Health and Nutrition

August 24, 2017


Filed under: Uncategorized — Doc Joe @ 4:39 pm

May 23, 2016

Specific change of histamine metabolism in acute magnesium-deficient young rats.

Filed under: Uncategorized — Doc Joe @ 4:11 pm
Drug Nutr Interact. 1987;5(2):89-96.

Specific change of histamine metabolism in acute magnesium-deficient young rats.


The effects of dietary magnesium (Mg) deficiency on histamine metabolism were studied. Young Wistar rats were fed a Mg-deficient diet (0.001% Mg diet) ad libitum for 8 days with control groups (0.07% Mg diet), food-restricted groups (0.21% Mg diet, but restricted to 5 g/rat/day), and refeeding groups (0.001% Mg diet for 6 days ad libitum, after that fed with a 0.21% Mg diet ad libitum for 2 days). Compared to the other groups, the plasma Mg level was markedly lower in the Mg-deficient group. A return from the lower Mg level to the controls took place after feeding them a 0.21% Mg diet for 2 days. Urinary histamine level increased rapidly after 4 days and reached a maximum on the eighth day of Mg deficiency. The high urinary histamine level in Mg-deficient rats decreased rapidly after feeding them a 0.21% Mg diet for 2 days. Histamine contents in some tissues increased on the eighth day of Mg deficiency. Other groups showed no significant change. The increased histamine content in Mg-deficient rats showed a tendency to return to control levels after feeding them a 0.21% Mg diet for 2 days. Histidine decarboxylase (HDC) activity in some tissues of Mg-deficient rats increased markedly. The increased HDC activity dropped nearly to control levels after feeding them a 0.21% Mg diet for 2 days. Diamine oxidase (DAO) activity in the duodenum was high in control rats. Duodenal DAO activity decreased gradually and reached half the value of controls on the eighth day of Mg deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

[PubMed – indexed for MEDLINE]

December 17, 2014

What’s the Real Cause of Heart Attacks?

Filed under: Uncategorized — Doc Joe @ 4:40 pm

By Thomas S. Cowan, MD

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 since 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 allow for any positive benefits, and, most seriously, has led many to adopt a low-fat 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.

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 For all interested in this important subject it is advised to read the entire website and watch the video on the website. The video above 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 the two articles found in the print version of 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.” Both articles are reprinted in full on the website.

Rebuttal of Conventional Theory

Until recently I believed, along with most physicians, that most heart attacks 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 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 bypass this area with coronary bypass grafting (CABG). Simple problem, simple solution.

The problems with this approach became apparent to me through a number of avenues. 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 presenting 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 heart attacks, 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 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 or additional new 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 above video, 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 artery. 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 heart attack 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 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 heart attacks one that, as it turns out, is equally invalid.

Meet the Unstable Plaque

We can now all agree that the entire focus of cardiology—upon 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 spokesmen have even suggested putting therapeutic doses of statins in the municipal water supplies.

Defendants 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 heart attack was carried out in Heidelberg in the 1970s.2 The study found that sufficient thrombosis to cause the heart attack was found in only twenty 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 heart attack, the more often the pathology report found stenosis; in addition, the longer the time between heart attack 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 heart attack event.

Another observation that puts into doubt the relevance of the coronary artery theory of heart attack 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 heart attack I.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 heart attack?

Second, it is clear from all pathology studies that thromboses of significant degrees evolve after the heart attack occurs, again leading to the question: what causes the heart attack 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-heart attack I to restore flow in those patients who do not have adequate collateral circulation to that part of their heart. So again, all the existing theories as to the relevance of the coronary arteries in the evolution of the heart attack are fraught with inconsistencies. If this is so, what then does cause 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 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 are 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: acetylcholine, 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,10 smoking 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 a heart attack? First comes a decrease in the tonic, healing activity of the parasympathetic nervous system—in the vast majority of cases the pathology for heart attack will not proceed unless this condition is met. Think of the person who is always pushing himself, who never takes time out, who has no hobbies, who constantly stimulates the adrenal cortex with caffeine or sugar, who does not nourish himself with real food and good fats, and who does not incorporate a regular pattern of eating and sleeping into his daily life.

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 p02 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 one hundred percent of heart attacks, 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 heart attack 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. It could not be clearer as to the true origin of this epidemic of heart disease.

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 g-strophanthin. 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. There are homeopathic versions of strophanthus available, which could be used. Another option that is effective but not ideal is an extract of the plant. The drawback is that the amount of ouabain is unknown.

Reprinted with kind permission of the Townsend Letter,

About the Author

Dr. Cowan has served as vice president of the Physicians Association for Anthroposophical Medicine and is a founding board member of the Weston A. Price Foundation. He is the principal author of The Fourfold Path to Healing and is co-author of The Nourishing Traditions Book of Baby and Child Care. Dr. Cowan lectures throughout the United States and Canada. Dr. Cowan is completing a book on the human heart that will be published by Chelsea Green Publishing in 2015.

August 24, 2014

Low vitamin D levels linked to increased risks after noncardiac surgery

Filed under: Uncategorized — Doc Joe @ 3:31 pm
ScienceDaily: Your source for the latest research news

August 15, 2014
Wolters Kluwer Health: Lippincott Williams and Wilkins

Patients with low blood levels of vitamin D are at increased risk of death and serious complications after noncardiac surgery, suggests a study in Anesthesia & Analgesia.

“Vitamin D concentrations were associated with a composite of in-hospital death, serious infections, and serious cardiovascular events,” according to the new research by Dr Alparslan Turan and colleagues of the Cleveland Clinic. They believe their results warrant further study to see if giving vitamin D supplementation before surgery can reduce the risk of these adverse outcomes.

Lower Vitamin D Levels Linked to Higher Surgical Risk

The researchers analyzed the relationship between vitamin D level and surgical outcomes in approximately 3,500 patients who underwent operations other than heart surgery between 2005 and 2011. Only patients who had available data on vitamin D levels around the time of surgery — from three months before to one month afterward — were included in the study.

The concentration of vitamin D (specifically, 25-hydroxyvitamin D) in blood samples was analyzed as a risk factor for death, cardiovascular events, or serious infections while in the hospital. The analysis included adjustment for other factors such as demographic characteristics, medical conditions, and type and duration of surgery.

Most patients did not meet the recommended 25-hydroxyvitamin D concentration of greater than 30 nanograms per milliliter (ng/mL). The median vitamin D level was 23.5 ng/mL — more than 60 percent of patients were in the range of vitamin D insufficiency (10 to 30 ng/mL). Nearly 20 percent had vitamin D deficiency (less than 10 ng/mL).

“Higher vitamin D concentrations were associated with decreased odds of in-hospital mortality/morbidity,” the researchers write. For each 5 ng/mL increase in 25-hydroxyvitamin D level, the combined risk of death, cardiovascular events, or serious infections decreased by seven percent.

Patients at the lowest level of 25-hydroxyvitamin D (less than 13 ng/mL) were at highest risk of death or serious complications. Those with higher vitamin D levels (up to 44 ng/mL) had about half the risk as those in the lowest group. The association with low vitamin D was statistically significant only for cardiovascular complications, although there were “strong trends” for mortality and infections.

Further Study Needed to Determine Cause and Effect

“Vitamin D deficiency is a global health problem,” according to Dr Turan and coauthors. In addition to protective cardiovascular and neurological effects, vitamin D plays an important role in the immune system.

The high rates of vitamin D insufficiency and deficiency in the surgical patients studied are consistent with previous findings in the general population. In recent years, studies have suggested that vitamin D levels may affect a wide range of health outcomes.

Patients undergoing surgery are at risk of cardiovascular and infectious complications, both of which may be aggravated by vitamin D deficiency. Previous studies found no increased risk of adverse outcomes related to vitamin D levels in patients undergoing cardiac surgery. It may be that the tissue injury and inflammation associated with heart surgery overwhelms any potential protective effect of vitamin D.

However, Dr Turan and colleagues note that their study had some important limitations of their study — especially the fact that it included only patients who had recent measurements of vitamin D levels. They may represent a less-healthy group, introducing a potential source of selection bias.

The study can’t determine whether there is any cause-and-effect relationship between vitamin D levels and the risk of adverse outcomes. Dr Turan and colleagues suggest a formal randomized trial to evaluate whether preoperative vitamin D supplementation can reduce the risk of serious complications and death after surgery.

Story Source:

The above story is based on materials provided by Wolters Kluwer Health: Lippincott Williams and Wilkins. Note: Materials may be edited for content and length.

Journal Reference:

  1. Alparslan Turan, Brian D. Hesler, Jing You, Leif Saager, Martin Grady, Ryu Komatsu, Andrea Kurz, Daniel I. Sessler. The Association of Serum Vitamin D Concentration with Serious Complications After Noncardiac Surgery. Anesthesia & Analgesia, 2014; 1 DOI: 10.1213/ANE.0000000000000096

February 1, 2014

Flax seeds can lower blood pressure

Filed under: Uncategorized — Doc Joe @ 3:54 pm


Abstract Title:

Potent antihypertensive action of dietary flaxseed in hypertensive patients.

Abstract Source:

Hypertension. 2013 Dec ;62(6):1081-9. Epub 2013 Oct 14. PMID: 24126178

Abstract Author(s):

Delfin Rodriguez-Leyva, Wendy Weighell, Andrea L Edel, Renee LaVallee, Elena Dibrov, Reinhold Pinneker, Thane G Maddaford, Bram Ramjiawan, Michel Aliani, Randolph Guzman, Grant N Pierce

Article Affiliation:

Delfin Rodriguez-Leyva


Flaxseed contains?-3 fatty acids, lignans, and fiber that together may provide benefits to patients with cardiovascular disease. Animal work identified that patients with peripheral artery disease may particularly benefit from dietary supplementation with flaxseed. Hypertension is commonly associated with peripheral artery disease. The purpose of the study was to examine the effects of daily ingestion of flaxseed on systolic (SBP) and diastolic blood pressure (DBP) in peripheral artery disease patients. In this prospective, double-blinded, placebo-controlled, randomized trial, patients (110 in total) ingesteda variety of foods that contained 30 g of milled flaxseed (4-6 tablespoons) or placebo each day over 6 months. Plasma levels of the ?-3 fatty acid ?-linolenic acid and enterolignans increased 2- to 50-fold in the flaxseed-fed group but did not increase significantly in the placebo group. Patient body weights werenot significantly different between the 2 groups at any time. SBP was ? 10 mm Hg lower, and DBP was ? 7 mm Hg lower in the flaxseed group compared with placebo after 6 months. Patients who entered the trial with a SBP ? 140 mm Hg at baseline obtained a significant reduction of 15 mm Hg in SBPand 7 mm Hg in DBP from flaxseed ingestion. The antihypertensive effect was achieved selectively in hypertensive patients. Circulating ?-linolenic acid levels correlated with SBP and DBP, and lignan levels correlated with changes in DBP. In summary, flaxseed induced one of the most potent antihypertensive effects achieved by a dietary intervention.

Study Type : Human Study
Additional Links

Additional Keywords : Phytotherapy : CK(357) : AC(58)

November 24, 2013

British doctors admit saturated fats are vital for good health, help naturally lower cholesterol without drugs.

Filed under: Uncategorized — Doc Joe @ 1:28 pm

British doctors admit saturated fats are vital for good health, help naturally lower cholesterol without drugs

by Ethan A. Huff, staff writer

(NaturalNews) Following the lead of Sweden, which recently denounced the conventional low-fat, high-carbohydrate “healthy” diet myth, a cohort of prominent British doctors and professors has come out to declare that saturated fats, which have been demonized for decades, are actually healthy. As reported by the U.K.’s Daily Express, British cardiologist Dr. Aseem Malhotra says that millions of people are now needlessly suffering from cardiovascular disease and obesity as a direct result of bad advice that told them to avoid eating fats.

Dr. Malhotra, an interventional cardiology specialist registrar at Croydon University Hospital in London, has conducted extensive research on the subject of fat intake and discovered that we have all basically been lied to. The oft recommended low-fat diet is actually a primary driver of both obesity and heart disease, he says, noting that the elimination of saturated and other healthy fats from the diets of millions of people worldwide has left them with more cardiovascular abnormalities, the opposite of what governments have long claimed.

In a recent study published in the British Medical Journal (BMJ), Dr. Malhotra clarifies the difference between artificial trans fats, which have repeatedly been shown to trigger the inflammatory processes in the body that lead to heart disease, and saturated fats, which occur naturally in foods like butter, coconut oil and palm oil. He dubs governmental preoccupation with the unsubstantiated dangers of saturated fats an “obsession,” noting that the real issue involves carbohydrates and sugars, which have been shown to trigger an uptick in harmful, low-density lipoprotein (LDL) cholesterol.

“Correlation is not causation,” stated Dr. Malhotra to the Daily Express, referring to now debunked studies that seemed to link saturated fats to heart disease. “Nevertheless, we were advised to cut fat intake to 30 percent of total energy and a fall in saturated fat to 10 percent.”

Diets high in saturated fat three times more effective than statins at lowering cholesterol

Though obviously ineffective at curbing obesity and heart disease, low-fat diets have continued to generate huge profits for the pharmaceutical industry, which now rakes in some $26 billion annually from the sale of cholesterol-lowering statin drugs. But Dr. Malhotra says statins are both harmful and ineffective, and that eating a diet high in saturated fat is actually three times more effective than statins at naturally lowering and balancing cholesterol levels.

“The assumption has been made that increased fat in the bloodstream is caused by increased saturated fat in the diet, whereas modern evidence is proving that refined carbohydrates and sugar in particular are actually the culprits,” adds Prof. David Haslam, chair of the National Obesity Forum.

Beyond this, a growing body of evidence now suggests that cholesterol is not even the issue. Since roughly 80 percent of the cholesterol in your bloodstream is actually made by your own body — your brain, in fact, is made of both cholesterol and saturated fat — there must be some other factor responsible for causing heart disease. This also means that artificially lowering your cholesterol with statin drugs is a bad idea, not only because they deprive your body of needed cholesterol, but also because they pose major risk factors like sexual dysfunction and muscle, nerve and organ damage.

“Focusing on an elevated blood cholesterol concentration as the exclusive cause of coronary heart disease is unquestionably the worst medical error of our time,” says Timothy Noakes, a professor at the University of Cape Town in South Africa. “After reviewing all the scientific evidence I draw just one conclusion — never prescribe a statin drug for a loved one.”

Sources for this article include:




June 4, 2013

Body mass index and musculoskeletal pain: is there a connection?

Filed under: Uncategorized — Doc Joe @ 2:06 pm

David R Seaman

Author Affiliations

National University of Health Sciences, SPC-Health Education Center, 7200 66th St, Pinellas Park, FL 33781, USA

Chiropractic & Manual Therapies 2013, 21:15 doi:10.1186/2045-709X-21-15
The electronic version of this article is the complete one and can be found online at:

Received: 14 January 2013
Accepted: 17 May 2013
Published: 20 May 2013

© 2013 Seaman; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.



Back pain is one of the most common complaints that patients report to physicians and two-thirds of the population has an elevated body mass index (BMI), indicating they are either overweight or obese. It was once assumed that extra body weight would stress the low back and lead to pain, however, researchers have reported inconsistencies association between body weight and back pain. In contrast, more recent studies do indicate that an elevated BMI is associated with back pain and other musculoskeletal pain syndromes due to the presence of a chronic systemic inflammatory state, suggesting that the relationship between BMI and musculoskeletal pains be considered in more detail.


To describe how an elevated BMI can be associated with chronic systemic inflammation and pain expression. To outline measurable risk factors for chronic inflammation that can be used in clinical practice and discuss basic treatment considerations.


Adiposopathy, or “sick fat” syndrome, is a term that refers to an elevated BMI that is associated with a chronic systemic inflammatory state most commonly referred to as the metabolic syndrome. The best available evidence suggests that the presence of adiposopathy determines if an elevated BMI will contribute to musculoskeletal pain expression. It is not uncommon for physicians to fail to identify the presence of adiposopathy/metabolic syndrome.


Patients with an elevated BMI should be further examined to identify inflammatory factors associated with adiposopathy, such as the metabolic syndrome, which may be promoting back pain and other musculoskeletal pain syndromes.


Back pain; Body mass index; Obesity; Metabolic syndrome; Inflammation

June 11, 2012

Sugar: The Bitter Truth

Filed under: Uncategorized — Doc Joe @ 3:19 pm

March 28, 2012

Oral Vitamin D Boosts Intranasal Steroid Effect in Rhinitis

Filed under: Uncategorized — Doc Joe @ 6:20 pm

Kate Johnson

March 12, 2012 (Orlando, Florida) — Adding an oral vitamin D supplement to regular intranasal corticosteroid dosing can improve symptoms of seasonal allergic rhinitis beyond that seen with corticosteroids alone in patients who are not vitamin D deficient, according to study results presented here at the American Academy of Allergy, Asthma and Immunology 2012 Annual Meeting.

The findings add to a number of reports at the meeting suggesting that vitamin D supplementation might be beneficial in patients with allergies.

“Vitamin D has been shown to play a role in innate immunity and the generation of antimicrobial peptides. It also has a number of immunological effects on T cells, dendritic cells, and macrophages,” said James Lane, BA, a researcher at the University of Chicago, Illinois, who presented the findings.

These findings must be viewed with caution, said lead investigator Fuad Baroody, MD, a pediatric head and neck surgeon at the University of Chicago. “This was a small study, a pilot study. More work needs to be done before people can run out and add vitamin D to intranasal steroids,” he said in an interview with Medscape Medical News.

In the double-blind placebo-controlled study, patients 18 to 45 years of age with seasonal allergic rhinitis received fluticasone propionate 200 µg/day, and were randomized to receive either vitamin D 4000 IU/day for 2 weeks (n = 17) or placebo (n = 18).

Subjects had at least a 2-year history of seasonal allergic rhinitis and a positive skin test to tree, grass, and/or ragweed.

At baseline, serum 25-hydroxy-vitamin D levels were within the normal range and similar in the vitamin D and placebo groups (29.6 vs 29.4 ng/dL). After 2 weeks, levels in the vitamin D group rose significantly from baseline to 37.2 ng/dL (P = .001); in the placebo group, there was no rise.

“There’s variation on what people consider appropriate levels of vitamin D,” explained Dr. Baroody. “Most recommendations are for levels around 30 or so. These were not vitamin-deficient people, but we bumped it up a little bit to within a still reasonable range, and nobody had side effects from having too much vitamin D.”

According to daily self-rated nasal symptoms, including sneezing, nasal congestion, and drip, subjects in both groups noted significant daytime improvements from baseline.

However, subjects in the vitamin D group noted a decreased symptom score of 6.9 points from baseline, which was statistically significant and superior to the 3.7 point drop in the placebo group (P = .04).

“Just giving vitamin D on top created a significant drop — almost a 50% drop,” said Dr. Baroody. “The magnitude is impressive, actually. If that is duplicated in a big trial, it would be pretty spectacular.”

Nighttime symptoms were not presented at the meeting, but Dr. Baroody said they were “not as spectacular.” As a result, the reduction in 24-hour symptom relief was not statistically different between the vitamin D and placebo groups (11.3 vs 7.6 points; P = .09).

Similarly, although there was a statistically significant improvement from baseline in quality of life in both groups (P = .0028), there was no significant difference between the vitamin D and placebo groups (2.5 vs 2.0 points).

“A change of 0.5 is considered to be clinically meaningful, and both groups had improvements well beyond that,” said Lane.

In response to a comment from the audience, Dr. Baroody acknowledged that perhaps the real strength of vitamin D supplementation in this group was not in better, but rather in faster, symptom control; all measures showed patients in the vitamin D group responding within 2 days and sustaining their response level.

“That’s an interesting way of looking at it. I will examine that in more detail,” he said.

“I think people don’t really know what the vitamin D story is,” Rachel Miller, MD, associate professor of medicine in pediatrics and environmental health sciences at Columbia University Medical Center in New York City, told Medscape Medical News.

“My bias is to do a randomized trial and see what vitamin D supplementation does, because most of the work so far has been observational. I know people are already doing it, but I personally look forward to more evidence from randomized trials.”

The study received no funding from industry. Mr. Lane and Dr. Miller have disclosed no relevant financial relationships. Dr. Baroody reports being on the speaker’s bureau for Merck and GlaxoSmithKline.

American Academy of Allergy, Asthma and Immunology (AAAAI) 2012 Annual Meeting: Abstract 510. Presented March 4, 2012.

April 13, 2011

Support for Chiropractic maintenace care?

Filed under: Uncategorized — Doc Joe @ 2:28 pm

Does maintained Spinal manipulation therapy for chronic non-specific low back pain result in better long term outcome?

Senna, Mohammed K.; Machaly, Shereen A.


Study Design. A prospective single blinded placebo controlled study was conducted.

Objective. to assess the effectiveness of spinal manipulation therapy (SMT) for the management of chronic non-specific low back pain (LBP) and to determine the effectiveness of maintenance SMT in long-term reduction of pain and disability levels associated with chronic low-back conditions after an initial phase of treatments.

Summary of background. SMT is a common treatment option for low back pain. Numerous clinical trials have attempted to evaluate its effectiveness for different subgroups of acute and chronic LBP but the efficacy of maintenance SMT in chronic non-specific LBP has not been studied.

Subjects and Methods. 60 patients with chronic, nonspecific LBP lasting at least 6 months were randomized to receive either (1) 12 treatments of sham SMT over a one-month period, (2) 12 treatments, consisting of SMT over a one-month period, but no treatments for the subsequent nine months, or (3) 12 treatments over a one-month period, along with “maintenance spinal manipulation” every two weeks for the following nine months. To determine any difference among therapies, we measured pain and disability scores, generic health status, and back-specific patient satisfaction at baseline and at 1-month, 4-month, 7-month and 10-month intervals.

Results: Patients in second and third groups experienced significantly lower pain and disability scores than first group at the end of 1-month period (P = 0.0027 and 0.0029 respectively). However, only the third group that was given spinal manipulations during the follow-up period showed more improvement in pain and disability scores at the 10-month evaluation. In the no maintained SMT group, however, the mean pain and disability scores returned back near to their pretreatment level.

Conclusion. SMT is effective for the treatment of chronic non specific LBP. To obtain long-term benefit, this study suggests maintenance spinal manipulations after the initial intensive manipulative therapy.

(C) 2011 Lippincott Williams & Wilkins, Inc.

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