suggested putting therapeutic doses of statins in the municipal water supplies.

Defenders of this theory point to angiogram studies that show the changes in these unstable plaques, claiming them as proof that unstable plaque is the true cause of the majority of MIs. As I will show, this acute thrombosis does happen in patients having heart attacks, but it is a consequence, not the cause of the MI.

What can pathology reports—as opposed to angiography studies—tell us about the role of unstable plaque in heart attacks? After all, pathology reports are the only accurate way of determining what actually happened during a heart attack, as opposed to angiograms, which are misleading and difficult to read.

The first major autopsy study of patients dying of MI was carried out in Heidelberg in the 1970s.2 The study found that sufficient thrombosis to cause the MI was found in only 20 percent of cases. The largest such study found sufficient thrombosis in only 41 percent of cases.3 The author, Baroldi, also found that the larger the area of the MI, the more often the pathology report found stenosis; in addition, the longer the time between MI and the death of the patient, the higher the percentage of stenosis.

Some researchers have used these two facts to cherry pick the numbers and make the stenosis rate seem high by studying only those with large MIs and those who live the longest after the MI event.

Another observation that puts into doubt the relevance of the coronary artery theory of MI is the fact that the proposed etiological mechanism of how thrombosed arteries cause ischemia is through cutting off the blood supply and thereby the oxygen supply to the tissues. To the enormous surprise of many investigators, the reality is that when careful measurements are done assessing the oxygen level of the myocardial cells, there is no oxygen deficit ever shown in an evolving MI.4 The oxygen levels (measured as pO2) do not change at all throughout the entire event. I will come back to this fact later when I describe what does change in every evolving MI ever studied. Again the question must be asked: if this theory is predicated on the lowering of the oxygen levels in the myocardial cells when in fact the oxygen levels don’t change, then what exactly does happen?

The conclusion is that while thrombosis associated with MI is a real phenomenon, it does not occur in more than 50 percent of cases— which leads to the question: why do the other 50 percent, those without an occlusion in the coronary arteries, even have an MI? Second, it is clear from all pathology studies that thromboses of significant degrees evolve after the MI occurs, again leading to the question: what causes the MI in the first place? The fact that thrombosis does occur after a heart attack also explains why emergency procedures—remember, the only patients who benefit from bypass and stents are critical, acute patients—can be helpful immediately post-MI to restore blood flow in those patients who do not have adequate collateral circulation to that part of their heart. So again, all the existing theories about the relevance of the coronary arteries in the evolution of the MI are fraught with inconsistencies. If this is so, then what causes heart attacks?

THE ETIOLOGY OF MYOCARDIAL ISCHEMIA

Any theory as to what causes myocardial ischemia must account for some consistent observations over the past fifty years. The most consistent risk factors for a person having heart disease are male sex, diabetes, cigarette use and psychological or emotional stress. Interestingly, in none of these is there a direct link to pathology of the coronary arteries—diabetes and cigarette use cause disease in the capillaries, not, as far as we know, in the large arteries. Also, we have learned over the past decades that the four main medicines of modern cardiology—beta-blockers, nitrates, aspirin, and statin drugs—all provide some benefits for heart patients (albeit all with serious drawbacks as well) and this observation must be accounted for in any comprehensive theory of myocardial ischemia.

heart doctor

HEART RATE VARIABILITY

The real revolution in the prevention and treatment of heart disease will come with increased understanding of the role played by the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart rate variability (HRV).

We have two distinct nervous systems: the first, the central nervous system (CNS), controls conscious functions such as muscle and nerve function; the second nervous system, the autonomic (or unconscious) nervous system (ANS), controls the function of our internal organs. The autonomic nervous system is divided into two branches, which in a healthy person are always in a balanced yet ready state. The sympathetic or “fight-or-flight” system is centered in our adrenal medulla; it uses the chemical adrenaline as its chemical transmission device and tells our bodies there is danger afoot—time to activate and run. It does so by activating a series of biochemical responses, the centerpiece of which is the glycolytic pathways, which accelerate the breakdown of glucose to be used as quick energy as we make our escape from the bear chasing us.

In contrast, the parasympathetic branch, centered in the adrenal cortex, uses the neurotransmitters acetylcholine (ACh), nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) as its chemical mediators; this is the “rest-and-digest” arm of the autonomic nervous system.

The particular nerve of the parasympathetic chain that supplies the heart with nervous activity is called the vagus nerve; it slows and relaxes the heart, whereas the sympathetic branches accelerate and constrict the heart. I believe it can be shown that an imbalance in these two branches is responsible for the vast majority of heart disease.

Using the techniques of heart rate variability (HRV) monitoring, which gives a real-time accurate depiction of autonomic nervous system status, researchers have shown in multiple studies5 that patients with ischemic heart disease have on average a reduction of parasympathetic activity of over one-third. Typically, the worse the ischemia, the lower the parasympathetic activity.6 Furthermore about 80 percent of ischemic events are preceded by a significant, often drastic, reduction in parasympathetic activity.7

By contrast, those with normal parasympathetic activity, who experience an abrupt increase in sympathetic activity (such as physical activity or an emotional shock), never suffer from ischemia.

In other words, without a preceding decrease in parasympathetic activity, activation of the sympathetic nervous system does not lead to MI.8 Presumably we are meant to experience times of excess sympathetic activity; this is normal life, with its challenges and disappointments. These shocks only become dangerous to our health in the face of an ongoing, persistent decrease in our parasympathetic, or life-restoring, activity.

The decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: ACh, NO, and cGMP. It is fascinating to note that women have stronger vagal activity than men, probably accounting for the sex difference in the incidence of MI.9 Hypertension causes a decrease in vagal activity,10smoking causes a decrease in vagal activity,11 diabetes causes a decrease in vagal activity,12 and physical and emotional stress cause a decrease in parasympathetic activity.13 Thus, all the significant risk factors suppress the regenerative nervous system activity in our heart.

On the other hand, the main drugs used in cardiology upregulate the parasympathetic nervous system. Nitrates stimulate NO production while aspirin and statin drugs also stimulate the production of ACh along with NO—that is, until they cause a rebound decrease in these substances which then makes the parasympathetic activity even worse.

Beta-blockers work by blocking the activity of the sympathetic nervous system, the increase of which is a central factor in the etiology of MI.

The bottom line: the risk factors for heart disease and the interventions used all affect the balance in our ANS. Whatever effects they may have on plaque and stenosis is of minor relevance.

HOW HEART ATTACKS OCCUR

So what is the sequence of events that leads to an MI? First comes a decrease in the tonic, healing activity of the parasympathetic nervous system—in the vast majority of cases the pathology for a heart attack will not proceed unless this condition is met. Think of those who are always pushing themselves, who never take time out, who have no hobbies, who constantly stimulate the adrenal cortex with caffeine or sugar, who do not nourish themselves with real food and good fats, who do not incorporate a regular pattern of eating and sleeping into their daily lives.

Then comes an increase in the sympathetic nervous system activity, usually a physical or emotional stressor. This increase in sympathetic activity cannot be balanced because of chronic parasympathetic suppression. The result is an uncontrolled increase of adrenaline, which directs the myocardial cells to break down glucose using aerobic glycolysis. Remember that in a heart attack there is no change in blood flow as measured by the pO2 in the cells. This step shunts the metabolism of the heart away from its preferred and most efficient fuel sources, which are ketones and fatty acids. This explains why heart patients often feel tired before their events. This also explains why a diet liberal in fat and low in sugar is crucial for heart health.

As a result of the sympathetic increase and resulting glycolysis, a dramatic increase in lactic acid production occurs in the myocardial cells; this happens in virtually 100 percent of MIs, with no coronary artery mechanism required.14,15 As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis prevents calcium from entering the cells,16 making the cells less able to contract. This inability to contract causes localized edema (swelling), dysfunction of the walls of the heart (hypokinesis, which is the hallmark of ischemic disease as seen on stress echoes and nuclear thallium stress tests), and eventually necrosis of the tissue—in other words, a heart attack. The localized tissue edema also alters the hemo-dynamics of the arteries embedded in that section of the heart, resulting in shear pressure, which causes the unstable plaques to rupture, further block the artery, and worsen the hemodynamics in that area of the heart.

Please note that this explanation alone explains why plaques rupture, what their role in the MI process is, and why they should indeed be addressed. Notice also that this explanation accounts for all the observable phenomena associated with heart disease and is substantiated by years of research. The true origin of this epidemic of heart disease could not be more clear.

NOURISHING THE PARASYMPATHETIC NERVOUS SYSTEM

If heart disease is fundamentally caused by a deficiency in the parasympathetic nervous system, then the solution is obviously to nurture and protect that system, which is the same as saying we should nurture and protect ourselves.

Nourishing our parasympathetic nervous system is basically the same as dismantling a way of life for which humans are ill-suited. This means avoiding the excesses of industrial civilization. The known things that nourish our parasympathetic nervous system are contact with nature, loving relations, trust, economic security (a hallmark of indigenous peoples the world over) and sex—this is a whole new world of therapy for ailing hearts.

The medicine that supports all aspects of the parasympathetic nervous system is an extract from the strophanthus plant called ouabain or gstrophanthin. G-strophanthin is an endogenous (made within us) hormone manufactured in our adrenal cortex from cholesterol and therefore inhibited by statin drugs.

G-strophanthin does two things that are crucial in this process—two actions provided by no other known medicine. First, it stimulates the production and liberation of ACh, the main neurotransmitter of the parasympathetic nervous system; secondly, and crucially, it converts lactic acid—the main metabolic culprit in this process—into pyruvate, one of the main and preferred fuels of the myocardial cells. In other words, it converts the central poison in this process into a nutrient. This may be what is meant in Chinese medicine when they say that the kidneys (that is, the adrenal glands, where ouabain is made) nourish the heart.

In my many years of using ouabain, I have not had a single patient have an MI while taking it. It is truly a gift to the heart.

Of course, I put all my patients on a WAPF-style heart-healthy diet, loaded with healthy fats and fat-soluble nutrients, and low in the processed carbs and sugars that are the hallmark of industrial, civilized life.

*This article was written by Dr. Tom Cowan, and was published on the Weston A. Price Foundation website. Thomas Cowan, MD is medical advisor to the Weston A. Price Foundation and a physician in private practice in San Francisco, California. He is the author of The Fourfold Path to Healing, which you can order from New Trends Publishing.Visit his website at http://www.fourfoldhealing.com. In our Ask the Doctor section, he takes health questions from readers and provides holistic suggestions for healing using diet, herbs, supplements, and movement.

To read the original article and sources to his work, please visit his journal page on the Weston A. Price website.

What causes heart attacks? (Part 1)

heart-attack-3-267x3001

The kidneys nourish the heart.
-Traditional Chinese medical texts.

The story of how I came to understand the cause, and therefore the appropriate treatment, of acute coronary syndrome involves fascinating elements of surprise and serendipity. I thought it best, therefore, to describe how this tale unfolded for me.

Acute Coronary Syndrome (ACS) describes a constellation of illnesses that include angina (chest pain), unstable angina (basically bad chest pain) and myocardial infarction (otherwise known as heart attack or MI). These three illnesses form a continuum, with angina as the mildest symptom and heart attack—when there is actual death of the heart cells—as the most severe. The history of thought about this group of illnesses is both fascinating and controversial.

It seems that heart attacks were rare in this country until about the 1930s. The incidence of fatal MIs quickly increased from about 3,000 per year during that decade to almost half a million per year during the 1950s. In fact, mid century, this formerly rare disease had become the leading cause of death in the US. The incidence has risen continually since then until just recently, when it seems that the tide may be turning a bit and the incidence lessening, or at least leveling off. Nevertheless, after decades of reckless fiddling with the American diet as a way to prevent heart disease, almost a million Americans still die from heart disease each year.

The Conventional Theory

As you can imagine, when it became clear that we were suffering from an epidemic of this disease, physicians and cardiologists developed an intense interest in the cause and possible treatment of the disease. Around the late 1940s, the medical establishment proposed a simple and plausible explanation for MI, and this explanation soon became universally accepted.

The current thinking about heart attacks focuses on the blood supply to the myocardial (heart) cells from the network of coronary arteries, that is, the arteries that supply blood to the heart itself. There are four main arteries, each supplying blood to a different region of the heart. Medical experts believe that when one or more of these arteries gets blocked with plaque, a condition called atherosclerosis, then the inside of the artery becomes narrowed, the blood flow becomes compromised and, in times of myocardial stress (such as exercise or emotional trauma), the insufficient blood flow causes damage to the particular region of the heart fed by the blocked artery. This diminished blood flow first causes pain (angina) and then, if more severe, death to the heart tissue.

Here was an elegant and plausible theory. Voilà! Case closed. The only thing left to figure out was what was causing the arterial blockages. This answer was famously supplied by Dr. Ancel Keys in the 1950s. Keys fingered cholesterol as the culprit, claiming that excess cholesterol floating around in the blood built up as plaque in the arteries. For over fifty years the theory has survived without any significant changes. In fact, if someone has a heart attack today, we often call it a “coronary,” referring to the presumed source of the problem, the coronary arteries.

This theory about the cause of heart attacks is so ingrained in our culture that until recently, even a medical skeptic like myself never really questioned it. My only issue with the theory centered on the material in the plaque, which research subsequently revealed to be mostly inflammatory debris, not cholesterol. But I never really gave any thought to the basic premise, namely, that blocked arteries cause heart attacks.

It should be mentioned that this theory about the cause of heart attacks has led to a massive industry devoted to its diagnosis and treatment. Angiograms (in which dye is injected into the vessels to see if they are blocked), bypasses, stents, angioplasties (like roto-rooters for blocked arteries), cholesterol- lowering drugs and lowfat, low-cholesterol diets are all based one hundred percent on the acceptance of blocked arteries as The Cause of acute coronary syndrome.

The whole debate in modern cardiology, both alternative and conventional, is how to stop the buildup of plaque or—more recently— how to prevent plaque in the arteries from breaking free and forming a clot, thereby completely blocking an artery already narrowed by the buildup.

heart copy

The Digitalis Connection

Around two years ago I received an email from the son-in-law of a recently deceased and apparently well-known Brazilian cardiologist, Quintilaino H. de Mesquita. Before he died, Dr. Mesquita had published a summary of twentynine years of research carried out at his cardiology hospital, data on what he called the “true cause and effective treatment of MIs.” His son-in-law and fellow researcher, Carlos Monteiro, emailed me a simple question, which was: “When you put your cancer patients on low-dose whole digitalis plant extract, does this lower their incidence of MIs?”

His question was actually a response to a series of articles describing the effectiveness of low-dose whole digitalis leaf extract in the treatment of a variety of cancers, which I had recently posted on my website, www.fourfoldhealing. com. I wrote back asking why he wanted to know this. He replied that in Dr. Mesquita’s groundbreaking study on what he called the myogenic (that is, arising from the muscle) theory of heart disease, he had stumbled on an unexpected result: the digitalis they were using to treat MIs had also dramatically lowered the incidence of cancer in their heart patients, and mine was the only website they found that mentioned this association.

As I had never heard of either the myogenic theory or of the use of digitalis for heart attack, I asked what this was all about. His response was a box of articles and books all published over the last fifty years that seemed to refute the coronary blockage theory of MIs and support what he called the myogenic theory. I spent the next two months poring over these studies until I became convinced that this was perhaps the biggest medical news of the decade, maybe of the entire century.

The Myogenic Theory

Briefly, the myogenic theory of MIs states that:

  1. The coronary obstruction theory does not adequately explain all the observed facts concerning MIs.
  2. The major etiologic (cause and effect) factor in an MI is a destructive chemical process; specifically, in situations of stress on the myocardial (heart muscle) tissue, often as a result of small vessel disease, the myocardial tissue gets insufficient oxygen and nutrients. This leads to destructive lactic acidosis in the tissue which, if unchecked, leads to death of the myocardial cells. This process is largely unrelated to coronary artery disease.
  3. The regular use of cardiotonics, primarily low-dose whole digitalis extracts or an extract of another herb called g-strophanthin, prevents this lethal acidosis and therefore prevents and corrects the true cause of this syndrome. The result is substantially lower morbidity and mortality from heart disease.

Let’s look at some of the data supporting these three conclusions. First, does the coronary obstruction theory adequately explain the observed facts? Interestingly, in the 1940s and 1950s, when the coronary blockage theory was first proposed, the majority of cardiologists did not accept it. They pointed out that while coronary arteries are not the only arteries to have plaque, the only tissue to suffer from decreased blood flow during a heart attack is that of the heart. In other words, no one has a spleen attack or a kidney attack, yet the arteries feeding these organs also get plaque buildup.

Furthermore, the medical literature reveals some surprising findings. In a 1998 paper by Mirakami,1 the author found that of those with an acute MI, 49 percent had a blockage, 30 percent had no coronary blockage, 14 percent had insufficient blockage to impair blood flow, and 7 percent had “another condition.” In a 1972 paper,2 a researcher named Roberts showed that in acute MIs, only 50-60 percent had evidence of sufficient blockage to impair blood flow. And a 25-year autopsy study of patients who died from an acute MI, carried out by Spain and Bradess, found that only 25 percent had sufficient blockage to account for their MI, while a total of 75 percent had only mild to moderate blockage.3 In a second paper,4 these same authors reported on a surprising discovery: when a heart attack is fatal, the longer the time elapsed between the MI and death (and then subsequent autopsy), the more likely they were to find significant blockages. If death occurred one hour after onset of an MI, only 16 percent had sufficient blockages to account for their MI; if death occurred 24 hours after the onset of an MI, the number with sufficient blockages to account for the heart attack increased to 53 percent. The authors concluded that the arterial blockages are a consequence, not a cause, of myocardial infarction.

As I looked into this subject further, I found that some of the most prominent cardiologists in our history were skeptical about the coronary artery theory of MI. For example, in 1972, Dr. George E. Burch stated, “The cardiac patient does not die from coronary disease, he dies from myocardial disease.”5 A 1980 editorial in the prestigious journal Circulation states, “These data support the concept that an occlusive coronary thrombus (otherwise known as a blockage) has no primary role in the pathogenesis of a myocardial infarct.”6 Finally, as recently as 1988, Dr. Epstein of the National Institutes of Health states: “They found that in an advanced state of narrowing of the coronary arteries, the supply of blood to the heart muscles is fully assured via collaterals that enlarge naturally in response to the blockage.”7 In fact, researchers have found that the more the coronaries narrow, the less danger there is of a heart infarct.

These shocking studies dovetail perfectly with a different study, one that rocked the world of cardiology, published in 1988 titled “Twenty years of coronary bypass surgery.”8 Referring to two major studies, the Veterans Administration (VA) study and the NIH Coronary Artery Surgery Study (CASS), the authors made the following statement: “Neither the VA nor the CASS has detected a significant difference in long-term survival between the medical and surgical treatment groups when all patients were included.” In other words, surgery to bypass blocked arteries did not improve the chances of patient survival—not the result one would expect if blocked arteries were the cause of heart attacks. Thus, evidence for the coronary artery theory of MI is not strong; in fact, it is actually refuted in the relevant literature.

The Theory Fits The Facts

So, if heart attacks are not the result of coronary artery disease, then what does cause all these MIs? The myogenic theory of Dr. Mesquita, in fact, fits all the current observations about this condition. The myogenic theory postulates that as a result of disease in the small vessels—the capillaries and small arterioles—which is a consequence of such factors as stress, diabetes, smoking and nutritional deficiencies, heart cells, which are very active metabolically, suffer from inadequate oxygen and nutrient supply. This oxygen and nutrient deficiency increases under stressful conditions. When this happens, the heart cells revert to their backup system, which is anaerobic fermentation for energy generation— very similar to what happens in your leg muscles when you run too far or too hard. The anaerobic fermentation produces lactic acid which collects in the tissues. Because the heart, unlike your leg muscles, cannot rest, the acidosis progresses if untreated, leading to actual death of the myocardial cells.

As a result of this necrotic process, inflammatory debris collects in the tissues, and it is this debris that is the actual source of the coronary artery blockages seen in death from acute MI. As you would predict, the longer the time period between the MI and death, the greater the likelihood of blockage—exactly as observed in the studies. The only conclusion one can draw from this is that the heart cells die first and only then does the artery become blocked with debris liberated at myocardial cell death, which is precisely the kind of debris that is found in these blockages. The current practice of flushing out arterial blockages can help remove the debris and restore blood flow to the compromised arterial system, but this in no way suggests that blocked arteries represent the primary event in the sequence leading to an MI. However, the whole emphasis on the coronary artery blockage is fundamentally a dead end and doomed to failure, whether it is approached from a surgical (bypass, stents, etc.) or a medical (cholesterol-lowering drugs, restricted diets, etc.) point of view.

file [Converted] copy

Myogenic Therapy

The myogenic theory points us to a very different kind of preventive treatment for heart disease, one that focuses on small vessel disease and the prevention of heart tissue acidosis. The theory also explains why stress, diabetes and smoking are such strong risk factors for MI, because these factors have all been shown to primarily affect small capillaries and small blood vessels, not the large coronary arteries. But the story gets even more interesting.

It turns out that there are simple, inexpensive and very effective compounds that effectively prevent lactic acidosis in the heart tissues. These medicines have been known for centuries as cardiotonics and have been used for treating heart disease in every traditional medical system in the world. The two best known are digitalis (the common foxglove) and strophanthus, an African vine. These plants are the source of so-called cardiac glycosides: digoxin and digitoxin from digitalis, and ouabain from strophanthus. The function of these compounds is to regulate the rhythm and power of the cardiac contraction and to prevent or reverse lactic acid buildup in the cardiac tissue. This is why these plants have been used for centuries to treat congestive heart failure, rhythm disturbances and other disorders of heart function.

The amazing thing is that these compounds are exact chemical copies of hormones made by our adrenal glands. And our adrenal glands produce these cardiotonics out of . . . cholesterol! Now we know why all the draconian dietary and pharmaceutical measures to lower cholesterol have not resulted in a decrease in the rates of MI, and why numerous studies have shown that as we age, those with the highest levels of cholesterol live the longest. When we lower cholesterol, we are depriving our bodies of the very substance they need to manufacture cardiotonics.

The myogenic theory also explains why stress can lead to heart attacks. In conditions of stress, our adrenal glands must work very hard to create numerous hormones that regulate the blood sugar and help the body heal. If the adrenal glands are weak or overloaded, production of cardiotonics goes on the back burner.

While there are few studies in the conventional literature that have considered the effectiveness of digitalis or strophanthus in the treatment of MI, Dr. Mesquita’s clinical results over twenty-nine years show a dramatic lowering of the death rate, recurrent MI rate, angina rate and all symptoms in the spectrum of acute coronary syndrome with the use of oral low-dose digitalis glycosides. These results are published in Teoria Miogenica Do Enfarte Miocardico, available through the Infarct Combat project website, www.infarctcombat.org.

Also, a German cardiologist, Dr. Berthold Kern, used g-strophanthin in a study for the German government which showed a dramatic reduction in MIs in his practice, down from the expected 400 to 20, with the use of this medicine.9 Furthermore, many reports are coming in from Germany in which doctors have noted a decrease of up to 81 percent in angina attacks with the use of oral g-strophanthin.10

In my practice, I generally use oral strophanthin in the form of the preparation known as Strodival for all my angina and MI patients, and I have uniformly recorded a decrease in angina episodes, improved exercise tolerance and, thus far, no MIs. When combined with a nourishing traditional diet, cod liver oil, high vitamin butter oil, CoQ10 (which helps strengthen the heart muscle) and Standard Process heart nutrients (Cardioplus, two capsules three times per day, and Cataplex E2, two tablets three times per day), I have seen a huge improvement in the lives of patients with this otherwise devastating condition. (Note: Both digitialis leaf and Strodival are prescription-only items which need to be prescribed by a doctor who is well versed in their use.)

The final irony is that the traditional Chinese doctors were correct. The kidneys (their way of referring to the adrenal glands) help the body deal with stress as well as make hormones (digoxin and ouabain) that keep our marvelous hearts healthy, strong and open to enjoy the full richness of life


Sidebars

Why Plaque Is A Problem

While plaque in the arteries leading to blockage may not be the main cause of heart disease, there is no doubt that the phenomena of athersclerosis (plaque formation) is a real problem in people, especially as we age. Certain sections of our arteries are subject to thickening and the formation of what is called fatty streaks for reasons that have to do with flow dynamics, that is, the velocity of blood flow and turbulence in that particular artery. A certain amount of thickening in places where the blood creates a lot of pressure on the arteries is normal and protective, and it therefore occurs in everyone. But the build up of plaque is a different situation and can lead to many problems. For example, blocked arteries in the legs can cause calf cramps and pain, which we refer to as intermittent claudication (leg pain while walking). In the brain, plaque formation leads to ischemic (lack of blood flow) stroke. In the kidneys, diminished blood flow due to plaque formation is a possible contributing factor in some cases of hypertension (high blood pressure). Likewise, blocked arteries leading to the liver or spleen can result in reduced function of these organs. The reasons for this plaque formation are unclear. Although scientists have long blamed such build up on high cholesterol levels in the blood, informed medical researchers today often cite inflammation in the vessels as the cause. Of course, this inflammation is secondary to other factors, such as stress, consumption of processed vegetable oils and nutrient deficiencies (particularly of vitamins A and C and minerals like copper). But plaque formation is not a sufficient explanation for the whole phenomena of myocardial ischemia. The reason the heart but not the spleen or the liver has “attacks” is because the energy use of the heart is so much higher and also because the heart can never rest. Because scientists have overlooked these factors, treatment of heart disease today is far less effective than it otherwise could be. The only other organ that might be said to suffer from an “attack” is the brain when a stroke occurs. However, strokes usually happen when a clot forms in one of the arteries feeding the brain. The process is not the same as lactic acid build up in the heart.

How To Protect Your Capillaries

  • Avoid high blood sugar: diabetes is a serious risk factor for capillary damage. A high-fat, low-carbohydrate diet is your best defense against diabetes. If you have diabetes, follow the protocol posted at www.westonaprice.org/moderndiseases/ diabetes.html.
  • Don’t smoke! Smoking is a risk factor for capillary damage.
  • Engage in moderate outdoor exercise.
  • Avoid commercial liquid vegetable oils, which are full of free radicals that can damage capillaries.
  • Follow a nutrient-dense traditional diet

Be Kind To Your Adrenal Glands

Since the adrenal glands, specifically the adrenal cortex (the outer portion of the adrenal gland), produce protective cardiotonics, an important strategy in protecting yourself against heart attack is to strengthen the ability of this important gland to work properly.

  • Avoid stimulants such as caffeine and related substances in coffee, tea and chocolate. Caffeine causes the adrenal medulla (the inner part of the adrenal gland) to produce adrenaline. In response, the adrenal cortex must produce a host of corticoid hormones that bring the body back into homeostasis. Repeated jolts of caffeine can lead to adrenal burnout, a situation in which the adrenal cortex is unable to produce the myriad of protective and healing substance for the body, including the cardiotonics.
  • Don’t try to lower your cholesterol—the cardiotonics are made from cholesterol.
  • Take cod liver oil for vitamin A. The body needs vitamin A to make all the adrenal cortex hormones from cholesterol. Vitamin A intake should be balanced with vitamin D (from cod liver oil) and vitamin K2 (from the fats and organ meats of grass-fed animals).
  • Don’t consume trans fats. Trans fats (from partially hydrogenated vegetable oils) interfere with the enzyme system needed for the production of adrenal cortex hormones.
  • Take care to avoid low blood sugar. When blood sugar drops too low, the adrenal glands go into overdrive to produce hormones that bring the blood sugar back up. This means avoiding sugar and not skipping meals. There is just no substitute for three good meals a day, at regular intervals, which contain adequate protein and plentiful amounts of good fat.

*This article was written by Dr. Tom Cowan, and was published on the Weston A. Price Foundation website. Thomas Cowan, MD is medical advisor to the Weston A. Price Foundation and a physician in private practice in San Francisco, California. He is the author of The Fourfold Path to Healing, which you can order from New Trends Publishing.Visit his website at http://www.fourfoldhealing.com. In our Ask the Doctor section, he takes health questions from readers and provides holistic suggestions for healing using diet, herbs, supplements, and movement.

To read the original article and sources to his work, please visit the journal page on the Weston A. Price website.

Nutrition: The Anti-Aging Factor

accountable-weight-loss-program-woman-1024x683

Due to increasing gains in life expectancy, by 2025 the number of people aged sixty-five and over will comprise 29 percent of the U.S. population. As a consequence of aging, the typical chronic diseases of the body and brain such as cardiovascular disease, cancer, hypertension, and Alzheimer’s disease (AD) will claim more and more precious human resources. To pursue good health as we age becomes more and more important in order to enjoy a disease-free and rewarding quality of life during our later decades.1

From the moment of our birth we begin to age. Aging can generally be defined as a progressive decline in the efficiency of biochemical and physiological processes after the reproductive phase of life.2 From one birthday to the next we are unaware of the fact that our cells, organs and bones are slowly losing some of their function. The common lament, “I am not as young as I used to be,” has become reality for the Baby Boomer Generation as it grows older.

With the appearance of the first crow’s feet, many men and women flock to cosmetic surgeons, anti-aging physician specialists, dietary supplements, and cosmetics counters to buy the newest anti-aging products, which are often laden with toxic chemicals. Americans spend millions on anti-aging therapies, according to Global Industry Analysts, which says that this spending will “push the U.S. market for antiaging products from about $80 billion now to more than $114 billion by 2015.”3 But the solution to feeling good and looking fit and healthy may not be so elusive or expensive, and in fact may be found only a few steps away—at your farmers’ market or in your own garden.

THE PHYSIOLOGY OF AGING

Aging has been predetermined in our genes, experts say, and cells can only divide forty to sixty times before they reach the “Hayflick Limit,” a theory advanced in 1961 by Leonard Hayflick at the Wistar Institute in Philadelphia, Pennsylvania. Structures at the end of chromosomes called telomeres protect cells from deterioration or fusion with other chromosomes. After each new replication the telomeres shorten until they reach a critical length when they stop dividing, begin to “age” and ultimately die.4  Scientific laboratories like SpectraCell now provide telomere testing as “a window into your cellular age.”5 DNA damage, exposure to toxins, irradiation, and activation of oncogenes (genetic material that carries the ability to induce cancer) also cause cell aging and death in healthy cells.6

On the other hand, a rare “genetic condition” called progeria—accelerated premature aging— can develop in infants and young children which is not actually genetic in nature yet appears through a “new” point mutation on a specific chromosome. These children quickly develop the typical symptoms of old age, such as hair loss, atherosclerosis, loss of eyesight, wrinkles and stiff joints, but the brain seems not to be affected and mental development is normal.7

An exception to the Hayflick limit is cancer cells, which appear to be immortal in their ability to continue reproducing. Because of a telomere-lengthening enzyme, mutation, viral infection, or production of chemicals such as the enzyme nagalase, which blocks the immune system from destroying them, they avoid normal programmed cell death (apoptosis).8

The most famous, oldest, and most commonly used immortal cell line, dubbed HeLa, originated in a tumor sample taken from an African-American woman, Henrietta Lacks, who is the subject of the recent book The Immortal Life of Henrietta Lacks.9 The tumor cells, harvested at Johns Hopkins Hospital, gave rise to the eponymous HeLa cell line which researchers have used continuously since her death in 1951 for numerous experiments, including Jonas Salk’s development of the polio vaccine. Contamination with human papillomavirus made them immortal.10 Neither Henrietta Lacks nor her family received one penny from the millions of dollars made from her uninformed and involuntary cell donation. Researchers have grown and used around twenty tons of her cells and research relating to this cell line has generated seventy-six thousand abstracts on Pub Med.11

Cancer cells aside, probably the most important factor in aging and living long with a good quality of life is nutrition. What we eat supplies the building blocks for our body’s cells, energy-producing mitochondria, enzymes, and co-factors that build or break the body. When a vital piece of this complex puzzle goes missing, the body scrambles to find substitute pieces. But the results may not look much like what nature intended. Disease and illness are the result.

The Standard American Diet (SAD) comprises a supermarket basket of industrially refined products whose packaging is sometimes more nutritious than the contents. Dominated by genetically modified corn and soy derivatives along with trans fats, refined and rancid vegetable oils, artificial colorings, flavorings, sweeteners, and high fructose corn syrup, the unpalatable and sickening ingredient list goes on and on. Coupled with pesticide-laden fruits and vegetables, suspicious animal products from factory and confinement operations, our standard commercial food supply is far from nutritious and is more likely dangerous. Fortunately there are many things that we can do to improve the quality of our meals and supply our bodies with the building blocks they need to function optimally all throughout life.12

AVOID SUGAR

Sugar has proved to be one of the most damaging substances to health and is a major factor in premature aging. Fructose in particular is an extremely potent pro-inflammatory agent that accelerates aging.13

Since its introduction to the New World, sugar consumption has progressively increased from less than five pounds per year per individual in 1850 up to one hundred fifty pounds in 2003.14 Between 1900 and 1967 the use of sugar more than doubled in the U.S. and U.K.15 In 1970, an additional sugar source, high-fructose corn syrup, was introduced into the industrial food supply.14

Fructose, contained naturally in some fruits and in the form of high fructose corn syrup, is a part of the fructose load, which the body processes differently from glucose. The body uses glucose for fuel but stores fructose in the form of triglycerides. Sucrose (cane or beet sugar) is half glucose and half fructose.16

Sugar forms advanced glycation end products (AGEs) when it reacts with amino acids and fats, a process which can occur in food itself during cooking and also in metabolic reactions inside the body.15 In cooking, the process is called the Maillard reaction, which gives breads and meats their browned, caramelized aroma and appearance. Searing meat and cooking at high heat form AGEs. Braising and stewing cuts of meat at lower temperatures and in “moist heat” environments in covered vessels are more healthful cooking methods because fewer AGEs are formed. AGEs are also responsible for colors and flavors in foods, such as in toasted bread, french fries, malt whiskey or beer, condensed milk, roasted coffee, caramel, chocolate syrup, and others.17 Pressure cooking can also contribute to the formation of AGEs because of the high temperatures generated during cooking.18

Glucose is the least reactive form of sugar and forms many fewer AGEs than fructose. In diabetic patients the concentration of fructose often surpasses that of glucose in the lens of the eye, causing cataract growth and blindness, and in nerves, causing neuropathies.19

Fructose is also a potent creator of AGEs that speed up the aging process.20 It does this in the conversion from fructose to fructose 1-phosphate, which drains the energy source, ATP, from the cells and promotes a dramatic inflammatory response.21 Gary Taubes explains in his books, Good Calories, Bad Calories and Why We Get Fat, that it is fructose, not saturated fats, that contribute to high insulin levels and insulin resistance, promoting adipocyte formation around the liver and midsection, and increasing insulin and leptin levels, all factors associated with premature aging.22 In addition, fructose elevates blood cholesterol, uric acid, urea nitrogen and lactate production.20

AGEs cause inflammation, which promotes heart disease, Alzheimer’s disease, diabetes, liver damage, and other chronic degenerative diseases. When receptors for AGEs bond with scar tissue in the endothelium of blood vessels, arterial plaques are formed. Collagen, the lens of the eye (cataracts), myelin, and DNA also accumulate AGEs. Glycation can be determined by a test for hemoglobin A1c, which is a marker of long-term blood sugar levels and how the body processes sugar.20

FLUORIDE HASTENS AGING

Fluoride has been added to community water supplies in the U.S. since the 1940s and continues to be a goal of the Public Health Service (PHS), which considers water fluoridation “one of the ten greatest achievements of the 20th century.” Yet for all this lip service to the victories of public health mandates, the PHS in fact has paid little attention to the harmful physical effects of fluoride on the human body. No government funds are available to explore the topic of fluoridation dangers. Existing research on fluoride’s insidious effects on the body comes from scientists in other countries such as India, where ground water contains extremely high amounts of fluoride and all want it out, not in. The Chinese government recently funded a series of studies on fluoride and IQ. 25,26

Ingestion of fluoride induces adverse effects not only in teeth and bones, but also in various soft tissues such as brain, skeletal muscle, kidney and liver, and interferes with reproductive functions, such as the production of sperm. Fluoride is a powerful central nervous system toxin and adversely affects brain function even at low doses, and causes neuron death along with impaired memory and learning. Fluoride disturbs the antioxidant enzyme activities in the brain. Fluoride fed to rats caused DNA damage in their brain cells and epigenetic changes in the brain tissue of offspring of the exposed rats.27

In rats treated with sodium fluoride (NaF) (the pharmaceutical form of fluoride), administration of vitamin D significantly lessened the skeletal and visceral abnormalities of skeletal fluorosis. Altered serum enzyme activities and lipids in the livers of male rats with fluorosis recovered to normal levels when the rats were given selenium. By improving mitochondrial membrane stability, selenium (Se) protected skeletal muscle cells damaged by fluoride through a disruption of energy metabolism in the mitochondria. 27

A recent Indian study showed that rats treated with NaF showed significantly enhanced activity of the pro-oxidants xanthine oxidase and lipid peroxidation, and decreased activity of the antioxidants catalase, superoxide dimutase, glutathione- s-tranferase, glutathione perioxidase, and glutathione reductase. Supplementation of Se along with NaF reversed the pro- and antioxidant systems towards normal levels. Selenium also increased general fluoride excretion. The accumulation of fluoride in the mouse brain was significantly less in mice treated with Se.27

Selenium is a necessary trace mineral in human nutrition and a potent antioxidant. The major biological form of Se is found in the amino acid selenocysteine. It is toxic in high doses. As a co-factor, it is required for the activity of a number of selenoenzymes involved in the stress response and in the maintenance of high tissue antioxidant levels.

Selenium acts nutritionally through its various selenoproteins to control the level of cellular hydroperoxides and the redox tone of the cell. Hydroperoxides can damage protein and cell organelles involved in the regulation and control of the body’s antioxidant glutathione peroxidase system, which plays a major role in the control of reactive oxygen species (ROS).28

Selenium appears to be an anti-aging nutrient in that it protects humans from the pro-oxidant effects of fluorides on the brain and body. Selenium is found in fish, shellfish, Brazil nuts, organ meats, poultry, dairy, onions, and in supplements of seleno-methionine. Supplements containing selenites are not useful and may be harmful.28

One of the most memorable fluoride researchers of all time was Dr. John Yiamouyiannis, a biochemist, researcher, and the editor of Chemical Abstracts Service, the world’s largest information center on chemicals. Dr. Yiamouyiannis demonstrated that fluoride caused cancer and that mortality rates were significantly higher in fluoridated communities. In 1993 he wrote in Fluoride: The Aging Factor that fluoride caused premature skin wrinkling through its effect on the breakdown and irregular formation of collagen in the skin, along with weakened tendons, ligaments, muscles, cartilage and bones, causing cases of irreversible arthritis. By studying populations in Turkey, India, and Italy where natural fluoride in the water is high, he saw the effects of crippling skeletal fluorosis.29

He revealed in his book that by 1981, scientists knew that fluoride inhibited enzymes by binding to their co-factors, such as magnesium and phosphate. At one part per million (ppm) fluoride changes the bonds holding the protein in place, disrupting the enzyme shape and activity and setting off an autoimmune reaction, with possible effects on the DNA molecule itself.29 The U.S. government claims that fluoridation at four parts per million is not harmful.25

Fluoride also blocks the migration of white blood cells to the site of infection in the body, damaging the immune system’s ability to destroy pathogens. Researchers discovered that fluoride perturbed the white blood cells’ components and function by stimulating their production of superoxide when at rest, thus releasing superoxides into the blood stream, damaging tissues and depleting energy reserves, processes associated with accelerated aging. Further, in the presence of infection, fluoride inhibited the cells’ production of superoxides— compounds that the cells normally employ against the challenge of a pathogen— thereby crippling white blood cells’ healthy response.29

Back in 1932 the dentist Dr. Weston Price reported a general disturbance of mineral metabolism and decreasing blood levels of iron, calcium, phosphorus, and potassium by fluorides. He wrote about his findings in the paper “Evidence of a need for fluorine in optimum amounts for plants and animal growth, and bone and tooth development with thresholds for injury.”26

To avoid fluoride’s detrimental effects on the body, avoid fluoridated water, and products made from it, such as soft drinks, beers, tea mixes, energy drinks, fruit juice mixes, and especially those products packaged in aluminum cans. Baby formula should never be mixed with fluoridated tap water. Mother’s milk is the beverage of choice for infants.25

If you live in an area where the community waters are fluoridated, a reverse osmosis system will remove it from your water. However, exposure to fluoride occurs not only through drinking and cooking, but also through bathing, showering, and watering the garden. Many vegetables and fruits are sprayed with a fluoride spray for storage and grown with fertilizers that contain fluoride.29

Fluoride occurs naturally in the soil and tea plants (Camellia sinensis) have a natural affinity for it—they take it up into their roots. Soils in parts of India, Turkey, and China, where most tea is grown, have high amounts of fluoride in the soil. Some tea is also sprayed with fluoride-containing pesticides. Especially high in fluoride is instant tea. Organic teas have somewhat lower fluoride content. Grapes and grape products such as raisins and wines are high in fluoride.25-26,29 People living near industrial areas with steel, fertilizer, aluminum, clay, glass, enamel and other manufacturing industries are exposed to high levels of fluorides in the air.29

FREE RADICAL THEORY OF AGING

Cells cannot live without oxygen, yet oxygen is the very source of free radicals that endanger the cells’ existence. The body uses molecular oxygen to produce energy via oxidative phosphorylation in the mitochondria. This energy production and other metabolic reactions generate free radicals which cause a condition called oxidative stress. This cellular damage affects proteins and DNA replication, and inhibits repair through many complex processes, including telomere shortening in the DNA components.30-31

Denham Harman, MD, PhD, the “father” of the free radical theory of aging, first proposed his hypothesis in 1965. Today it is the most widely accepted theory used to explain the aging process. Harman claimed that aging is the result of oxidative stress due to reactive oxygen species (ROS)—also called free radicals—generated by a multitude of endogenous and environmental processes. They are highly reactive molecules that can directly damage the structures of cells and their lipids and proteins, as well as DNA. Other cellular sources of superoxide radicals include xanthine oxidase activity which forms the superoxide anion followed by the generation of hydrogen peroxide. Neutrophils, eosinophils, and macrophages are also sources of cellular ROS.32

In the body, free radicals are produced in the mitochondria during detoxification reactions (cytochrome 450), in peroxisomes, and during inflammation. ROS can be produced from outside sources such as xenobiotics, chlorinated compounds, fluorides, environmental agents, metals, ions and radiation.30

The body possesses multiple endogenous defense mechanisms to protect it from ROS by weakening and destroying those substances. These mechanisms take the form of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase) and the non-enzymatic antioxidant molecules (vitamin E, vitamin C, vitamin A, ubiquinone and others), which include the sulfur-containing antioxidants (glutathione, theoredoxin, alpha lipoic acids), melatonin, carotenoids, flavonoids, and polyphenols. The best dietary choice to fight aging is first and foremost avoidance of industrial fats and oils, which are just loaded with free radicals. Use butter, cook in saturated fats, and make your own salad dressing with olive oil.

Next, include foods and botanicals that contain multiples of anti-oxidant nutrients: the anti-aging powerhouses of garlic, curcumin, herbs, blueberries, and so on, which contain potent free radical scavengers.30

Catalase is a very important enzyme which protects the cell from oxidative damage by ROS. It is involved in the quick conversion of hydrogen peroxide (H2O2), produced in many reactions, to water and oxygen. Hydrogen peroxide is produced as a potent antimicrobial agent in the immune response when cells are infected with a pathogen. It is also a byproduct of normal cellular respiration, and is formed from the superoxide anion by the action of superoxide dismutase. Fuel your catalase production by eating foods like meat which contains sulfur, iron and methionine. 32

Catalase has one of the highest turnover rates for all enzymes: one molecule of catalase can convert approximately six million molecules of hydrogen peroxide to water and oxygen each minute.62 Catalase deficiency has been implicated in diabetes type 2, and in schizophrenia, atherosclerosis and other chronic diseases.32

Despite the presence of the cell’s antioxidant defense system to counteract oxidative damage from ROS, oxidative damage accumulates during the life cycle and has been implicated in aging and age-dependent diseases such as cardiovascular disease, cancer, neurodegenerative disorders and other chronic conditions. It becomes extremely important to supply the body with building materials needed for enzyme and antioxidant production through diet and supplementation to lessen the processes that lead to aging.30-32

PROBIOTICS FOR HEALTHY GUT AGING

Aging is accompanied by lower levels of gastric acid, an increase in stomach pH, and delayed stomach emptying, all of which contribute to a shift toward gut dysbiosis and a loss of microbial diversity. A lifetime history of antibiotic use destroys healthy colonies of probiotic bacteria and leads to increasing numbers of pathogenic bacteria, such as Clostridium difficile (C. diff ), especially in those receiving antibiotic therapy. Studies show 21 percent of hospitalized patients with C. diff infections compared to 1.6 percent in the community at large.

The most important characteristic of age-related gut dysbiosis is the decline in the abundance, diversity and adhesive properties of Bifidobacterium species, which have important anti-infective and immunomodulatory functions. Lower levels are associated with an increased susceptibility to gastrointestinal and systemic infections as well as inflammatory conditions. This status leads to a decline in immunological function accompanied by an increase in inflammation, called “inflamm-aging,” a characteristic of many chronic diseases such as cardiovascular disease, Alzheimer’s disease, type 2 diabetes, osteoporosis and cancer. Aging is also accompanied by a decrease in innate as well as adaptive immunity, termed “immunosenescence,” which relates to an increased susceptibility to infections and autoimmunity.

One of the most important strategies to healthful aging and long life is to maintain a healthy immune system via the gut. Centenarians studied have healthy immune factors and the portion of healthy Bifidobacterium species ranging from 53 to 87 percent compared to 40 percent found in healthy younger people.

“Bifidobacterium strains isolated from healthy centenarians have been shown to enhance both immune function and intestinal function in healthy mice following oral administration. These findings provide tantalizing evidence that healthy centenarians are characterized by a gastrointestinal microbiota containing more numerous, diverse Bifidobacterium populations that possess more valuable immunomodulatory properties than are even present in younger healthy people. Other studies show that preserved immune function modulated by a balanced gut microbiota is a characteristic of healthy elderly people at any age.”40

Centenarians and especially those over one hundred years of age are examples of those who have learned to age successfully and well. What factors contribute to that longevity? Some of the longest lived people come from the Bulgarian mountains near the Greek border where fermented milk products have a long tradition in the local diet. The bacterium that ferments milk to yogurt is known as Lactobacillus bulgaricus and researchers from around the world have come to Bulgaria to study the fermented milk. A typical Bulgarian centenarian eats yogurt three times a day, “sometimes with bread crumbs.” In existing pockets of longevity in locations around the world, like the native peoples studied by Dr, Weston Price, these peoples continue to eat their native diets of mostly fresh and unprocessed foods, and are generally isolated from most of the worst influences of modern civilization. They enjoy lives of moderation, sleep well and walk and work outdoors. They benefit from sunny, pollution-free, and oxygen-rich mountain living. 41

THE AGING BRAIN

The brain also ages and neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s, can be blamed on the processes of aging. Cerebral volume decreases and ventricles expand. Plasticity—the ability to change and function—decreases, as do the gray matter cells composed of neurons involved in senses, emotions, self-control, and muscle control, as do the memory parts of neurons, called dendritic spines.42-44

Increasing numbers of neurofibrillary tangles, accumulated tau proteins, and amyloid plaques are found in the brains of Alzheimer’s disease (AD) patients. Recent theories have connected aluminum deposits in the brain to the formation of fibrillary tangles, the hallmark of AD. Aluminum is a neurotoxin involved in the development of AD. It is contained in vaccines, absorbed from aluminum cookware, and is an ingredient in antiperspirants, coated aspirin, and many over-the-counter medications. “Aluminum’s contribution to AD is based upon at least seven independently derived observations that at physiologically realistic concentrations, aluminum strongly promotes amyloid aggregation and accumulation, a key feature of AD neuropathology.”45-47

Vitamin D is extremely important in the maintenance of a healthy brain and makes the antimicrobial peptide cathelicidin, which suppresses herpes simplex virus-1 (HSV-1) flareups, otherwise silent except for the appearance of cold sores. HSV-1 has been implicated in AD. The best source of vitamin D is the sun. As a fat-soluble vitamin, it is found in fat-based foods such as cod liver oil, pastured butter and lard from pastured pork. Vitamin D supplements are not always effective because they lack vitamin D’s partners, vitamin A and vitamin K2, which work in tandem with vitamin D.48

A recent study found that melatonin protects neurons against the damage of AD.46 Melatonin is produced from serotonin in the pineal gland located in the inner brain. With aging, the pineal gland becomes calcified, thus less functional. But calcification has also been observed in young children. About 40 percent of Americans have calcified pineals by age seventeen.50 “Calcium, phosphorus and fluoride deposits increase with aging and are likely to cause decreased melatonin production and abnormal pineal function, which could contribute to a variety of effects in humans.”51 Upon examination in many studies, the pineal gland had the highest fluoride concentrations in the body, higher than bone or teeth.52 This contributes to accelerated sexual maturation in females.53

Cognitive impairment is related to ROS. Inflammation is the most controllable risk factor in oxidative stress.54 Antioxidants like fat-soluble vitamins A, D, E, and K, as well as B and C vitamins, and omega-3 fatty acids, are recommended to reduce oxidative stress.23

Neurotransmitters like serotonin and their receptors change with aging.54 Dopamine synthesis declines as well as the number of dopamine receptors. DNA damage accumulates with age in the brain.55-56 Saturated fats and fats from cod liver oil are extremely helpful in regulating the oxidative stress in the brain as we age.

IN CONCLUSION

Although there are many other nutritional giants that could be included in your arsenal, they cannot all be discussed here. Overall, the basic advice that we learned as children to “eat a variety of foods from many colors” still applies. Of course man cannot live on fruits and vegetables alone. Saturated fats, especially those from pastured animals and poultry, are most important in the diet to promote a happy, healthy brain and body. Follow the principles of the Weston A. Price Foundation diet which includes generous amounts of vitamins, minerals, trace minerals, good fats, high quality proteins, and probiotic foods flavored with unprocessed sea salt.59-61

Avoid industrial fats and oils, processed foods, refined sweeteners and fluoridated water.

In addition to good nutrition, other lifestyle practices such as those listed in the sidebar below all provide pieces to the puzzle that can help create a good life crowned with satisfaction, pleasure, health, and fulfillment as we age.58

*This article is written by Sylvia Onusic, and was published on the Weston A. Price Foundation website. For the original article and sources to her work, please visit here.

Sylvia P. Onusic, PhD, CNS, LDN, a board-certified and licensed nutritionist, writer and researcher, is a frequent contributor to the journal. Her background is in foods, nutrition, and public health. As “Your Public Health Advocate,” she keeps you current on controversial topics in health and nutrition, analyzes studies in the field, and provides nutrition counseling services through her website at drsylviaonusic.com.