If you’re feeling stressed out or you know that you’re in for a bad day, you might want to eat a handful of walnuts to relieve the pressure. According to one study by researchers at Penn State University, a diet rich in walnuts and walnut oil may prepare the body to deal better with stress.

The researchers wanted to examine how walnuts and walnut oil, which contain polyunsaturated fats, influence blood pressure at rest and under stress.  That’s because people who have an exaggerated biological response to stress are at higher risk of heart disease.  According to the researchers, they wanted to find out if omega 3-fatty acids from plant sources would blunt cardiovascular responses to stress.

In the study 22 healthy adults with elevated LDL cholesterol followed three different diets for six weeks each. The participants were subjected to stress either by giving a speech or immersing a foot in cold water. The results, published in the Journal of the American College of Nutrition, showed that when participants were following a diet that included walnuts and walnut oil, their blood pressure and stress responses were lower.

The “average” American diet does not include any nuts on a daily basis and the diet found to be effective to reduce the stress reaction included about 9 whole walnuts as an average serving.  That may be all it takes for you to feel the calming effects.

A quarter cup of walnuts provides over 90% of the recommended daily value of omega-3 fats.  Previous studies had already shown that omega-3 fatty acids like the alpha linolenic acid found in walnuts and flax seeds, can reduce LDL (the so-called bad) cholesterol, and may also reduce inflammation.

Walnuts are rich in healthy fats, dietary fiber, minerals, vitamins, antioxidants and phytosterols, and have long been associated with heart health.  The U.S. Food and Drug Administration allows walnut providers to make the health claim that “eating 1.5 ounces per day of walnuts as part of a diet low in saturated fat and cholesterol may reduce the risk of heart disease.”

Besides its beneficial effects on blood pressure and inflammation, walnuts have also been shown to be an excellent source of antioxidants, help to prevent gallstones, improve sleep by boosting melatonin, protect bone health and prevent weight gain.

Now this study points out that walnuts and walnut oil reduce blood pressure during stressful periods. And since we can’t completely avoid all the stresses in our lives, it’s good to know that such a simple and convenient snack could help us deal with the pressure.

Pomegranate Found To Prevent Coronary Artery Disease Progression

The future of cardiovascular disease prevention and treatment will not be found in your medicine cabinet, rather in your kitchen cupboard or in your back yard growing on a tree.

A study published in the journal Atherosclerosis confirms that pomegranate extract may prevent and/or reverse the primary pathology associated with cardiac mortality: the progressive thickening of the coronary arteries caused by the accumulation of fatty materials known as atherosclerosis.[i]

Mice with a genetic susceptibility towards spontaneous coronary artery blockages were given pomegranate extract via their drinking water for two weeks, beginning at three weeks of age. Despite the fact that pomegranate treatment actually increased cholesterol levels associated with very low density lipoprotein-sized particles, the treatment both reduced the size of the atherosclerotic plaques in the aortic sinus (the dilated opening above the aortic valve) and reduced the proportion of coronary arteries with occlusive atherosclerotic plaques.

Remarkably, the researchers also found that pomegranate extract treatment resulted in the following 7 beneficial effects:

1. Reduced levels of oxidative stress
2. Reduced monocytie chemotactic protein-1, a chemical messenger (chemokine) associated with inflammatory processes within the arteries.
3. Reduced lipid accumulation in the heart muscle
4. Reduced macrophage infiltration in the heart muscle
5. Reduced levels of monocyte chemotactic protein-1 and fibrosis in the myocardium
6. Reduced cardiac enlargement
7. Reduced ECG abnormalities

How can something as benign and commonplace as a fruit extract reverse so many aspects of coronary artery disease, simultaneously, as evidenced by the study above?  The answer may lie in the fact that our ancestors co-evolved with certain foods (fruits in particular) for so long that a lack of adequate quantities of these foods may directly result in deteriorating organ function.  Indeed, two-time Nobel Prize winner Linus Pauling argued that vitamin C deficiency is a fundamental cause of cardiovascular disease, owing to the fact that our hominid primate ancestors once had year-round access to fruits, and as a result lost the ability to synthesize it.

There’s another obvious clue as to how pomegranate may work its artery opening magic. Anyone who has ever tasted pomegranate, or consumed the juice, knows it has a remarkable astringency, giving your mouth and gums that dry, puckering mouth feel. This cleansing sensation is technically caused, as with all astringents, by shrinking and disinfecting your mucous membranes.

Anyone who drinks pomegranate juice, or is lucky enough to eat one fresh, can understand why it is so effective at cleansing the circulatory system. Nature certainly planted enough poetic visual clues there for us: its juice looks like blood, and it does resemble a multi-chambered heart, at least when you consider its appearance in comparison to most other fruits.

Indeed, your mouth and your arteries are lined with the same cell type: epithelial cells. Together, they make up the epithelium, one of four basic tissue types within animals, along with connective tissue, muscle tissue and nervous tissue, and which comprises the interior walls of the entire circulatory system. So, when you feel that amazing cleansing effect in your mouth, this is in fact akin to what your circulatory system – and the epithelium/endothelium lining the inside of your veins and arteries – “feels” as well.

The Pomegranate “Artery Cleaning” Clinical Trial

Published in Clinical Nutrition in 2004 and titled, “Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation,” Israeli researchers discovered pomegranate, administered in juice form over the course of a year, reversed plaque accumulation in the carotid arteries of patients with severe, though symptomless, carotid artery stenosis (defined as 70–90% blockage in the internal carotid arteries).

The study consisted of nineteen patients, 5 women and 14 men, aged 65-75, non-smokers. They were randomized to receive either pomegranate juice or placebo. Ten patients were in the pomegranate juice treatment group and 9 patients that did not consume pomegranate juice were in the control group. Both groups were matched with similar blood lipid and glucose concentrations, blood pressure, and with similar medication regimens which consisted of blood-pressure lowering (e.g. ACE inhibitors, β-blockers, or calcium channel blockers) and lipid lowering drugs (e.g. statins).

The ten patients in the treatment group group received 8.11 ounces (240 ml) of pomegranate juice per day, for a period of 1 year, and five out of them agreed to continue for up to 3 years.

The remarkable results were reported as follows:

“The mean intima media thickness the left and right common carotid arteries in severe carotid artery stenosis patients that consumed pomegranate juice for up to 1 year was reduced after 3, 6, 9 and 12 months of pomegranate juice consumption by 13%, 22%, 26% and 35%, respectively, in comparison to baseline values.”

You can only imagine what would happen if a pharmaceutical drug was shown to reverse plaque build up in the carotid arteries by 13% in just 3 months! This drug would be lauded the life-saving miracle drug, and not only would be promoted and sold successfully as a multi-billion dollar blockbuster, but discussion would inevitably follow as to why it should be mandated.

While these results are impressive, if not altogether groundbreaking for the field of cardiology, they may be even better than revealed in the stated therapeutic outcomes above.  When one factors in that the carotid artery stenosis increased 9% within 1 year in the control group, the pomegranate intervention group may have seen even better results than indicated by the measured regression in intima media thickness alone.  That is, if we assume that the pomegranate group had received no treatment, the thickening of their carotid arteries would have continued to progress like the control group at a rate of 9% a year, i.e. 18% within 2 years, 27% within 3 years. This could be interpreted to mean that after 3 years of pomegranate treatment, for instance, the thickening of the arteries would have been reduced over 60% beyond what would have occurred had the natural progression of the disease been allowed to continue unabated.  

3 Ways How Pomegranate Heals The Cardiovascular System

The researchers identified three likely mechanisms of action behind pomegranate’s observed anti-atherosclerotic activity:

• Antioxidant properties: Subjects receiving pomegranate saw significant reductions in oxidative stress, including decreases in autoantibodies formed against ox-LDL, a form of oxidized low density lipoprotein associated with the pathological process of atherosclerosis. Decreases in oxidative stress were measurable by an increase in the blood serum enzyme paraoxonase 1 (PON1) of up to 91% after 3 years; PON1 is an enzyme whose heightened activity is associated with lower oxidative stress. All of this is highly relevant to the question of pomegranate’s anti-atherosclerotic activity because of something called the lipid peroxidation hypothesis of atherosclerosis, which assumes that it is the quality of the blood lipids (i.e. whether they are oxidized/damaged or not), and not their quantity alone that determine their cardiotoxicity/atherogenicity. Essentially, pomegranate prevents the heart disease promoting effects of oxidative stress.
• Blood Pressure Lowering Properties: The intervention resulted in significant improvement in blood pressure: the patient’s systolic blood pressure was reduced 7%, 11% ,10%, 10% and 12% after 1, 3, 6, 9, and 12 months of pomegranate consumption, respectively, compared to values obtained before treatment. Pomegranate’s ability to reduce systolic blood pressure indicates it has a healing effect on the endothelium, or the inner lining of the artery which fails to relax fully in heart disease; a condition known as endothelial dysfunction.
• Plaque Lesion Stabilization: Because two of the ten patients on PJ (after 3 and 12 months) experienced clinical deterioration, carotid surgery was performed and the lesions were analyzed to determine the difference in their composition to those who did not receive pomegranate. The researchers noticed four distinct positive differences in the composition of the pomegranate-treated lesions: 1. Reduced Cholesterol Content: “The cholesterol content in carotid lesions from the two patients that consumed PJ was lower by 58% and 20%, respectively, in comparison to lesions obtained from CAS patients that did not consume PJ (Fig. 3A).” 2.     Reduced Lipid Peroxides: “[T]he lipid peroxides content in lesions obtained from the patients after PJ consumption for 3 or 12 months was significantly reduced by 61% or 44%, respectively, as compared to lesions from patients that did not consume PJ (Fig. 3B). 3.     Increased Reduced Glutathione Content: “A substantial increase in the lesion reduced glutathione (GSH) content, (GSH is a major cellular antioxidant) by 2.5-fold, was observed after PJ consumption for 3 or 12 months, (Fig. 3C). 4.     Reduced LDL Oxidation: “LDL oxidation by lesions derived from the patients after PJ consumption for 3 or 12 months, was significantly (Po0.01) decreased by 43% or 32%, respectively, in comparison to LDL oxidation rates obtained by lesions from CAS patients that did not consume PJ (Fig. 3D).”

Essentially these results reveal that not only does pomegranate reduce the lesion size in the carotid arteries, but “the lesion itself may be considered less atherogenic after PJ consumption, as its cholesterol and oxidized lipid content decreased, and since its ability to oxidize LDL was significantly reduced.”

This finding is quite revolutionary, as presently, the dangers of carotid artery stenosis are understood primarily through the lesion size and not by assessing for the quality of that lesion. This dovetails with the concept that the sheer quantity of lipoproteins (i.e. “cholesterol”) in the blood can not accurately reveal whether those lipoproteins are actually harmful (atherogenic); rather, if lipoproteins are oxidized (e.g. ox-LDL) they can be harmful (or representative of a more systemic bodily imbalance), whereas non-oxidized low density lipoprotein may be considered entirely benign, if not indispensable for cardiovascular and body wide health. Indeed, in this study the researchers found the pomegranate group had increased levels of triglycerides and very low density lipoprotein, again, underscoring that the anti-atherosclerotic properties likely have more to do with the improved quality of the physiological milieu within which all our lipoproteins operate than the number of them, in and of itself.

Finally, it should be pointed out that all the patients in this study were undergoing conventional, drug-based care for cardiovascular disease, e.g. cholesterol- and blood pressure-lowering agents. Not only did the pomegranate treatment not appear to interfere with their drugs, making it a suitable complementary/adjunct therapy for those on pharmaceuticals, but it should be pointed out that the control group’s condition got progressively worse (e.g. the mean IMT increased 9% within 1 year), speaking to just how ineffective drugs are, or how they may even contribute to the acceleration of the disease process itself.

Further Validation of Pomegranate’s Artery-Clearing Properties

Pomegranate’s value in cardiovascular health may be quiet broad, as evidenced by the following experimentally confirmed properties:

• Anti-inflammatory: Like many chronic degenerative diseases, inflammation plays a significant role in cardiovascular disease pathogenesis. There are five studies on GreenMedInfo.com indicating pomegranate’s anti-inflammatory properties.[iii]
• Blood-Pressure Lowering: Pomegranate juice has natural angiotensin converting enzyme inhibiting properties, [iv] and is a nitric oxide enhancer, two well-known pathways for reducing blood pressure. [v] Finally, pomegranate extract rich in punicalagin has been found reduce the adverse effects of perturbed stress on arterial segments exposed to disturbed flow.[vi]
• Anti-Infective: Plaque buildup in the arteries often involves secondary viral and bacterial infection, including hepatitis C and Chlamydia pneumoniae.[vii] Pomegranate has a broad range of anti-bacterial and anti-viral properties.
• Antioxidant: One of the ways in which blood lipids become heart disease-promoting (atherogenic) is through oxidation. LDL, for instance, may be technically ‘elevated’ but harmless as long as it does not readily oxidize. Pomegranate has been found to reduce the oxidative stress in the blood, as measured by serum paraoxonase levels.  One study in mice found this decrease in oxidative stress was associated with 44% reduction in the size of atherosclerotic lesions. [viii]
• Ant-Infective: While it is commonly overlooked, cardiovascular disease, and more particularly atherosclerosis, is connected to infection. Dentists know this, which is why they often prescribe antibiotics following dental work which releases bacteria into systemic circulation. Plaque in the arteries can also harbor viral pathogens. Pomegranate happens to have potent antiviral and antibacterial properties relevant to cardiovascular disease initiation and progression. It has been studied to combat the following infectious organisms:
  1. Avian Influenza
  2. Candida
  3. Escherichia Coli
  4. Hepatitis B
  5. HIV
  6. Influenza A
  7. Poxviruses
  8. Salmonella
  9. SARS
  10. Staphylococcus auerus
  11. Vaccinia virus
  12. Vibrio (Cholera) virus

For additional research on pomegranate’s heart friendly properties read our article: Research: Pomegranate May Reverse Blocked Arteries, and to learn more about it’s broadly therapeutic properties read: 100+ Health Properties of Pomegranate Now Includes Helping Diabetics.

Also, view our dedicated research section on reversing arterial plaque: Clogged Arteries

Resources

• [i] Aishah Al-Jarallah, Fatima Igdoura, Yi Zhang, Christine B Tenedero, Elizabeth J White, Melissa E Macdonald, Suleiman A Igdoura, Bernardo L Trigatti. The effect of pomegranate extract on coronary artery atherosclerosis in SR-BI/APOE double knockout mice. Atherosclerosis. 2013 May ;228(1):80-9. Epub 2013 Mar 7. PMID: 23528829

• [ii] Michael Aviram, Mira Rosenblat, Diana Gaitini, Samy Nitecki, Aaron Hoffman, Leslie Dornfeld, Nina Volkova, Dita Presser, Judith Attias, Harley Liker, Tony Hayek. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr. 2004 Jun;23(3):423-33. PMID: 15158307

• [iii] GreenMedInfo.com, Pomegranate’s Anti-Inflammatory Properties

• [iv] Mahalaxmi Mohan, Harshal Waghulde, Sanjay Kasture. Effect of pomegranate juice on Angiotensin II-induced hypertension in diabetic Wistar rats. Phytother Res. 2009 Dec 17. PMID: 20020514

• [v] Filomena de Nigris, Maria Luisa Balestrieri, Sharon Williams-Ignarro, Francesco P D’Armiento, Carmela Fiorito, Louis J Ignarro, Claudio Napoli. The influence of pomegranate fruit extract in comparison to regular pomegranate juice and seed oil on nitric oxide and arterial function in obese Zucker rats. Nitric Oxide. 2007 Aug ;17(1):50-4. Epub 2007 May 5. PMID: 17553710

• [vi] Filomena de Nigris, Sharon Williams-Ignarro, Vincenzo Sica, Lilach O Lerman, Francesco P D’Armiento, Russell E Byrns, Amelia Casamassimi, Daniela Carpentiero, Concetta Schiano, Daigo Sumi, Carmela Fiorito, Louis J Ignarro, Claudio Napoli. Effects of a pomegranate fruit extract rich in punicalagin on oxidation-sensitive genes and eNOS activity at sites of perturbed shear stress and atherogenesis.Cardiovasc Res. 2007 Jan 15;73(2):414-23. Epub 2006 Sep 1. PMID: 17014835

• [vii] Yasunori Sawayama, Kyoko Okada, Shinji Maeda, Hachiro Ohnishi, Norihiro Furusyo, Jun Hayashi. Both hepatitis C virus and Chlamydia pneumoniae infection are related to the progression of carotid atherosclerosis in patients undergoing lipid lowering therapy. Fukuoka Igaku Zasshi. 2006 Aug;97(8):245-55. PMID: 17087362

• [viii] M Aviram, L Dornfeld, M Rosenblat, N Volkova, M Kaplan, R Coleman, T Hayek, D Presser, B Fuhrman. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr. 2000 May ;71(5):1062-76. PMID: 10799367

Millions believe depression is caused by ‘serotonin deficiency,’ but where is the science in support of this theory?

“Depression is a serious medical condition that may be due to a chemical imbalance, and Zoloft works to correct this imbalance.”

Herein lies the serotonin myth.

As one of only two countries in the world that permits direct to consumer advertising, you have undoubtedly been subjected to promotion of the “cause of depression.” A cause that is not your fault, but rather; a matter of too few little bubbles passing between the hubs in your brain! Don’t add that to your list of worries, though, because there is a convenient solution awaiting you at your doctor’s office…

What if I told you that, in 6 decades of research, the serotonin (or norepinephrine, or dopamine) theory of depression and anxiety has not achieved scientific credibility?

You’d want some supporting arguments for this shocking claim.

So, here you go:

The Science of Psychiatry is Myth

Rather than some embarrassingly reductionist, one-deficiency-one-illness-one-pill model of mental illness, contemporary exploration of human behavior has demonstrated that we may know less than we ever thought we did.  And that what we do know about root causes of mental illness seems to have more to do with the concept of evolutionary mismatch than with genes and chemical deficiencies.

In fact, a meta-analysis of over 14,000 patients and Dr. Insel, head of the NIMH, had this to say:

“Despite high expectations, neither genomics nor imaging has yet impacted the diagnosis or treatment of the 45 million Americans with serious or moderate mental illness each year.”

To understand what imbalance is, we must know what balance looks like, and neuroscience, to date, has not characterized the optimal brain state, nor how to even assess for it.

A New England Journal of Medicine review on Major Depression, stated:

” … numerous studies of norepinephrine and serotonin metabolites in plasma, urine, and cerebrospinal fluid as well as postmortem studies of the brains of patients with depression, have yet to identify the purported deficiency reliably.”

The data has poked holes in the theory and even the field of psychiatry itself is putting down its sword. One of my favorite essays by Lacasse and Leo has compiled sentiments from influential thinkers in the field – mind you, these are conventional clinicians and researchers in mainstream practice – who have broken rank, casting doubt on the entirety of what psychiatry has to offer around antidepressants:

Humble Origins of a Powerful Meme

In the 1950s, reserpine, initially introduced to the US market as an anti-seizure medication, was noted to deplete brain serotonin stores in subjects, with resultant lethargy and sedation. These observations colluded with the clinical note that an anti-tuberculosis medication, iproniazid, invoked mood changes after five months of treatment in 70% of a 17 patient cohort. Finally, Dr. Joseph Schildkraut threw fairy dust on these mumbles and grumbles in 1965 with his hypothetical manifesto entitled “The Catecholamine Hypothesis of Affective Disorders” stating:

“At best, drug-induced affective disturbances can only be considered models of the natural disorders, while it remains to be demonstrated that the behavioral changes produced by these drugs have any relation to naturally occurring biochemical abnormalities which might be associated with the illness.”

Contextualized by the ripeness of a field struggling to establish biomedical legitimacy (beyond the therapeutic lobotomy!), psychiatry was ready for a rebranding, and the pharmaceutical industry was all too happy to partner in the effort.

Of course, the risk inherent in “working backwards” in this way (noting effects and presuming mechanisms) is that we tell ourselves that we have learned something about the body, when in fact, all we have learned is that patented synthesized chemicals have effects on our behavior. This is referred to as the drug-based model by Dr. Joanna Moncrieff. In this model, we acknowledge that antidepressants have effects, but that these effects in no way are curative or reparative.

The most applicable analogy is that of the woman with social phobia who finds that drinking two cocktails eases her symptoms. One could imagine how, in a 6 week randomized trial, this “treatment” could be found efficacious and recommended for daily use and even prevention of symptoms. How her withdrawal symptoms after 10 years of daily compliance could lead those around her to believe that she “needed” the alcohol to correct an imbalance. This analogy is all too close to the truth.

Running With Broken Legs

Psychiatrist Dr. Daniel Carlat has said:

“And where there is a scientific vacuum, drug companies are happy to insert a marketing message and call it science. As a result, psychiatry has become a proving ground for outrageous manipulations of science in the service of profit.”

So, what happens when we let drug companies tell doctors what science is? We have an industry and a profession working together to maintain a house of cards theory in the face of contradictory evidence.

We have a global situation in which increases in prescribing are resulting in increases in severity of illness (including numbers and length of episodes) relative to those who have never been treated with medication.

To truly appreciate the breadth of evidence that states antidepressants are ineffective and unsafe, we have to get behind the walls that the pharmaceutical companies erect. We have to unearth unpublished data, data that they were hoping to keep in the dusty catacombs.

A now famous 2008 study in the New England Journal of Medicine by Turner et al sought to expose the extent of this data manipulation. They demonstrated that, from 1987 to 2004, 12 antidepressants were approved based on 74 studies. Thirty-eight were positive, and 37 of these were published.  Thirty-six were negative (showing no benefit), and 3 of these were published as such while 11 were published with a positive spin (always read the data not the author’s conclusion!), and 22 were unpublished.

In 1998 tour de force, Dr. Irving Kirsch, an expert on the placebo effect, published a meta–analysis of 3,000 patients who were treated with antidepressants, psychotherapy, placebo, or no treatment and found that only 27% of the therapeutic response was attributable to the drug’s action.

This was followed up by a 2008 review, which invoked the Freedom of Information Act to obtain access to unpublished studies, finding that, when these were included, antidepressants outperformed placebo in only 20 of 46 trials (less than half!), and that the overall difference between drugs and placebos was 1.7 points on the 52 point Hamilton Scale.  This small increment is clinically insignificant, and likely accounted for by medication side effects strategically employed (sedation or activation).

When active placebos were used, the Cochrane database found that differences between drugs and placebos disappeared, given credence to the assertion that inert placebos inflate perceived drug effects.

The finding of tremendous placebo effect in the treatment groups was also echoed in two different meta-analyses by Khan et al who found a 10% difference between placebo and antidepressant efficacy, and comparable suicide rates. The most recent trial examining the role of “expectancy” or belief in antidepressant effect, found that patients lost their perceived benefit if they believed that they might be getting a sugar pill even if they were continued on their formerly effective treatment dose of Prozac.

The largest, non-industry funded study, costing the public $35 million dollars, followed 4000 patients treated with Celexa (not blinded, so they knew what they were getting), and found that half of them improved at 8 weeks. Those that didn’t were switched to Wellbutrin, Effexor, or Zoloft OR “augmented” with Buspar or Wellbutrin.

Guess what? It didn’t matter what was done, because they remitted at the same unimpressive rate of 18-30% regardless with only 3% of patients in remission at 12 months.

How could it be that medications like Wellbutrin, which purportedly primarily disrupt dopamine signaling, and medications like Stablon which theoretically enhances the reuptake of serotonin, both work to resolve this underlying imbalance? Why would thyroid, benzodiazepines, beta blockers, and opiates also “work”? And what does depression have in common with panic disorder, phobias, OCD, eating disorders, and social anxiety that all of these diagnoses would warrant the same exact chemical fix?

Alternative options

As a holistic clinician, one of my bigger pet peeves is the use of amino acids and other nutraceuticals with  “serotonin-boosting” claims. These integrative practitioners have taken a page from the allopathic playbook and are seeking to copy-cat what they perceive antidepressants to be doing.

The foundational “data” for the modern serotonin theory of mood utilizes tryptophan depletion methods which involve feeding volunteers amino acid mixtures without tryptophan and are rife with complicated interpretations.

Simply put, there has never been a study that demonstrates that this intervention causes mood changes in any patients who have not been treated with antidepressants.

In an important paper entitled Mechanism of acute tryptophan depletion: Is it only serotonin?, van Donkelaar et al caution clinicians and researchers about the interpretation of tryptophan research. They clarify that there are many potential effects of this methodology, stating:

“In general, several findings support the fact that depression may not be caused solely by an abnormality of 5-HT function, but more likely by a dysfunction of other systems or brain regions modulated by 5-HT or interacting with its dietary precursor. Similarly, the ATD method does not seem to challenge the 5-HT system per se, but rather triggers 5HT-mediated adverse events.”

So if we cannot confirm the role of serotonin in mood and we have good reason to believe that antidepressant effect is largely based on belief, then why are we trying to “boost serotonin”?

Causing imbalances

All you have to do is spend a few minutes on http://survivingantidepressants.org/ or http://beyondmeds.com/ to appreciate that we have created a monster. Millions of men, women, and children the world over are suffering, without clinical guidance (because this is NOT a part of medical training) to discontinue psychiatric meds. I have been humbled, as a clinician who seeks to help these patients, by what these medications are capable of. Psychotropic withdrawal can make alcohol and heroin detox look like a breeze.

An important analysis by the former director of the NIMH makes claims that antidepressants “create perturbations in neurotransmitter functions” causing the body to compensate through a series of adaptations which occur after “chronic administration” leading to brains that function, after a few weeks, in a way that is “qualitatively as well as quantitatively different from the normal state.”

Changes in beta-adrenergic receptor density, serotonin autoreceptor sensitivity, and serotonin turnover all struggle to compensate for the assault of the medication.

Andrews, et al., calls this “oppositional tolerance,” and demonstrate through a careful meta-analysis of 46 studies demonstrating that patient’s risk of relapse is directly proportionate to how “perturbing” the medication is, and is always higher than placebo (44.6% vs 24.7%). They challenge the notion that findings of decreased relapse on continued medication represent anything other than drug-induced response to discontinuation of a substance to which the body has developed tolerance. They go a step further to add:

“For instance, in naturalistic studies, unmedicated patients have much shorter episodes, and better long-term prospects, than medicated patients. Several of these studies have found that the average duration of an untreated episode of major depression is 12–13 weeks.”

Harvard researchers also concluded that at least fifty percent of drug-withdrawn patients relapsed within 14 months. In fact:

“Long-term antidepressant use may be depressogenic . . . it is possible that antidepressant agents modify the hardwiring of neuronal synapses (which) not only render antidepressants ineffective but also induce a resident, refractory depressive state.”

So, when your doctor says, “You see, look how sick you are, you shouldn’t have stopped that medication,” you should know that the data suggests that your symptoms are withdrawal, not relapse.

Longitudinal studies demonstrate poor functional outcomes for those treated with 60% of patients still meeting diagnostic criteria at one year (despite transient improvement within the first 3 months). When baseline severity is controlled for, two prospective studies support a worse outcome in those prescribed medication:

One in which the never-medicated group experienced a 62% improvement by six months, whereas the drug-treated patients experienced only a 33% reduction in symptoms, and another WHO study of depressed patients in 15 cities which found that, at the end of one year, those who weren’t exposed to psychotropic medications enjoyed much better “general health”; that their depressive symptoms were much milder”; and that they were less likely to still be “mentally ill.” 

I’m not done yet. In a retrospective 10-year study in the Netherlands, 76% of those with unmedicated depression recovered without relapse relative to 50% of those treated.

Unlike the mess of contradictory studies around short-term effects, there are no comparable studies that show a better outcome in those prescribed antidepressants long term.

First Do No Harm

So, we have a half-baked theory in a vacuum of science that that pharmaceutical industry raced to fill. We have the illusion of short-term efficacy and assumptions about long-term safety. But are these medications actually killing people?

The answer is yes.

Unequivocally, antidepressants cause suicidal and homicidal behavior. The Russian Roulette of patients vulnerable to these “side effects” is only beginning to be elucidated and may have something to do with genetic variants around metabolism of these chemicals.  Dr. David Healy has worked tirelessly to expose the data that implicates antidepressants in suicidality and violence, maintaining a database for reporting, writing, and lecturing about cases of medication-induced death that could make your soul wince.

What about our most vulnerable?

I have countless patients in my practice who report new onset of suicidal ideation within weeks of starting an antidepressant. In a population where there are only 2 randomized trials, I have grave concerns about postpartum women who are treated with antidepressants before more benign and effective interventions such as dietary modification and thyroid treatment. Hold your heart as you read through these reports of women who took their own and their childrens’ lives while treated with medications.

Then there is the use of these medications in children as young as 2 years old. How did we ever get the idea that this was a safe and effective treatment for this demographic? Look no further than data like Study 329, which cost Glaxo Smith Klein 3 billion dollars for their efforts to promote antidepressants to children. These efforts required ghost-written and manipulated data that suppressed a signal of suicidality, falsely represented Paxil as outperforming placebo, and contributes to an irrepressible mountain of harm done to our children by the field of psychiatry.

RIP Monoamine Theory

As Moncrieff and Cohen so succinctly state:

“Our analysis indicates that there are no specific antidepressant drugs, that most of the short-term effects of antidepressants are shared by many other drugs, and that long-term drug treatment with antidepressants or any other drugs has not been shown to lead to long-term elevation of mood. We suggest that the term “antidepressant” should be abandoned.”

So, where do we turn?

The field of psychoneuroimmunology dominates the research as an iconic example of how medicine must surpass its own simplistic boundaries if we are going to begin to chip away at the some 50% of Americans who will struggle with mood symptoms, 11% of whom will be medicated for it.

There are times in our evolution as a cultural species when we need to unlearn what we think we know. We have to move out of the comfort of certainty and into the freeing light of uncertainty. It is from this space of acknowledged unknowing that we can truly grow. From my vantage point, this growth will encompass a sense of wonder – both a curiosity about what symptoms of mental illness may be telling us about our physiology and spirit, as well as a sense of humbled awe at all that we do not yet have the tools to appreciate. For this reason, honoring our co-evolution with the natural world, and sending the body a signal of safetythrough movement, diet, meditation, and environmental detoxification represents our most primal and most powerful tool for healing.

Bayer’s headaches don’t stop with Monsanto-related buyer’s remorse. Their most iconic pharmaceutical — aspirin — which they once marketed as a ‘wonder drug’ is now being revealed to have no benefits to older adults, and may even cause significant harm. 

I’ve been writing about the underreported dangers and overstated health benefits of aspirin for some years now. Sometimes it feels like swimming upstream, given how often mainstream reporting and thinking associates so-called “low-dose” aspirin usage with some kind of ‘wonder drug’ for the prevention of cardiovascular disease. But the truth is now catching up to this marketing hype, as evidenced by this recent ABC news headline: “Daily aspirin may be harmful for healthy, older adults, large study finds.”

According to the new report, healthy patients, 70 and older (65 for blacks and Hispanics), experienced no health benefits from taking aspirin. This is based on research published last month in the New England Journal of Medicine, titled, “Effect of Aspirin on Disability-free Survival in the Healthy Elderly.” As summarized by a Forbes article advising older, healthy adults to “Toss Your Aspirin”:

“A major study conducted in the United States and Australia that enrolled about 19,000 healthy adults, 70 years and older (65 years and older for blacks and Hispanics in the United States), found that an enteric-coated, aspirin that is similar to the dose of a baby aspirin increased the risk of death, did not reduce the risk of heart disease or disability or dementia or cancer. In fact, the increase in mortality was attributed primarily to cancer. And those taking aspirin also had an increased risk of bleeding. Overall there was nothing in the plus column for aspirin. And no benefit was found in any particular subgroup.”

The study’s co-author Dr. Anne Murray, a geriatrician and epidemiologist at the Hennepin Healthcare Research Institute and the University of Minnesota, Minneapolis, was quoted as saying:

“We knew there would an increased risk of bleeding with aspirin, because there has always been…But not only did it not decrease risk of disability or death, it did not decrease the risk of heart attack and stroke, and there was an increase in the rate of death.”

Why and How Does Aspirin Cause Harm?

The obvious problem with aspirin is that it’s actually not a natural substance, comprised as it is of xenobiotic chemicals alien to the human body and its delicate metabolism.  In my previous article on the topic, “The Evidence Against Aspirin And For Natural Alternatives,” I discuss this in detail:

“As far back as the 5th century BC, the Greek physician Hippocrates wrote about the use of a bitter powder extracted from willow bark that reduced fevers and eased aches and pains.  Native Americans also used an infusion of willow bark for similar purposes. What was this remarkable “healing” principle within the bark that relieved disease?

 

Known as salicylic acid (from the Latin salix, willow tree), this pain-killing compound is widely distributed throughout plants, where it functions as a hormone.  The more vegetables and fruits you consume, the more likely you are to have a physiologically significant concentration of salicylic acid in your blood. This is why, for instance, vegans and vegetarians generally have higher levels than most grain- and meat-based consumers. [1]

 

The chemical acetyl-salicylic acid, commonly known as aspirin, is a synthetic form of salicylic acid, a compound which is formed when salicin, a bitter compound naturally found within plants like white willow bark, is broken down within the human body. Salicylic acid can also be synthesized endogenously from benzoic acid, and its urinary metabolite, salicyluric acid, has been found to overlap levels in patients on low-dose aspirin regimens. Cell research indicates that salicylic acid compounds (known as salicyclates) actually compare surprisingly well to aspirin in reducing inflammatory activity.[2]

 

While salicylic acid is found naturally in plants as salicylates, acetyl-salicylic acid does not exist in nature, is not formed as byproduct of natural salicylate consumption,[3] and is produced only through industrial synthesis. For example, this is one method of synthesis:  

Acetylsalicylic acid is prepared by reacting acetic anhydride with salicylic acid at a temperature of <90 deg C either in a solvent (e.g., acetic acid or aromatic, acyclic, or chlorinated hydrocarbons) or by the addition of catalysts such as acids or tertiary amines.”[4]

Also, the chemical modification of natural salicylic acid with an acetyl group results in the acetylation of hemoglobin,[5]essentially chemically altering the natural structure-function of our red blood cells and subsequent hemodynamics. In essence, aspirin, a semi-synthetic compound, makes the blood tissue itself semi-synthetic.

This could be why aspirin has been linked to such a broad range of unintended adverse health effects, including but not limited to:

• Gastric Ulcer [6]

• Hearing Loss/Tinnitus[7] [8] [9] [10] [11] [12]

• Cerebral Bleeding [13]

• Influenza Mortality [14]

• Reye Syndrome

• Crohn’s Disease[15]

• Helicobacter Pylori Infection[16]

We have a section on our database dedicated to indexing the under-reported, unintended adverse effects of aspirin, related to 50 diseases which can be viewed here: Aspirin Side Effects. We also have a section which indexes research on natural compounds studied to prevent, reduce or reverseAspirin-Induced Toxicity.

According to US EPA statistics, up to 500 thousand pounds of the chemical was produced in the United States in 1998 alone.[17]  Millions the world over take it for pain relief, including your typical headache, but also for the prevention of heart attacks and stroke.

Taking a “baby aspirin,” i.e. an 81 mg dose, is considered safer — which it is relative to a 325 mg “adult dose” – but is known to cause widespread and significant gastroduodenal damage.  A study published in 2009 in the journal Currrent Medical Research & Opinion titled, “Gastroduodenal toxicity of low-dose acetylsalicylic acid: a comparison with non-steroidal anti-inflammatory drugs,” found the following:

“Data suggest that ASA causes significant gastroduodenal damage even at the low doses used for cardiovascular protection. These effects (both systemic and possibly local) may be pharmacodynamically distinct from the gastroduodenal toxicity seen with NSAIDs.”[18]

Another 2009 study found that 80% of healthy individuals who uses short-term (14 days), low-dose aspirin experienced small intestinal toxicity, including small bowel mucosal breaks and mucosal inflammation. [19]  Also, there are reports of esophageal mucosal lesions induced by low-dose aspirin and other antiplatelet medications mimicking esophageal malignancy.[20]

Data suggest that ASA [aspirin]causes significant gastroduodenal damage even at the low doses used for cardiovascular protection. These effects (both systemic and possibly local) may be pharmacodynamically distinct from the gastroduodenal toxicity seen with NSAIDs.[21]

Hemorrhagic side effects, in fact, are one of the greatest challenges facing those who use aspirin for prevention.  By taking a drug which prevents clotting, aspirin can work too well, resulting in bleeding disorders or events, some of which may be life-threatening, even lethal.”

If Aspirin is So Dangerous and Ineffective, What’s the Natural Alternative?

With tens of thousands dying each year from opioid drug overdose, and with thousands more succumbing to the cardiotoxicity of commonly used NSAID drugs like ibuprofen, it is important for people to know about one natural alternative to aspirin that has been studied to be far superior both in safety and effectiveness, and which may have over a dozen significant side benefits. That substance is pycnogenol, or French maritime pine bark extract.

A 1999 clinical study published in Thrombotic Research found that when habitual smokers were given either 500 mg of aspirin or anywhere between 100-200 mg of pycnogenol, the pycnogenol group experienced equivalent platelet aggregation inhibiting effects but with much lower bleeding times:

“Thus, smoking-induced enhanced platelet aggregation was inhibited by 500 mg Aspirin as well as by a lower range of 100-125 mg Pycnogenol. Aspirin significantly (p<0.001) increased bleeding time from 167 to 236 seconds while Pycnogenol did not.These observations suggest an advantageous risk-benefit ratio for Pycnogenol.”

This is a highly significant finding, as aspirin-induced bleeding can result in significantly increased morbidity and mortality. To learn more, read my article on the topic: The Powerful Aspirin Alternative Your Doctor Never Told You About.

The science has never been clearer: flaxseed deserves to be top of the list of the world’s most important medicinal foods. For just pennies a day it may protect against dozens of life-threatening health conditions. 

Many of us have been enculturated to think about the nutritional dimension of our food intake in terms of the government’s recommended daily allowances (RDAs), focusing on getting the “right” amounts of carbohydrate, proteins, fats, vitamins, and minerals. However, I believe this focus on the quantifiable dimensions of food versus the qualitative/informationl elements has profoundly lead us astray. We bear witness to this in the fact that Americans are some of the most overfed yet simultaneously malnourished people on the planet. It is no wonder that we we are dying by the droves, with heart disease and cancer representing the most common (and also most preventable) causes of premature death.

What if there was a nutrient-packed super-food which costs pennies a day that can greatly reduce the risk of dying not only these, but dozens of other life-threatening conditions? Would you take it? The good news is there already is: welcome to the amazing nutritional/medicinal potential of flaxseed!

70 Reasons To Consume Flaxseed Daily

Admittedly, the title of this article is a bit over the top. Wouldn’t five good reasons, or even just one good reason be enough to consume it more regularly? After all, think of the millions of people around the world who take aspirin daily only because it promises to reduce the risk for one condition: namely, prevention of heart attack. A practice, incidentally, that is dubious at best, and for which natural and likely far safer and effective alternatives may exist. If we can establish the preventive value of flaxseed in only one serious condition, perhaps this alone would be compelling enough to convince our readers to start incorporating it into their daily dietary regimen. However, for those nutrition geeks out there who like to read the first-hand research, here’s our flaxseed database page, wherein you will find all the abstracts we have gathered on the topic of this seed’s immense potential in preventing and/or treating up to 70 different health conditions.

7 Flaxseed Healing Highlights

Below you will find our top 7 reports on flaxseed’s immense health benefits, including their role in preventing and/or reversing the #1 and #2 killers, namely, cardiovascular disease and cancer.

1. They Can Heal Your Arteries
2. They Can Contain Beneficial Plant Estrogens
3. They Can Reduce Your Breast Cancer Mortality by 70% 
4. They Can Protect Against Ovarian Cancer
5. They Protect Against Radiation Toxicity
6. They Can Dilate Your Arteries
7. They Can Treat Carpal Tunnel Syndrome

For those who are interested in how best to take advantage of flaxseed’s many health benefits, but are unsure what is the best way to consume it, we address some of the most common questions below.

Should I Eat The Seeds Ground or Whole? 

First, keep in mind that flaxseeds are Nature’s ingenious design for preserving the precious cargo inside: highly therapeutic, though fragile polyunsaturated fatty acids, amino acids, and other fat soluble vitamins. This also means that you don’t have to worry about refrigerating it. Once the seed is ground up and exposed to air, light, ambient fluctuations in temperature, and time, it begins to “go bad,” i.e. oxidize and degrade. This is why many make a daily practice of grinding up their own seeds in a coffee grinder to ensure maximum freshness. While I think this is a great idea, not everyone will have the time or desire to adhere to this daily routine. This is why some purchase pre-ground flaxseed. I am not against the practice. My only stipulation is that the buyer make sure the manufacturer has nitrogen-flushed the container so that oxygen didn’t get into the package at the time of manufacture.

The same rule applies to flaxseed oil. The company manufacturing the oil should maintain optimal freshness via nitrogen flushing the container, which will preferably be in non-chemical leaching glass. Also, opt for a high lignan form of the oil when available because you lose this valuable component of the seed material when you produce oil concentrate.  Flaxseed has one of the highest levels of naturally occurring lignans known, and this is why if you are consuming the oil you may also wish to supplement with whole or ground flaxseed so that you benefit from these highly therapeutic compounds.

As far as whole flaxseed, make sure that you chew it well, if you primary objective is to obtain the beneficial nutrients, lignans, and fiber from them. Also, consider that flaxseed produces a very soothing mucilaginous gel when exposed and/or soaked in water. You can pre-soak a tablespoon in a glass of water overnight to produce a very good concoction for constipation by drinking it in the morning.  Because flaxseed will naturally soak up water, remember not to consume too much dry, whole flaxseed without adequate hydration, as it could be a bit binding – the exact opposite effect that it will naturally have when consumed in the correct manner.

Which is Better? Flaxseed Oil or The Seed? 

Hands down, this is the most common question I have fielded. The truth is that one is not better than the other for general preventive health purposes. For optimal protection I would suggest using both. However, there are some important things to consider when incorporating either of these forms into your diet:

• Never heat flaxseed oil: All oils rich in monounsaturated and polyunsaturated fatty acids are prone to enhanced oxidation (rancidity) when heated. This means that you would not cook with flaxseed oil, opting for naturally saturated (and therefore more heat stabile) fats like palm, coconut oil or ghee (clarified butter) instead.
• Get creative with flaxseed meal: Flaxseed meal is an excellent addition to smoothies or for sprinkling on foods that have a higher glycemic index, e.g. pasta, cereal. The flaxseed meal will slow the breakdown of the starchy carbohydrates and therefore blunt blood sugar spikes and concomitant elevations in insulin. Also, the fiber is excellent for helping to contribute to regularity (it is useful both for going too much and not enough). The key, of course, is to always stay hydrated when using flaxseed, as it can cause significant binding in a dehydrated individual.
• Flaxseed is full of good fats: Keep in mind that flaxseed is a potent source of omega-3 fatty acids, containing a 4:1 ratio of omega 3 to omega 6 fatty acids. This is a great way to balance out the predominant ratios in the Standard American Diet, which is so heavy in corn, canola, soy, and peanut oils, all of which have several orders of magnitude more omega 6 than omega 3.

How Much Should I Take?

Generally, a tablespoon or two of meal a day is a good dose for ensuring you are getting a physiologically significant amount. The same goes for the oil. I have personally consumed five tablespoons of meal a day without any harm, and have used a good amount of the flaxseed oil in place of olive oil as salad dressing (I happen to like the taste of flaxseed better). Everyone will be different, so go with your intuition if you are just experimenting. If you are sick, consult your health practitioner or dietary coach to obtain specific recommendations. Also, listen to your body. If you aren’t finding flaxseed agrees with you, then back off on the amount or stop it until you find another dietary intervention that does work for you. Another alternative that has many of the same health benefits is chia seed.

Just the Nutritional Facts

We’ll leave you with some nutritional snapshots of flaxseed from the more quantitative perspective, so that it is clear how valuable it is in human nutrition simply as a source of both macronutrients and micronutrients, above and beyond its clearly medicinal function  (a reflection of what I would call it’s “therapeutic information” content) in the wide range of health conditions our database shows. The information below is based on 1 cup (168 grams) worth of flaxseed whole.

Flaxseed Protein and Amino Acid Content

Flaxseed Vitamin Content

Flaxseed Mineral Content

Flaxseed Fatty Acids

For more nutritional data on flaxseed, visit the Nutritiondata.com website.

It may come as a surprise to some, especially those with conventional medical training, but the default state of the body is one of ceaseless regeneration.  Without the flame-like process of continual cell turnover within the body – life and death ceaselessly intertwined – the miracle of the human body would not exist.

In times of illness, however, regenerative processes are overcome by degenerative ones. This is where medicine may perform its most noble feat, nudging the body back into balance with foods, herbs, nutrients, healing energies, i.e. healing intention. Today, however, drug-based medicine invariably uses chemicals that have not one iota of regenerative potential; to the contrary, they almost always interfere with bodily self-renewal in order to suppress the symptoms against which they are applied.

Despite the outright heretical nature of things which stimulate healing and regeneration vis-à-vis the conventional medical system which frowns upon, or is incredulous towards, spontaneous remission in favor of symptom suppression and disease management, over the course of the past few years of trolling MEDLINE we have collected a series of remarkable studies on the topic…

Nerve Regeneration – There are actually a broad range of natural compounds with proven nerve-regenerative effects. A 2010 study published in the journal Rejuvenation Research, for instance, found a combination of blueberry, green tea and carnosine have neuritogenic (i.e. promoting neuronal regeneration) and stem-cell regenerative effects in an animal model of neurodegenerative disease. [1] Other researched neuritogenic substances include:

1. Curcumin
2. Lion’s Mane Mushroom
3. Apigenin (compound in vegetables like celery)
4. Blueberry
5. Ginseng
6. Huperzine
7. Natto
8. Red Sage
9. Resveratrol
10. Royal Jelly
11. Theanine
12. Ashwaganda
13. Coffee (trigonelline)

There is another class of nerve-healing substances, known as remyelinating compounds, which stimulate the repair of the protective sheath around the axon of the neurons known as myelin, and which is often damaged in neurological injury and/or dysfunction, especially autoimmune and vaccine-induced demyelination disorders.  It should also be noted that even music and falling in love have been studied for possibly stimulating neurogenesis, regeneration and/or repair of neurons, indicating that regenerative medicine does not necessary require the ingestion of anything; rather, a wide range of therapeutic actionsmay be employed to improve health and well-being, as well.

[View the first-hand biomedical citations on these neuritogenic substance visit our Neuritogenic Research page on the topic]

Liver Regeneration – Glycyrrhizin, a compound found within licorice, and which we recently featured as a powerful anti-SARS virus agent,  has also been found to stimulate the regeneration of liver mass and function in the animal model of hepatectomy. Other liver regenerative substances include:

1. Carvacrol (a volatile compound in oregano)
2. Curcumin
3. Korean Ginseng
4. Rooibos
5. Vitamin E

[view the first-hand biomedical citations on the Liver Regeneration research page]

Beta-Cell Regeneration – Unfortunately, the medical community has yet to harness the diabetes-reversing potential of natural compounds. Whereas expensive stem cell therapies, islet cell transplants, and an array of synthetic drugs in the developmental pipeline are the focus of billions of dollars of research, annually, our kitchen cupboards and backyards may already contain the long sought-after cure for type 1 diabetes. The following compounds have been demonstrated experimentally to regenerate the insulin-producing beta cells, which are destroyed in insulin dependent diabetes, and which once restored, may (at least in theory) restore the health of the patient to the point where they no longer require insulin replacement.

1. Gymenna Sylvestre (“the sugar destroyer”)
2. Nigella Sativa (“black cumin”)
3. Vitamin D
4. Curcumin (from the spice Turmeric)
5. Arginine
6. Avocado
7. Berberine (found in bitter herbs such as Goldenseal and Barberry)
8. Bitter Melon
9. Chard (yes, the green leafy vegetables)
10. Corn Silk
11. Stevia
12. Sulforaphane (especially concentrated in broccoli sprouts)

[view the first-hand biomedical citations on the Beta Cell Regeneration research page]

Hormone Regeneration – there are secretagogues, which increase the endocrine glands’ ability to secrete more hormone, and there are substances that truly regenerate hormones which have degraded (by emitting electrons) into potentially carcinogenic “transient hormone” metabolites. One of these substances is vitamin C. A powerful electron donor, this vitamin has the ability to contribute electrons to resurrect the form and function of estradiol (estrogen; E2), progesterone, testosterone, for instance. [2] In tandem with foods that are able to support the function of glands, such as the ovaries, vitamin C may represent an excellent complement or alternative to hormone replacement therapy.

Cardiac Cell Regeneration – Not too long ago, it was believed that cardiac tissue was uniquely incapable of being regenerated. A new, but rapidly growing body of experimental research now indicates that this is simply not true, and there is a class of heart-tissue regenerating compounds known as neocardiogenic substances.  Neocardiogenic substances are able to stimulate the formation of cardiac progenitor cells which can differentiate into healthy heart tissue, and they include the following:

1. Resveratrol
2. Siberian Ginseng (Eleuthero)
3. Red Wine Extract
4. Geum Japonicum
5. N-acetyl-cysteine

Another remarkable example of cardiac cell regeneration is through what is known as fetomaternal trafficking of stem cells through the placenta. In a recent article we discussed the amazing process known as “fetal microchimerism” by which the fetus contributes stem cells to the mother which are capable of regenerating her damaged heart cells, and possibly a wide range of other cell types.

Cartilage/Joint/Spine Regeneration – Curcumin and resveratrol have been shown to improve recovery from spinal cord injury.  Over a dozen other natural compounds hold promise in this area, which can be viewed on our Spinal Cord Injury page.  As far as degenerative joint disease, i.e. osteoarthritis, there are a broad range of potentially regenerative substances, with 50 listed on our osteoarthritis research page.

Ultimately, regenerative medicine threatens to undermine the very economic infrastructure that props up the modern, drug-based and quite candidly degenerative medical system. Symptom suppression is profitable because it guarantees both the perpetuation of the original underlying disease, and the generation of an ever-expanding array of additional, treatment-induced symptoms.

This is the non-sustainable, infinite growth model which shares features characteristic of the process of cancer itself – a model, which by its very nature, is doomed to fail and eventually collapse. Cultivating diets, lifestyles and attitudes conducive to bodily regeneration can interrupt this pathological circuit, and help us to attain the bodily freedom that is a precondition for the liberation of the human soul and spirit, as well.

Additional related articles: 

• Brain Regeneration: Why It’s Real & How To Do It
• How Music Can Support Brain Regeneration & Healing
• How WHOLE Turmeric Heals The Damaged Brain
• Boost Memory, Regenerate Neurons with This Ancient Plant
• Broccoli Can Stimulate Brain Regeneration
• The Flame of Cell Life-Death In The Miracle of Regeneration

References

[1] NT-020, a natural therapeutic approach to optimize spatial memory performance and increase neural progenitor cell proliferation and decrease inflammation in the aged rat. Rejuvenation Res. 2010 Jun 29. Epub 2010 Jun 29. PMID: 20586644

[2] Photo-induced regeneration of hormones by electron transfer processes: Potential biological and medical consequences. Radiat Phys Chem Oxf Engl 1993. Updated 2011 Aug ;80(8):890-894. PMID: 21814301

There is evidence for the potential therapeutic use of curcumin in over 700 conditions, these ten are some of the most compelling applications. 

1) Depression

People suffering from major depressive disorder were given 1g of curcumin or placebo for 8 weeks in a double-blind study. The curcumin was significantly more effective than placebo. Curcumin was also effective for the serious and difficult to treat atypical depression (J Affect Disord 2014;167:368-75).

A 6 week study gave 1g of curcumin (standardized for 88% curcuminoids), 20mg of Prozac or both to 45 people suffering from major depressive disorder. The difference between the 3 groups was not significant, but the combination worked slightly better than either treatment alone. 62.5% of the curcumin group and 64.7% of the Prozac group responded. 77.8% responded when they were combined. There was no significant difference between the treatments in improvement on the Hamilton Depression Scale (HAMD): the Prozac group improved by 12.6 points, the curcumin group by a slightly better 14 points and the combination group by 14.8 points. Patients’ treatment ratings were not significantly different, but the herb did better than the drug: 70.5% of those on Prozac said their treatment was good or excellent compared to 75% on curcumin and 83.3% on the combination (Phytother Res 2014;28:579-85).

Other recent research shows that curcumin improves the efficacy of antidepressants. When 108 adults added 1g of curcumin or placebo to their meds for 6 weeks, the curcumin significantly improved the antidepressant effect (J Clin Psychopharmacol 2015;35:406-10).

A meta-analysis of curcumin and depression included 6 studies that added curcumin or placebo to therapy. There was a significant reduction in symptoms of depression in the curcumin group compared to the placebo group. Curcumin had to be taken for at least 6 weeks at a dose of 1g. It worked better on middle-aged people than on older people, and it worked better for longer durations (Phytother Res 2016;30:175-183).

2) Arthritis

Curcumin lowers pain scores significantly better than placebo: 60% of people on placebo still have to take NSAIDs, while only 32% of people on curcumin do (J Orthop Sci 2014;19:933-9). A second study compared 1500mg of curcuminoids to placebo. The curcuminoids significantly reduced osteoarthritis scores, including scores for pain and stiffness. The curcuminoid group reduced the need for painkillers by 84% compared to 19% in the placebo group (Phytother Res 2014;28:1625-31).

Curcumin is also superior to pain killing drugs. When people with osteoarthritis were given turmeric extract or ibuprofen, 91% of those taking curcumin reported moderate to high satisfaction versus 80.4% taking ibuprofen (J Altern Comp Med 2009;15:891-897). And in another ibuprofen comparison, scores improved significantly in both groups, but the curcumin was safer (Clin Intrerv Aging 2014;9:451-8). A third controlled study also found curcumin to be more effective than ibuprofen. Improvements in pain scores were greater on curcumin, and 91% of those on curcumin reported moderate to high satisfaction compared to 80.4% of those on ibuprofen (Arthritis Rheum 2001;44:2531-8).

When researchers conducted a systematic review and meta-analysis of all randomized controlled studies of turmeric extracts and curcumin for osteoarthritis, they found that about 1g of turmeric/curcumin a day significantly reduced pain and significantly improved WOMAC osteoarthritis scores. Turmeric/curcumin was as effective as pain meds (J Food Med 2016;19(8):717-29).

A recent review included 15 studies: 13 of the studies were randomized. Among the randomized studies, 5 compared curcumin to placebo, and 4 compared it to NSAIDs. Others compared it to “best treatment,” chondroitin or glucosamine. People using curcumin had improvements in pain, physical function and quality of life. They also were able to take fewer pharmaceutical painkillers and experienced reduced side effects from drug treatment. The curcumin seemed to work in part by preventing the death of chondrocytes, which prevents loss of cartilage, and by reducing inflammation and free radical damage (Drug Des Devel Ther 2016;10:3029–3042).

For rheumatoid arthritis, curcumin is as effective as the powerful NSAID phenylbutazone (Indian J Med Res 1980;71:632-4). When curcumin was compared to the NSAID diclofenac sodium for rheumatoid arthritis, the herb was significantly more effective and safer (Phytother Res 2012;26:1719-25).

3) Diabetes

In perhaps one of the most amazing diabetes studies, 237 prediabetics were given either curcumin (containing 750mg curcuminoids) or placebo twice a day for 9 months in a double-blind study. 16.4% of prediabetics on placebo went on to develop type 2 diabetes. 0% of those on curcumin did! The curcumin group had significantly better insulin producing beta-cell function and significantly less insulin resistance. So, curcumin may actually stop the development of diabetes (Diabetes Care 2012;35:2121-7). A review of the literature on curcumin and diabetes/prediabetes shows that curcumin lowers glucose and improves beta cell function (Int J Endocrinol Metab 2014; 12: e18081).

A recent review of the literature on curcumin and diabetes revealed that studies on diabetics and prediabetics show that curcumin lowers glucose and improves beta cell function (Int J Endocrinol Metab 2014; 12: e18081).

4) Colitis

This double-blind study included 50 people with mild to moderate ulcerative colitis who were not responding to the drug mesalamine. They all stayed on the mesalamine, but, while half added a placebo, half added 3g a day of curcumin for one month. By the end of the study, mesalamine still wasn’t working: none of the people who added a placebo to the drug were in remission. But, 53.8% of those who added curcumin were in clinical remission. When you look not just at complete remission but at how many people were helped by the herb, while only 12.5% responded to the addition of the placebo, 65.3% responded when they started taking curcumin. Again, that is a significant advantage with the herb. 38% of the curcumin group achieved endoscopic remission versus none in the placebo group (Clinical Gastroenterology and Hepatology 2015;13(8):1444-1449.e1).

A small, previous pilot study also found curcumin to help inflammatory bowel disease (Dig Dis Sci 2005;50(11):2191-3).

5) Ulcers

A study included 60 people with ulcers and H. pylori infections. They were all getting standard medical treatment for the H. pylori, but, while some added a placebo, some added a low dose of 500mg curcumin a day. At the end of the 4 week study, although the curcumin did not seem to benefit H. pylori infection more than the placebo, it was significantly better at alleviating the symptoms of the ulcers. The people taking the curcumin had significantly better improvement on total symptoms according to the Hong Kong dyspepsia index (HKDI). They also had significantly greater improvement specifically in upper abdominal dull ache, stomach pain prior to meals and belching. At the end of the study, 27.6% of the curcumin group had no dyspepsia versus only 6.7% of the placebo group: a significant difference. It would be interesting to see what a more typical larger dose of curcumin would do (Drug Res (Stuttg) 2016;66(8)444-448).

6) PMS

This double-blind, placebo-controlled study gave either a placebo or 100mg of curcumin twice a day for three menstrual cycles to seventy women who suffered from PMS. They took the curcumin for ten days each cycle, starting a week before the start of menstruation. The curcumin lowered mean PMS symptom scores significantly more than the placebo (Neuropeptides 2015 Nov 11. pii:S0143-4179(15)00118-3).

7) Anti-Aging

Telomeres are the protective DNA and protein caps on the ends of chromosomes. They shorten with each cell division, and when they reach a critical length, the cell finally dies. These telomeres help to determine how long you will live. Telomere shortness is a marker of aging, disease and premature death. The longer they are, the longer you are likely to live. In ground breaking preliminary research curcumin showed the ability to lengthen telomeres (PLoS One 2014;9:e101251).

8) Cognition

In the first study of curcumin and cognition and mood, 60 healthy people between the ages of 60 and 85 were given either curcumin or a placebo. The double-blind study found that curcumin significantly improves working memory, fatigue, fatigue caused by stress, calmness and contentedness (J Psychopharmacol 2014;doi:10.1177/0269881114552744). When 37 people between 50 and 90 who did not suffer from dementia were given either curcumin or a placebo in a second double-blind study that lasted 18 months, memory and attention improved significantly on curcumin compared to placebo (Am J Geriatr Psychiatry 2017; doi.org/10.1016/j.jagp.2017.10.010).

When forty adults between 51 and 84 who had mild memory complaints but no dementia were given curcumin or a placebo for 18 months in a double-blind study, curcumin significantly improved memory and attention compared to the placebo. Memory improved by 28%. Curcumin also mildly improved mood. Curcumin may work because it decreases plaque and tangle accumulation in the brain and acts as an anti-inflammatory (Am J Geriatr Psychiatry 2018;26(3):266-77).

One of the unfortunate complications of diabetes is dementia. The cognitive impairment begins developing while the person is still pre-diabetic. In a double-blind study, people who were sixty or older and who were prediabetic were given a single dose of 1g of turmeric at breakfast. After six hours, measures of working memory showed a significant improvement from a score of 2.6 to 2.9 on a 3-point scale in the ones given the turmeric. Measurements in the study suggested that the turmeric may be even more effective in healthy people with no prediabetes (Asia Pac J Clin Nutr2014;23:581-91).

9) Cancer

Curcumin is one of the most promising and exciting cancer treatments. Curcumin is loaded with promise for both the prevention and treatment of cancer. A review of curcumin in cancer therapy has concluded that it has anti-cancer effects at several stages of cancer: carcinogenesis (formation), cell proliferation (growth), apoptosis (safe death specifically of cancer cells), metastasis (spread) and angiogenesis (the formation of blood vessels by the tumour that allow it to feed itself and grow). It also concluded that curcumin increases the effectiveness of chemotherapy and radiation while protecting from their side effects (Curr Probl Cancer 2007;31:243-305).

Curcumin is very versatile, helping against prostate, breast, colon, skin, liver, cervical, stomach and oral cancer. In fact, curcumin helps fight virtually any form of cancer. Research has found curcumin to powerfully induce apoptosis in even the toughest cases of prostate cancer, the hormone independent variety (Prostatic Cancer Prostatic Dis 2000).

Most recently, research has identified curcumin as one of the most powerful natural compounds for killing cancer stem cells. Cancer stem cells represent a paradigm shift in the treatment of cancer. Current cancer treatments target proliferating cells in tumours but are powerless against cancer stem cells. Cancer stem cells have the incredible ability to “self-renew,” making them virtually immortal. They originate the cells that make up tumours and then playa role in every single phase of cancer, form initiation to progression, invasion and metastasis (Int J Mol Sci 2015;16:15727-42).

10) Heart Health

Curcumin helps heart health in a number of important ways. It lowers cholesterol and triglycerides and protects cholesterol from free radical damage (Indian J Physiol Pharmacol 1992; Age 1995; Nutr J 2017;16(1):68). Curcumin can also help protect against atherosclerosis by preventing blood platelets from sticking together (Thromb Res 1995; Arzneimforsch 1986) and by reducing elevated levels of fibrinogen (Mech Ageing Dev 2000), which can cause atherosclerosis.

Recent research has also shown that curcumin is valuable for blood pressure and blood vessel health. In fact, it may be as beneficial as exercise. 32 healthy, but sedentary, postmenopausal women were put in a group that took 150mg of curcumin a day or in a group that exercised or in a group that did neither. After 8 weeks, blood pressure had dropped in the curcumin and exercise group but not in the control group. Blood vessel elasticity, an important factor in atherosclerosis, also improved in both treatment groups but not in the control group. The improvements in the curcumin and exercise groups were similar (Nutr Res 2012).

The endothelial wall is a layer of cells that lines the inside of the heart and blood vessels. If the endothelial wall gets damaged, cholesterol can be deposited on it and plaque can develop, leading to blocked arteries and atherosclerosis. Flow-mediated dilation (FMD) is a measure of endothelial dysfunction and blood vessel health. It is an important indicator of early stage atherosclerosis. A double-blind study gave 59 healthy people a placebo, 50mg of curcumin or 200mg of curcumin every day for 8 weeks. The people who got the 200mg dose of curcumin had improvement in endothelial function, as measured by FMD. Compared to the placebo, FMD improved by a “clinically substantial” 3%. That would translate into a 39% reduction in the risk of cardiovascular disease (Journal of Nutrition and Metabolism 2016;dx.doi.org/10.1155/2016/1089653).

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Heart disease while still the #1 cause of mortality in the developed world, can be prevented and even reversed disease with nutrition, according to a growing body of scientific research.

Considering that heart disease is the #1 cause of death in the developed world, anything that can prevent cardiac mortality, or slow or even reverse the cardiovascular disease process, should be of great interest to the general public.

Sadly, millions of folks are unaware of the extensive body of biomedical literature that exists supporting the use of natural compounds for preventing and even reversing heart disease.

Instead, they spend billions buying highly toxic cholesterol-lowering pharmaceuticals with known cardiotoxicity, among 300 other proven side effects, simply because their doctor told them to do so.

So, with this in mind, let’s look at the biomedical literature itself.

Three Natural Substances that Reduce the Risk of Heart-Related Death

• Omega-3 Fatty Acids: There is a robust body of research indicating that the risk of sudden cardiac death is reduced when consuming higher levels of omega-3 fatty acids. Going all the way back to 2002, the New England Journal of Medicine published a study titled,  “Blood levels of long-chain n-3 fatty acids and the risk of sudden death,” which found  “The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease.” Another 2002 study, published in the journal Circulation, found that Omega-3 fatty acid supplementation reduces total mortality and sudden death in patients who have already had a heart attack.[i] For additional research, view our dataset on the topic of Omega-3 fatty acids and the reduction of cardiac mortality. It should be noted that the best-selling cholesterol drug class known as statins may actually reduce the effectiveness of omega-3 fats at protecting the heart. This has been offered as an explanation as to why newer research seems to show that consuming omega-3 fats does not lower the risk of cardiac mortality.
• Vitamin D: Levels of this essential compound have been found to be directly associated with the risk of dying from all causes. Being in the lowest 25% percent of vitamin D levels is associated with a 26% increased rate of all-cause mortality.[ii]  It has been proposed that doubling global vitamin D levels could significantly reduce mortality.[iii]Research published in the journal Clinical Endocrinology in 2009 confirmed that lower vitamin D levels are associated with increased all-cause mortality but also that the effect is even more pronounced with cardiovascular mortality.[iv] This finding was confirmed the same year in the Journal of the American Geriatric Society, [v] and again in 2010 in the American Journal of Clinical Nutrition.[vi]
• Magnesium: In a world gone mad over taking inorganic calcium supplementation for invented diseases such as T-score defined “osteopenia” or “osteoporosis,”despite their well-known association with increased risk of cardiac mortality, magnesium’s role in protecting against heart disease cannot be overstressed. It is well-known that even the accelerated aging of the heart muscle experienced by those in long space flight is due to magnesium deficiency. In 2010, the Journal of Biomedical Sciences reported that cardiovascular risks are significantly lower in individuals who excrete higher levels of magnesium, indicating its protective role.[vii]  Another study published in the journal Atherosclerosis in 2011 found that low serum magnesium concentrations predict cardiovascular and all-cause mortality.[viii] Remember that when you are looking to ‘supplement’ your diet with magnesium go green. Chlorophyll is green because it has a magnesium atom at its center. Kale, for example, is far better a source of complex nutrition than magnesium supplements. But, failing the culinary approach, magnesium supplements can be highly effective at attaining a therapeutic and/or cardioprotective dose.

For an additional list of compounds that may reduce cardiac mortality, including cocoa, tea, wine and yes, even cholesterol itself, view our Reduce Cardiac Mortality page.

Four Natural Compounds Which May Unclog the Arteries

• Pomegranate: this remarkable fruit has been found in a human clinical study to reverse the carotid artery thickness (i.e. blockage) by up to 29% within 1 year. [ix] There are a broad range of mechanisms that have been identified which may be responsible for this effect, including: 1) lowering blood pressure 2) fighting infection (plaque in arteries often contains bacteria and viruses) 3) preventing cholesterol oxidation 4) reducing inflammation.[x]
• Arginine: Preclinical and clinical research indicates that this amino acid not only prevents the progression of atherosclerosis but also reverses pathologies associated with the process. (see also: Clogged Arteries and Arginine). One of the mechanisms in which it accomplishes this feat is by increasing the production of nitric oxide which is normally depressed in blood vessels where the inner lining has been damaged (endothelium) resulting in dysfunction.
• Garlic: Not only has garlic been found to reduce a multitude of risk factors associated with arteriosclerosis, the thickening and hardening of the arteries, but it also significantly reduces the risk of heart attack and stroke.[xi]  In vitro research has confirmed that garlic inhibits arteriosclerotic plaque formation.[xii]  Aged garlic extract has also been studied to inhibit the progression of coronary artery calcification in patients receiving statin therapy.[xiii] And let us not forget, garlic’s benefits are extremely broad. We have identified over 150 diseases that this remarkable culinary and medicinal herb has been confirmed to be of potential value in treating and preventing and which can be viewed here: Garlic Health Benefits.
• B-Complex: One of the few vitamin categories that has been confirmed in human studies to not only reduce the progression of plaque buildup in the arteries but actually reverse it is B-complex. A 2009 study published in the journal Stroke found that high dose B-complex vitamin supplementation significantly reduces the progression of early-stage subclinical atherosclerosis in healthy individuals.[xiv] More remarkably, a 2005 study published in the journal Atherosclerosis found a B-vitamin formula decreased the carotid artery thickness in patients at risk for cerebral ischemia.[xv] Another possible explanation for these positive effects is the role B-vitamins have in reducing the production of homocysteine, an artery and otherwise blood vessel scarring amino acid.[xvi]

For additional research on artery unclogging substances visit our page dedicated to the topic Unclogging Arteries.

Additional Heart Unfriendly Things To Avoid

No discussion of preventing cardiac mortality would be complete without discussing things that need to be removed in order to reduce risk, such as:

• NSAIDs: Drugs like aspirin, ibuprofen, and Tylenol, have well-known association with increased cardiac mortality. Review six studies on the topic here: NSAID Cardiotoxicity.
• Statin Drugs: It is the height of irony that the very category of drugs promoted to millions globally as the standard of care for primary and secondary prevention of cardiovascular disease and cardiac mortality are actually cardiotoxic agents, linked to no less than 300 adverse health effects. Statin drugs have devastating health effects. Explore the research here: Statin Drug Health Effects.
• Wheat: while this connection is rarely discussed, even by those who promote grain-free and wheat free diets, wheat has profound cardiotoxic potential, along with over 200 documented adverse health effects: Wheat Toxicity. And why wouldn’t it, when the very countries that eat the most of it have the highest rate of cardiovascular disease and heart-related deaths? For an in-depth explanation read our article: Wheat’s Cardiotoxicity: As Serious As A Heart Attack.

Finally, for additional research on the topic of heart health promoting strategies visit our Health Guide: Heart Health. Interested in healing an injured heart? Read about cardiac tissue regeneration: 6 Bodily Tissues That Can Be Regenerated Through Nutrition.

References

• [i] Roberto Marchioli, Federica Barzi, Elena Bomba, Carmine Chieffo, Domenico Di Gregorio, Rocco Di Mascio, Maria Grazia Franzosi, Enrico Geraci, Giacomo Levantesi, Aldo Pietro Maggioni, Loredana Mantini, Rosa Maria Marfisi, G Mastrogiuseppe, Nicola Mininni, Gian Luigi Nicolosi, Massimo Santini, Carlo Schweiger, Luigi Tavazzi, Gianni Tognoni, Corrado Tucci, Franco Valagussa,. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105(16):1897-903. PMID: 11997274

• [ii] Michal L Melamed, Erin D Michos, Wendy Post, Brad Astor. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008 Aug 11;168(15):1629-37. PMID: 18695076

• [iii] W B Grant. An estimate of the global reduction in mortality rates through doubling vitamin D levels. Eur J Clin Nutr. 2011 Jul 6. Epub 2011 Jul 6. PMID: 21731036

• [iv] Stefan Pilz, Harald Dobnig, Giel Nijpels, Robert J Heine, Coen D A Stehouwer, Marieke B Snijder, Rob M van Dam, Jacqueline M Dekker. Vitamin D and mortality in older men and women. Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18. PMID: 19226272

• [v] Adit A Ginde, Robert Scragg, Robert S Schwartz, Carlos A Camargo. Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009 Sep;57(9):1595-603. Epub 2009 Jun 22. PMID: 19549021

• [vi] Karl Michaëlsson, John A Baron, Greta Snellman, Rolf Gedeborg, Liisa Byberg, Johan Sundström, Lars Berglund, Johan Arnlöv, Per Hellman, Rune Blomhoff, Alicja Wolk, Hans Garmo, Lars Holmberg, Håkan Melhus. Plasma vitamin D and mortality in older men: a community-based prospective cohort study. Am J Clin Nutr. 2010 Oct;92(4):841-8. Epub 2010 Aug 18. PMID: 20720256

• [vii] Yukio Yamori, Takashi Taguchi, Hideki Mori, Mari Mori. Low cardiovascular risks in the middle aged males and females excreting greater 24-hour urinary taurine and magnesium in 41 WHO-CARDIAC study populations in the world. J Biomed Sci. 2010;17 Suppl 1:S21. Epub 2010 Aug 24. PMID: 20804596

• [viii] Thorsten Reffelmann, Till Ittermann, Marcus Dörr, Henry Völzke, Markus Reinthaler, Astrid Petersmann, Stephan B Felix. Low serum magnesium concentrations predict cardiovascular and all-cause mortality. Atherosclerosis. 2011 Jun 12. Epub 2011 Jun 12. PMID: 21703623

• [ix] Sayer Ji, Research: Pomegranate May Reverse Blocked Arteries

• [x] GreenMedInfo.com, Pomegranate’s Health Benefits

• [xi] G Siegel, A Walter, S Engel, A Walper, F Michel. [Pleiotropic effects of garlic].Wien Med Wochenschr. 1999;149(8-10):217-24. PMID: 10483684

• [xii] Günter Siegel, Frank Michel, Michael Ploch, Miguel Rodríguez, Martin Malmsten. [Inhibition of arteriosclerotic plaque development by garlic]. Wien Med Wochenschr. 2004 Nov;154(21-22):515-22. PMID: 15638070

• [xiii] Matthew J Budoff, Junichiro Takasu, Ferdinand R Flores, Yutaka Niihara, Bin Lu, Benjamin H Lau, Robert T Rosen, Harunobu Amagase. Inhibiting progression of coronary calcification using Aged Garlic Extract in patients receiving statin therapy: a preliminary study. Prev Med. 2004 Nov;39(5):985-91. PMID: 15475033

• [xiv] Howard N Hodis, Wendy J Mack, Laurie Dustin, Peter R Mahrer, Stanley P Azen, Robert Detrano, Jacob Selhub, Petar Alaupovic, Chao-ran Liu, Ci-hua Liu, Juliana Hwang, Alison G Wilcox, Robert H Selzer,. High-dose B vitamin supplementation and progression of subclinical atherosclerosis: a randomized controlled trial.Stroke. 2009 Mar;40(3):730-6. Epub 2008 Dec 31. PMID: 19118243

• [xv] Uwe Till, Peter Röhl, Almut Jentsch, Heiko Till, Andreas Müller, Klaus Bellstedt, Dietmar Plonné, Horst S Fink, Rüdiger Vollandt, Ulrich Sliwka, Falko H Herrmann, Henning Petermann, Reiner Riezler. Decrease of carotid intima-media thickness in patients at risk to cerebral ischemia after supplementation with folic acid, Vitamins B6 and B12. Atherosclerosis. 2005 Jul;181(1):131-5. Epub 2005 Feb 16. PMID: 15939064

• [xvi] Claudio Maldonado, Chirag V Soni, Nathan D Todnem, Sathnur Pushpakumar, Dorothea Rosenberger, Srikanth Givvimani, Juan Villafane, Suresh C Tyagi. Hyperhomocysteinemia and sudden cardiac death: potential arrhythmogenic mechanisms. Curr Vasc Pharmacol. 2010 Jan;8(1):64-74. PMID: 19485933

“Though Mother Nature’s formulas are proprietary, she does not grant patents”

~ Sayer Ji

Some of the most powerful medicines on the planet are masquerading around as foods and spices. While they do not lend themselves to being patented, nor will multi-billion dollar human clinical trials ever be funded to prove them efficacious, they have been used since time immemorial to both nourish our bodies, and to prevent and treat disease.

So valued were these in ancient times that they were worth their weight in gold, and entire civilizations either rose to great power or collapsed as a result of their relationship to them.

What is even more amazing is that many of these “plant allies” are found growing in our backyards, and often sitting there in our refrigerators and spice racks, neglected and under appreciated.  In fact, many of us use these daily unaware that this is why we don’t get sick as often as those who do not incorporate them into their diet. Let’s look at a few examples….

Garlic

With the increasing prevalence of multi-drug resistant bacteria and the failure of the conventional, drug-based model to develop effective solutions against them (nor accepting responsibility for creating them), spices have regained their once universal reign as broad spectrum infection-fighters with sometimes life-saving power. Garlic, in fact, has several hundred therapeutic properties, confirmed by a growing body of scientific research, which you can view directly on GreenMedInfo.com.[i]  One quick example of garlic’s power, is in killing multi-drug resistant tuberculosis (MDR-TB), which the mainstream media has termed the “white plague,” roiling the masses with a fear of drug-resistant (but not plant-extract resistant) they are made to believe they are defenseless against.  Last year an article was published in a peer-reviewed scientific journal showing that garlic was capable of inhibiting a wide range of multiple drug resistant tuberculosis strains.[ii] The authors concluded “The use of garlic against MDR-TB may be of great importance regarding public health.”  Garlic’s anti-infective properties do not end with MDR-TB, as it has been demonstrated to inhibit the following pathogens as well:

• Amoeba Entamoeba histolytica (parasite)
• Cholera
• Clostridium
• Cytomegalovirus
• Dermatophytoses (a type of topical fungal infection)
• Haemophilus Influenzae
• Helicobacter Pylori
• Herpes Simplex Virus Type 1
• Herpes Simplex Virus Type 2
• Klebsiella
• Methicillin-resistant Staphylococcus A. (MRSA)
• Parainfluenza Virus
• Peridontal Infection
• Pneumococcal Infections
• Pseudomonas aeruginosa
• Streptococcus Mutans
• Streptococcus Infections: Group A
• Streptococcus Infections: Group B
• Streptococcus pyrogenes
• Thrush (oral fungal infection)

This amazing list underscores how important it is to keep a supply of garlic close by!

Honey

Bees produce a wide range of therapeutic substances beyond honey, e.g. propolis, bee venom, royal jelly, beeswax, bee pollen, etc., but this sweet, sticky stuff that we all love to dip our paw into occasionally, is the most well-known and most copiously consumed of them all – and for good reason, it tastes great!  But did you know that this sweet treat is one of nature’s most powerful healing agents, as well? Here is just a smattering of some of honey’s more scientifically researched health benefits and/or applications:

• Aspirin-Induced Gastrointestinal Toxicity  (honey  coats the delicate linings of the stomach, preventing aspirin-induced lesions and bleeding)
• Bacterial Infections
• Burns
• Candida infection (despite the fact that honey contains sugar, it demonstrates anti-fungal properties)
• Conjunctivitis
• Dental plaque (a recent study showed that Manuka honey was a viable alternative to chemical mouthwash in dissolving dental plaque)[iii]
• Dermatitis
• Diabetic Ulcer
• Herpes-related ulcers
• MRSA (especially for Manuka honey)

There are many more uses for honey than covered here. Needless to say, replacing synthetic sweeteners or highly processed sugars or high fructose corn syrup with a moderate amount of honey may be a great preventative health step to take.

Apples

An apple a day does in fact keep the doctor away, especially cancer specialists it would seem.  For instance, one of the most well-established health benefits of consuming apples is to reduce the risk of colorectal cancer. The more apples you consume, the less likely you are to develop this potentially fatal disease.  To view the 5 studies that reference this relationship, go to the GreenmedInfo.com apple research page where you will also find 50 other health benefits of apple or apple byproducts (e.g. apple vinegar) consumption which include:

• Aging, Reduce Rate
• Allergies
• Allopecia (Hair Loss)
• Diarrhea
• Insulin Resistance
• Liver Cancer
• Radiation Induced Illness
• Staphylococcol Infection

Sunlight

This one may throw some of you off, but sunlight possesses both energy and information with real, metabolic value and is therefore a source of usable energy for the body – and so, in a very real sense it can be considered a form of food that we consume through our skin by way of its built in, melanin-based “solar panels.”  Not only does adequate sunlight exposure result in the production of vitamin D, a hormone-like substance that regulates over 2,000 genes in the human body — and as a result prevents or ameliorates hundreds of vitamin D deficiency associated health conditions — but sunlight exposure itself has a unique set of health benefits not reducible to simply vitamin D production alone.  One of the more interesting studies performed on sunlight exposure, based on data gathered from over 100 countries and published earlier this year in the journal Anticancer Research, showed that there was “a strong inverse correlations with solar UVB for 15 types of cancer,” with weaker, though still significant evidence for the protective role of sunlight in 9 other cancers. Here are some additional benefits of sunlight exposure:

• Alzheimer’s Disease
• Depression
• Dopamine Deficiency
• Dermatitis
• Influenza
• Multiple Sclerosis
• Psoriasis

Turmeric

This is quite possibly the world’s most important herb. Named “Kanchani,” or literally “Golden Goddess,” in the ancient Indian healing tradition, its healing properties have been deeply appreciated, if not revered for countless centuries. In fact, I believe it is a physical embodiment of compassion. Turmeric has been scientifically documented to have over 800 applications in disease prevention and treatment. It also has been shown to modulate over 150 distinct biological and genetic/epigenetic pathways of value in health, demonstrating a complexity as well as gentleness that no drug on the planet has ever been shown to possess.

As there are too many health conditions that turmeric may benefit to list, we are listing the top 10 as determined by the GreenMedInfo algorithm which calculates both the evidence quantity (number of articles) and evidence quality (human study valued higher than animal, and so on). Also, the number in parentheses denotes the number of studies on the database demonstrating the beneficial relationship.

• Oxidative Stress (160)
• Inflammation (51)
• DNA Damage (48)
• Lipid Peroxidation (34)
• Colorectal Cancer (24)
• Breast Cancer (60)
• Colon Cancer (52)
• Chemically-Induced Liver Damage (34)
• Alzheimer’s Disease (34)
• Tumors (23)

For a more in depth look at the 1500+ studies on our site on Turmeric (and its primary polyphenol Curcumin), watch the video below and please share it with others if you find the information compelling.

References

[i] GreenMedInfo.com, Garlic Research Page: http://www.greenmedinfo.com/substance/garlic

[ii] Pak J Pharm Sci. 2011 Jan;24(1):81-5. PMID: 21190924

[iii] Contemp Clin Dent. 2010 Oct ;1(4):214-7. PMID: 22114423

Magnesium deficiency is often misdiagnosed because it does not show up in blood tests – only 1% of the body’s magnesium is stored in the blood.

We thirst for magnesium rich water.

Most doctors and laboratories don’t even include magnesium status in routine blood tests. Thus, most doctors don’t know when their patients are deficient in magnesium, even though studies show that the majority of Americans are deficient in it.

Consider Dr. Norman Shealy’s statements, “Every known illness is associated with a magnesium-deficiency” and that, “magnesium is the most critical mineral required for electrical stability of every cell in the body. A magnesium-deficiency may be responsible for more diseases than any other nutrient.” The truth he states exposes a gapping hole in modern medicine that explains a good deal about iatrogenic death and disease. Because magnesium-deficiency is largely overlooked, millions of Americans suffer needlessly or are having their symptoms treated with expensive drugs when they could be cured with magnesium supplementation.

One has to recognize the signs of magnesium thirst or hunger on their own since allopathic medicine is lost in this regard. It is really something much more subtle then hunger or thirst but it is comparable. In a world though where doctors and patients alike do not even pay attention to thirst and important issues of hydration, it is not hopeful that we will find many recognizing and paying attention to magnesium thirst and hunger, which is a dramatic way of expressing the concept of magnesium deficiency.

Few people are aware of the enormous role magnesium plays in our bodies. It is by far the most important mineral in the body. After oxygen, water, and basic food, magnesium may be the most important element needed by our bodies; vitally important, yet hardly known. It is more important than calcium, potassium or sodium and regulates all three of them. Millions suffer daily from magnesium deficiency without even knowing it

In fact, there happens to be a relationship between what we perceive as thirst and deficiencies in electrolytes. I remember a person asking, “Why am I dehydrated and thirsty when I drink so much water?” Thirst can mean not only lack of water but it can also mean that one is not getting enough nutrients and electrolytes. Magnesium, Potassium, Bicarbonate, Chloride and Sodium are some principle examples and that is one of the reasons magnesium chloride is so useful.

Magnesium Torment (Deficiency)

You know all those years, when doctors used to tell their patients ‘its all in your heads,’ were years the medical profession was showing its ignorance. It is a torment to be magnesium deficient on one level or another. Even if it’s for the enthusiastic sport person whose athletic performance is down, magnesium deficiency will disturb sleep and background stress levels and a host of other things that reflect on the quality of life. Doctors have not been using the appropriate test for it – their serum blood tests just distort their perceptions. Magnesium has been off their radar screens through the decades that magnesium-deficiencies have snowballed.

Symptoms of Magnesium Deficiency

The first symptoms of deficiency can be subtle – as most magnesium is stored in the tissues, leg cramps, foot pain, or muscle ‘twitches’ can be the first sign. Other early signs of deficiency include loss of appetite, nausea, vomiting, fatigue, and weakness. As magnesium-deficiency worsens, numbness, tingling, seizures, personality changes, abnormal heart rhythms, and coronary spasms can occur.

A full outline of magnesium-deficiency was beautifully presented in a recent article by Dr. Sidney Baker. “Magnesium-deficiency can affect virtually every organ system of the body. With regard to skeletal muscle, one may experience twitches, cramps, muscle tension, muscle soreness, including back aches, neck pain, tension headaches and jaw joint (or TMJ) dysfunction. Also, one may experience chest tightness or a peculiar sensation that he can’t take a deep breath. Sometimes a person may sigh a lot.”

“Symptoms involving impaired contraction of smooth muscles include constipation; urinary spasms; menstrual cramps; difficulty swallowing or a lump in the throat-especially provoked by eating sugar; photophobia, especially difficulty adjusting to oncoming bright headlights in the absence of eye disease; and loud noise sensitivity from stapedius muscle tension in the ear.”

“Other symptoms and signs of magnesium-deficiency and discuss laboratory testing for this common condition. Continuing with the symptoms of magnesium deficiency, the central nervous system is markedly affected. Symptoms include insomnia, anxiety, hyperactivity and restlessness with constant movement, panic attacks, agoraphobia, and premenstrual irritability. Magnesium-deficiency symptoms involving the peripheral nervous system include numbness, tingling, and other abnormal sensations, such as zips, zaps and vibratory sensations.”

“Symptoms or signs of the cardiovascular system include palpitations, heart arrhythmias, and angina due to spasms of the coronary arteries, high blood pressure and mitral valve prolapse. Be aware that not all of the symptoms need to be present to presume magnesium deficiency; but, many of them often occur together. For example, people with mitral valve prolapse frequently have palpitations, anxiety, panic attacks and premenstrual symptoms. People with magnesium deficiency often seem to be “uptight.” Other general symptoms include a salt craving, both carbohydrate craving and carbohydrate intolerance, especially of chocolate, and breast tenderness.”

Magnesium is needed by every cell in the body including those of the brain. It is one of the most important minerals when considering supplementation because of its vital role in hundreds of enzyme systems and functions related to reactions in cell metabolism, as well as being essential for the synthesis of proteins, for the utilization of fats and carbohydrates. Magnesium is needed not only for the production of specific detoxification enzymes but is also important for energy production related to cell detoxification. A magnesium deficiency can affect virtually every system of the body.

Like water we need magnesium everyday. There is an
eternal need for magnesium as well as water and when
magnesium is present in water life and health are enhanced.

One of the principle reason doctors write millions of prescriptions for tranquilizers each year is the nervousness, irritability, and jitters largely brought on by inadequate diets lacking magnesium. Persons only slightly deficient in magnesium become irritable, highly-strung, and sensitive to noise, hyper-excitable, apprehensive and belligerent. If the deficiency is more severe or prolonged, they may develop twitching, tremors, irregular pulse, insomnia, muscle weakness, jerkiness and leg and foot cramps.

If magnesium is severely deficient, the brain is particularly affected. Clouded thinking, confusion, disorientation, marked depression and even the terrifying hallucinations of delirium tremens are largely brought on by a lack of this nutrient and remedied when magnesium is given. Because large amounts of calcium are lost in the urine when magnesium is under supplied, the lack of this nutrient indirectly becomes responsible for much rampant tooth decay, poor bone development, osteoporosis and slow healing of broken bones and fractures. With vitamin B6 (pyridoxine), magnesium helps to reduce and dissolve calcium phosphate kidney stones.

Magnesium deficiency may be a common factor associated with insulin resistance. Symptoms of MS that are also symptoms of magnesium deficiency include muscle spasms, weakness, twitching, muscle atrophy,  an inability to control the bladder, nystagmus (rapid eye movements), hearing loss, and osteoporosis.  People with MS have higher rates of epilepsy than controls.  Epilepsy has also been linked to magnesium deficiencies.[1]

Another good list of early warning symptoms suggestive of magnesium insufficiency:

• Physical and mental fatigue
• Persistent under-eye twitch
• Tension in the upper back, shoulders and neck
• Headaches
• Pre-menstrual fluid retention and/or breast tenderness

Possible manifestations of magnesium deficiency include:

• Low energy
• Fatigue
• Weakness
• Confusion
• Nervousness
• Anxiousness
• Irritability
• Seizures (and tantrums)
• Poor digestion
• PMS and hormonal imbalances
• Inability to sleep
• Muscle tension, spasm and cramps
• Calcification of organs
• Weakening of the bones
• Abnormal heart rhythm

Severe magnesium deficiency can result in low levels of calcium in the blood (hypocalcemia). Magnesium deficiency is also associated with low levels of potassium in the blood (hypokalemia). Magnesium levels drop at night, leading to poor REM (Rapid Eye Movement) sleep cycles and unrefreshed sleep. Headaches, blurred vision, mouth ulcers, fatigue and anxiety are also early signs of depletion.

We hear all the time about how heart disease is the number one health crisis in the country, about how high blood pressure is the “silent killer”, and about how ever increasing numbers of our citizens are having their lives and the lives of their families destroyed by diabetes, Alzheimer’s disease, and a host of other chronic diseases.

Signs of severe magnesium deficiency include:

• Extreme thirst
• Extreme hunger
• Frequent urination
• Sores or bruises that heal slowly
• Dry, itchy skin
• Unexplained weight loss
• Blurry vision that changes from day to day
• Unusual tiredness or drowsiness
• Tingling or numbness in the hands or feet
• Frequent or recurring skin, gum, bladder or vaginal yeast infections

But wait a minute, aren’t those the same symptoms for diabetes? Many people have diabetes for about 5 years before they show strong symptoms. By that time, some people already have eye, kidney, gum or nerve damage caused by the deteriorating condition of their cells due to insulin resistance and magnesium deficiency. Dump some mercury and arsenic on the mixture of etiologies and pronto we have the disease condition we call diabetes.

Magnesium deficiency is synonymous with diabetes and is at the root of many if not all cardiovascular problems.

Magnesium deficiency is a predictor of diabetes and heart disease both; diabetics both need more magnesium and lose more magnesium than most people. In two new studies, in both men and women, those who consumed the most magnesium in their diet were least likely to develop type 2 diabetes, according to a report in the January 2006 issue of the journal Diabetes Care. Until now, very few large studies have directly examined the long-term effects of dietary magnesium on diabetes. Dr. Simin Liu of the Harvard Medical School and School of Public Health in Boston says, “Our studies provided some direct evidence that greater intake of dietary magnesium may have a long-term protective effect on lowering risk,” said Liu, who was involved in both studies.

The thirst of diabetes is part of the body’s response to excessive urination. The excessive urination is the body’s attempt to get rid of the extra glucose in the blood. This excessive urination causes the increased thirst. But we have to look at what is causing this level of disharmony. We have to probe deeper into layers of cause. The body needs to dump glucose because of increasing insulin resistance and that resistance is being fueled directly by magnesium deficiency, which makes toxic insults more damaging to the tissues at the same time.

When diabetics get too high blood sugars, the body creates “ketones” as a by-product of breaking down fats. These ketones cause blood acidity which causes “acidosis” of the blood, leading to Diabetic Ketoacidosis (DKA), This is a very dangerous condition that can lead to coma and death. It is also called “diabetic acidosis”, “ketosis”, “ketoacidosis” or “diabetic coma”. DKA is a common way for new Type 1 diabetics to be diagnosed. If they fail to seek medical advice on symptoms like urination, which is driving thirst they can die of DKA.

Oral magnesium supplements reduce erythrocyte[2] dehydration.[3] In general, optimal balances of electrolytes are necessary to maintain the best possible hydration. Diabetic thirst is initiated specifically by magnesium deficiency with relative calcium excess in the cells. Even water, our most basic nutrient starts having a hard time getting into the cells with more going out through the kidneys.

Autism and Magnesium Deficiency

When dealing with autism spectrum and other neurological disorders in children it is important to know the signs of low magnesium: restless, can’t keep still, body rocking, grinding teeth, hiccups, noise sensitive, poor attention span, poor concentration, irritable, aggressive, ready to explode, easily stressed. When it comes to children today we need to assume a large magnesium deficiency for several reasons.

1) The foods they are eating are stripped of magnesium because foods in general, as we shall see below are declining in mineral content in an alarming way.

2) The foods many children eat are highly processed junk foods that do not provide real nutrition to the body.

3) Because most children on the spectrum are not absorbing the minerals they need even when present in the gut. Magnesium absorption is dependent on intestinal health, which is compromised totally in leaky gut syndromes and other intestinal problems that the majority of autism syndrome disorders.

4) Because the oral supplements doctors rely on are not easily absorbed, because they are not in the right form and because magnesium in general is not administered easily orally.

Modern medicine is supposed to help people not hurt them, but with their almost total ignorance of magnesium doctors end up hurting more than they help for many of the medical interventions drive down magnesium levels when they should be driving them up. Many if not most pharmaceutical drugs drive magnesium levels into very dangerous zones and surgery done without increasing magnesium levels is much more dangerous then surgery done with.

The foundation of medical arrogance is actually medical ignorance and the only reason ignorance and arrogance rule the playing field of medicine is a greed lust for power and money. Human nature seems to be at its worst in modern medicine when it should be at its best. It is sad that people have to suffer needlessly and extraordinarily tragic that allopathic medicine has turned its back on the Hippocratic Oath and all that it means.

For additional research on Magnesiun Deficiency, read the following articles:

• Magnesium’s Importance Far Greater Than Previously Imagined
• What We Learned From The Accelerated Aging of Astronauts
• 7 Reasons to Get More Magnesium

Consult our Magnesium research database on the therapeutic role of magnesium in over 190 conditions:

Additional Resources

• First published: Magnesium Thirst Magnesium Hunger

• [1] http://www.nhfw.info/magnesium.html

• [2] Red blood cells are also known as RBCs, red blood corpuscles (an archaic term), haematids or erythrocytes (from Greek erythros for “red” and kytos for “hollow”, with cyte translated as “cell” in modern usage). The capitalized term Red Blood Cells is the proper name in the US for erythrocytes in storage solution used in transfusion medicine.

• [3] J. Clin. Invest. 100(7): 1847-1852 (1997). doi:10.1172/JCI119713. The American Society for Clinical Investigation

New research shows that treatment with this powerhouse combination restores euthyroid status in Hashimoto’s thyroiditis. What’s more, you can easily obtain the therapeutic dosages from foods

One in ten women and one in fifty men suffers from Hashimoto’s thyroiditis, an autoimmune thyroid disease (1, 2). Although genetic susceptibility contributes to risk, nutritional factors such as vitamin D, iron, iodine, and selenium are implicated in the induction and pathogenesis of Hashimoto’s, underscoring the role of therapeutic nutrition in potentially reversing autoimmunity (3).

Immune Dysregulation Triggers Hashimoto’s Thyroiditis

The mechanism implicated in Hashimoto’s thyroiditis is activation of auto-aggressive lymphocytes, or white blood cells directed against self which trigger production of antibodies against enzymes involved in thyroid hormone production and storage called thyroid peroxidase (TPO) and thyroglobulin (TG) (4). Development of anti-thyroid antibodies, which are correlated with progressive thyroid damage and lymphocytic inflammation (5), represent an 8-fold and 25-fold increased risk of the subsequent development of clinical hypothyroidism in women and men, respectively (6).

As a result of autoantibody formation, inflammatory cytokine production, and migration of immune cells towards the thyroid gland, auto-destruction of thyroid epithelial cells occurs and hypothyroidism is the end product (2). As a compensatory reaction, levels of the upstream pituitary hormone thyroid stimulating hormone (TSH) rise in an attempt to prompt the remaining thyroid cells to increase thyroid hormone production (2). Once levels of TSH meet an arbitrary diagnostic threshold, which was established based on a reference group uncorrected for chronic or occult disease (7), Hashimoto’s patients are unilaterally offered levothyroxine, a synthetic analogue of thyroxine (T4) that is the conventional treatment of choice.

However, even when thyroid parameters return to so-called normal levels, a significant proportion of patients on thyroid hormone replacement continue to report fatigue and diminished quality of life (8). This is unsurprising, since thyroid replacement therapy does nothing to arrest the underlying autoimmune pathogenesis responsible for Hashimoto’s, but rather applies a hormonal band-aid to keep symptoms at bay. This failure to practice root-cause resolution medicine, and address the immune dysregulation that invokes Hashimoto’s in the first place, also accounts for the three-fold increased likelihood of developing another autoimmune disease after the first autoimmune diagnosis (9).

Selenium Deficiency: A Global Problem

A rare element on our planet, the name selenium is derived from the Greek word “σελήνη” or “Selene,” meaning moon, since its appearance is bright and gray when melted (10). The concentration of selenium in igneous bedrock is lower than for any other nutrient element (11). Selenium is a Goldilocks nutrient, demonstrating a U-shaped relationship with disease, as both selenium excess and deficiency are associated with adverse health outcomes (12).

Selenium content in foods is predicated upon the selenium in the soil, which is dictated in turn by geochemical, geological, and climactic variables (11). In fact, selenium is often depleted from soil due to accelerated soil erosion or anthropogenic fires, for example (11). Although selenium is added to some commercial fertilizers, uptake by plants is poor and varies widely, as evidenced by a fifteen-fold variability in the capacity of Brassica vegetables to accumulate selenium (13).

Signs of compromised selenium status include nail whitening, muscle weakness, cardiomyopathy, hair loss, change in hair color, and growth retardation (14). Risk factors for selenium depletion, for reasons not completely elucidated, include advancing age, smoking, and consumption of white rice, alcohol, coffee, and eggs (15). Deficiency of selenium is widespread, affecting half a billion to one billion people worldwide (11).

However, researchers propose that the vast majority of people globally have suboptimal selenostasis, or maintenance of a physiological concentration of selenium, putting them at significant risk for cancer, heart diseases, diabetes, severe infections such as human immunodeficiency virus (HIV), thyroid disease, and inflammatory conditions where oxidative stress is involved in the etiology (13, 14). Because the physiological roles of selenium are so diverse, with crucial roles in metabolism, cellular growth and homeodynamics, immune-endocrine function, and viral defense, the effects of selenium deficiency can be grave (12).

Selenium Ameliorates Hashimoto’s Thyroiditis

Initial interest in selenium as a therapeutic option emerged from studies demonstrating a higher incidence of Hashimoto’s thyroiditis in regions with severe selenium deficiency (4). Observational studies, in addition, illustrated that selenium can reduce thyroid autoimmunity, hypothyroidism, and postpartum thyroiditis (3). Multiple studies have reproduced the findings that selenium, administered as the sole treatment in concert with thyroid replacement therapy, significantly reduces production of anti-thyroid peroxidase (anti-TPO) antibodies in patients with Hashimoto’s thyroiditis (16, 17).

Moreover, selenium supplementation in patients with autoimmune thyroiditis significantly improves both quality of life and ultrasonographic thyroid morphology (12). Not only that, but supplementation with selenium in Graves’ disease, a thyroid-directed autoimmune disorder that results in the opposite extreme, hyperthyroidism, also improves Graves’ orbitopathy and delays progression of ocular disorders (12).

Lastly, another study of selenium supplementation in 2143 pregnant women with Hashimoto’s thyroiditis showed that 200 micrograms of selenomethionine per day during the pregnancy and postpartum periods decreases the progression of autoimmune thyroiditis (18). Remarkably, “They found a reduction of TPOAb levels, improved thyroid echogenicity, decreased incidence of thyroid dysfunction in the postpartum period, and decreased permanent hypothyroidism” (12). Researchers therefore conclude that selenium deficiency is quintessential to both the pathogenesis of Hashimoto’s thyroiditis and Graves’ disease (4).

Function of Selenium in the Thyroid Gland

An essential micronutrient with pleiotropic effects, selenium participates in the function of at least 25 so-called selenoproteins, or enzymes that use selenium as a cofactor (19). The thyroid, however, represents the biggest reservoir of selenium content per gram of tissue (12). Because selenoenzymes are key to regulation of the immune system, even mild selenium deficiency can lead to development of autoimmune thyroid disease (4).

Selenium is especially important to the function of enzymes such as glutathione peroxidase (GPX) and thioreductase (TX), which protect thyrocytes from toxic concentrations of hydrogen peroxide and lipid hydroperoxides which result from thyroid hormone synthesis (12). Glutathione peroxidase in particular is critical to glandular protection, and more broadly protects the lipid bilayer of cell membranes and cellular and extracellular constituents from oxidative damage, neutralizing the harmful effects of reactive oxygen species (ROS) that are a byproduct of cellular metabolism (20).

In addition, because expression of iodothyronine deiodinases (DIO) are dependent upon sufficient selenium, selenium deficiency can negatively affect thyroid hormone status (14). Deiodinases, enzymes which control thyroid hormone turnover, are also responsible for converting the largely inactive pro-hormone, T4, to the metabolically active thyroid hormone, T3, through the removal of an iodine atom from the external ring (21).

Food-Based Approaches to Selenium Sufficiency

The richest source of selenium is the Brazil nut from the Amazon region (20). Whether their selenium content is sufficient to restore selenostasis, however, has been a source of contention in holistic medical communities.

One study of patients on hemodialysis with depressed selenium levels, however, revealed that consumption of one Brazil nut per day for three months significantly elevates both plasma and erythrocyte selenium levels (20). Not only that, but the activity of the antioxidantenzyme glutathione peroxidase was significantly augmented after the Brazil nut intervention (20). The authors discuss the salience of these findings to public health:

Recommendations to include as few as one Brazil nut per day in the diet would avoid the need for fortification of food supplements to improve their Se [selenium] status. Food sources are preferable to alternative supplementation practices because they are sustainable, less expensive, and present a lower risk of toxicity compared with supplementation. (20)

In another three-month placebo-controlled trial conducted in New Zealand, subjects were randomized to receive two Brazil nuts per day, to provide approximately 100 micrograms of selenium, or an equivalent supplemental dose of selenomethionine (22). The Brazil nut intervention was found to increase plasma selenium, plasma glutathione peroxidase, and whole blood glutathione peroxidase as well as the selenomethionine supplement (22). Therefore, these two studies highlight the utility of including Brazil nuts in the diet to confer selenostasis and boost antioxidant defense mechanisms.

In addition, according to the National Institutes of Health (NIH), seafoods and organ meats are considered the richest food sources of selenium (23). For example, three ounces of halibut or sardines contains approximately 50 micrograms of selenium, but this is still less than the amount of selenium per serving contained in Brazil nuts by a factor of ten (23). Other botanical sources of selenium include fennel, Chinese knotweed, mountain buchu, ladyslipper, stevia, cramp bark, hawthorn, grapes, and thyme (USDA, 2016). Food-based approaches are preferable to supplemental, since selenosis, or selenium excess, can arise when selenium ingestion exceeds 400 micrograms per day, which has been shown to happen with misformulated supplements (24).

Myo-Inositol is Critical to Thyroid Function

A recent novel approach undertaken by researchers is combining selenium with myo-inositol. Myo-inositol is one of the most representative inositol compounds, and a precursor to the synthesis of phosphoinositides which play a role in the phosphatidylinositol signal transduction pathway that occurs across the plasma membrane (4). In effect, myo-inositol acts as a calcium-mobilizing second messenger, overseeing the activity of hormonal signaling pathways such as follicle-stimulating hormone (FSH), insulin, and thyroid stimulating hormone (TSH) (4). Binding of TSH to its receptor on the surface of thyroid triggers two different post-receptor cascades, one of which is dependent upon inositol and regulates the iodination of thyroglobulin to form thyroid hormones (4).

Due to its role in thyroid signaling cascades, researchers set out to explore the effect of myo-inositol and selenium in patients with a mild form of thyroid failure called subclinical hypothyroidism, characterized by levels of TSH between 3 and 6 mIU/L (25). This TSH is considered suboptimal by new standards from the National Health and Nutrition Examination Survey (NHANES) III data, which consider normal TSH to fall under 4.12 mIU/L, and some researchers have proposed that the upper limit of TSH should be even lower at 2.5 to 3.0 mIU/L (7). Therefore, the population studied here is considered to be in the preliminary stages of waning thyroid function.

In this study, 86 Hashimoto’s thyroiditis patients with normal levels of free thyroxine (fT4) and free triiodothyronine (fT3) , elevated serum antithyroid peroxidase (TPOAb) and/or antithyroglobulin (TgAb), and mildly elevated TSH were enrolled alongside one hyperthyroid patient with a TSH of approximately 0.14 μU/ml (4). All patients received oral supplements containing 600 mg myo-inositol plus 83 μg selenium in the form of L-selenomethionine for six months, taken on an empty stomach (4).

Selenium & Myo-Inositol Restore Euthyroid Status in Hashimoto’s Thyroiditis

Not only did thyroid autoantibodies significantly decrease post-treatment, but TSH effectively normalized, and serum free T3 and free T4 levels increased slightly but significantly compared to baseline (4). Of note, is that the combination of selenium and myo-inositol not only decreased thyroid peroxidase (TPO) antibodies, but also decreased thyroglobulin (TG) antibodies, whereas selenium as the sole treatment only lowered TPO (4).

Paradoxically, the treatment had a normalizing effect on TSH regardless of pre-treatment TSH value, as evidenced by restoration of the TSH value into normal range for the hyperthyroid patients (4). Therefore, myo-inositol functions in a fashion analogous to adaptogens, lowering TSH when it is too high and increasing it when it is too low (4). Subjective symptomatology also significantly improved, with patients reporting significantly increased quality of life after the combination intervention (4). Researchers theorize that myo-inositol is so effective, because,

It can be speculated that impairment of the inositol-dependent TSH signaling pathway may be, at least in part, one cause of thyroid malfunctioning and that, by increasing the availability of Myo-Ins at cellular level, it is possible to improve TSH sensitivity of the thyroid follicular cell. (4)

In their study, published in the International Journal of Endocrinology, Nordio and Basciani discuss that restoration of TSH signal transduction via myo-inositol is important, since it modulates release of thyroid hormones, promotes iodine uptake by the thyroid gland, saves thyrocytes from apoptosis, induces growth and differentiation of thyroid cells, and prevents the formation of thyroid carcinoma cells (4). Their concluding thoughts should impart hope to patients with Hashimoto’s:

Therefore, the conclusion of our study is that the supplementation of Myo-Ins-Se is able to restore the euthyroid state as well as improve the wellbeing of Hashimoto’s patients with [subclinical hypothyroidism]… Bearing in mind also the safety of these two molecules’ usage, accentuated by the absence of side effects, the Myo-Ins-Se combination can be considered a very efficacious and safe therapy for AIT treatment. (4)

These results were confirmed in an earlier randomized, double-blinded, placebo-controlled study in 48 women with Hashimoto’s thyroiditis who had TSH levels between 4.01 mIU/L and 9.99 mIU/L (2). Patients either received 83 micrograms of selenomethionine per day, or an equivalent dose of selenium plus 600 mg of myo-inositol for six months (2). In all patients receiving the combination treatment, ultrasound echogenicity was significantly improved, alongside significant decreases in TSH concentrations that did not occur in the group receiving selenium therapy alone (2). In this study, autoantibody titers significantly decreased in both groups (2).

Food Sources of Myo-Inositol

Obtaining nutrients from foods is the preferable approach due to their presence in a whole-food complex and because of the presence of synergistic components. Encouragingly, researchers have found high myo-inositol diets to be ranked more palatable than diets low in myo-inositol, which demonstrates the ease of incorporating food-based sources myo-inositol sources (26).

Fresh fruits and vegetables, in general, possess higher myo-inositol content than canned, frozen, processed, or salt-free products (26). Extraordinarily high amounts of myo-inositol are found in cantaloupe and citrus fruits such as oranges, grapefruit, and lime (26). Other fruit sources high in myo-inositol include blackberry, kiwi, nectarine, mango, prunes, cherries, peaches, pears, watermelon, apple, and carob fruit (26, 27).

Good vegetable sources of myo-inositol, on the other hand, include Brussels sprouts, lima beans, navy beans, green beans, artichoke, okra, eggplant, cabbage, asparagus spears, banana pepper, hubbard squash, collard greens, tomato, zucchini, and bell peppers (26). Compared to other grains, oats contained considerably higher levels of myo-inositol (26).

By maximizing foods with high myo-inositol content, research has shown that it is possible to achieve myo-inositol intakes of 1500 mg per 1800 kcal ingested (26), which is more than double the dose needed for thyroid benefits according to the aforementioned studies. Moreover, research has elucidated that virtually all of ingested myo-inositol is absorbed from the gastrointestinal tract, so bioavailability from foods appears to be high (26).

Therefore, by increasing inclusion of these foods, alongside a holistic diet and lifestyle program and the food sources of selenium discussed in a previous section, patients with Hashimoto’s thyroiditis can address elements underlying immune dysregulation that precipitate thyroid autoimmunity in the first place—and look forward to the prospect of permanent remission.

References

1. Chandrashekara, S. (2012). The treatment strategies of autoimmune disease may need a different approach from conventional protocol: A review. Indian Journal of Pharmacology, 44(6), 665-671.
2. Nordio, M., & Pajalich, R. (2013). Combined treatment with Myo-inositol and selenium ensures euthyroidism in subclinical hypothyroidism patients with autoimmune thyroiditis. Journal of Thyroid Research, 424163.
3. Hu, S., & Rayman, M.P. (2017). Multiple Nutritional Factors and the Risk of Hashimoto’s Thyroiditis. Thyroid, 27(5), 597-610.
4. Nordio, M., & Basciani, S. (2017). Treatment with Myo-Inositol and Selenium Ensures Euthyroidism in Patients with Autoimmune Thyroiditis. International Journal of Endocrinology.
5. Sturniolo, G., & Mesa, J. (2013). Selenium supplementation and autoimmune thyroid diseases. Endocrinology & Nutrition, 60(8), 423-426.
6. Vanderpump, M.P.J. et al. (1995) The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickam Survey. Clinical Endocrinology, 43, 55–68.
7. Wartofsky, L., & Dickey, R.A. (2005). The evidence for a narrower thyrotropin reference range is compelling. Journal of Clinical Endocrinology & Metabolism, 90(9), 5428-5488.
8. Costantini, A., & Pala, M.I. (2014). Thiamin and Hashimoto’s Thyroiditis: A Report of Three Cases. The Journal of Alternative and Complementary Medicine, 20(3), 208-2011.
9. Cojocaru, M., Cojocaru, I.M., & Silosi, I. (2010). Multiple autoimmune syndrome. Maedica, 5(2), 132-134.
10. Duntas, L., & Benvenga, S. (2015). Selenium: an element for life. Endocrine, 48(3), 756-775.
11. Haug, A. et al. (2007). How to use the world’s scarce selenium resources efficiently to increase the selenium concentration in food. Microbial Ecology in Health and Disease, 19(4), 209-228.
12. Ventura, M, Melo, M., & Carrilho, F. (2017). Selenium and Thyroid Disease: From Pathophysiology to Treatment. International Journal of Endocrinology, 1297658.
13. Combs, G.F. Jr. (2001). Se in global food systems. British Journal of Nutrition, 85, 517-547.
14. Kawai, M. et al. (2018). Thyroid hormone status in patients with severe selenium deficiency. Clinical Pediatric Endocrinology, 27(2), 67-74.
15. Park, K. et al. (2011). Demographic and lifestyle factors and selenium levels in men and women in the U.S. Nutrition Research and Practice, 5(4), 357-364.
16. Zagrodzki, P., & Kryczyk, J. (2014). The importance of selenium in Hashimoto’s disease. Postepy Hig Med Dosw (Online), 68, 1129-1137
17. van Zuuren, E.J. et al. (2014). Selenium supplementation for Hashimoto’s Thyroiditis: Summary of a Cochrane Systematic Review. European Thyroid Journal, 3(1), 25-31. doi: 10.1159/000356040
18. Negro, R. et al. (2007). The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. The Journal of Clinical Endocrinology and Metabolism, 92(4), 1263–1268.
19. Dharmasena, A. (2014). Selenium supplementation in thyroid associated ophthalmopathy: an update. International Journal of Ophthalmology, 7(2), 365–375.
20. Stockler-Pinto, M.B. et al. (2010). Effect of Brazil nut supplementation on the blood levels of selenium and glutathione peroxidase in hemodialysis patients. Nutrition, 26(11-12), 1065-1069.
21. Kohrle, J. et al. (2005). Selenium, the thyroid, and the endocrine system. Endocrine Reviews, 26(7), 944–984.
22. Thomson, C.D. et al. (2008). Brazil nuts: an effective way to improve selenium status. American Journal of Clinical Nutrition, 87(2), 379-384.
23. National Institutes of Health: Office of Dietary Supplements. (2018). Selenium: Fact Sheet for Health Professionals. Retrieved from https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/
24. MacFarquhar, J.K. et al. (2010). Acute selenium toxicity associated with a dietary supplement. Archives of Internal Medicine, 170(3), 256-261.
25. Fatourechi, V. (2009). Subclinical hypothyroidism: an update for primary care physicians. Mayo Clinic Proceedings, 84(1), 65–71.
26. Clements, R.S. Jr., & Darnell, B. (2018). Myo-inositol content of common foods: development of a high-myo-inositol diet. The American Journal of Clinical Nutrition, 33, 1957-1967.
27. United States Department of Agriculture, Agricultural Research Service. (1992-2016). Dr. Duke’s Phytochemical and Ethnobotanical Databases. Home Page, http://phytochem.nal.usda.gov/ http://dx.doi.org/10.15482/USDA.ADC/1239279

Written By: Sayer Ji  founder of Greenmedinfo.com

Millions of pounds are consumed annually, yet it may be more like a drug than a food and just as damaging and addictive as alcohol…

Fructose, which literally means “fruit sugar,”* sounds so sweet and innocent. And indeed, when incorporated into the diet in moderate amounts in the form of fruit – always organic and raw, when possible – it’s about as pure and wholesome as any biomolecule inseparably complexed with vitamins, fiber, plant stem cells, antioxidants, etc. i.e. as a whole food, can get.

Not so for industrially processed fructose in isolate form, which may be as addictive as alcohol,[i] and perhaps even morphine [ii] [iii]and which according to USDA research published in 2008 into major trends in U.S. food consumption patterns, 1970-2005, we now consume at the rate of at least 50 lbs a year — the ‘800 ounce gorilla’ in the room.[iv]

Our dietary exposure to fructose, of course, is primarily through either sugar (sucrose), which is a disaccharide comprised of 50% fructose and 50% glucose by weight, or through high-fructose corn syrup (HFCS), which is mostly a 55% fructose and 45% glucose blend of monosaccharides, but goes as high as 90% fructose and 10% glucose in HFCS-90 form.  Pasteurized fruit juices are another concentrated source of fructose, but increasingly even pasteurized fruit juice is being adulterated with additional sugar or HFCS for reasons that have mostly to do with protecting the manufacturer’s bottom line.

Because high-fructose corn syrup contains free-form monosaccharides of fructose and glucose, it cannot be considered biologically equivalent to sucrose, which has a glycosidic bond that links the fructose and glucose together, and which slows its break down in the body. The attempt by the HFCS industry to re-label their product as “corn sugar,” which was recently denied by the FDA,[v] belies their anxiety about the differences, and also reveals growing awareness among the public of isolated fructose’s inherently toxic properties.

The reality is that fructose can cause far more damage than glucose, and we must look beyond caloric equivalences to understand this. While in times of need (e.g. starvation, post-workout glycogen depletion), fructose is as effective as glucose in replenishing glycogen stores, in “hypercaloric” states of excess

consumption, it can lead to a process known as glycation whereby a sugar binds with protein or lipid molecules, often resulting in damage to cells and tissues.

For example, in vitro studies show that fructose damages proteins seven times more rapidily than glucose through a process known as protein fructosylation, which is when a sugar undergoes a Maillard reaction with a protein, which basically results in the caramelization (browning) of blood and tissue contents, “gumming up the works.” For example, if you try baking a pastry made with fructose, instead of white sugar, it will brown much more rapidly as a result of this Maillard reactivity.

Fructose actually shares great resemblance to alcohol (ethanol), such as being capable of stimulating dopamine production in our brain, as well as sharing similar metabolic pathways and effects on the liver (e.g. fatty liver). Their great similarities make even more sense when you consider that fructose can easily be converted into ethanol with a pinch of yeast in order to make alcoholic beverages.

So toxic is “purified” fructose that here at GreenMedInfo we have indexed research on over 70 adverse health effects associated with the risk factors and conditions constellated around Metabolic Syndrome, which include:

• Insulin Resistance (32 studies)
• Fatty Liver (22 studies)
• Obesity (13 studies)
• Hypertension (10 studies)
• Elevated Uric Acid (9 studies)
• Elevated Triglycerides (14 studies)
• Belly Fat (2 studies)
• Cardiovascular Diseases (4 studies)
• Liver Stress (6 studies)
• Pancreatic Cancer (2 studies)
• Leptin Resistance (2 studies)

To view the first hand research on 70+ forms of fructose toxicity click the hyperlink.

Like many foods consumed en masse, which may have a lesser known dark side (e.g. wheat), our global fixation on fructose may reveal something about it’s hitherto under appreciated addictive properties.

Fructose’s Drug-like Hold On Our Bodies

Fructose addiction and alcoholism, in fact, share a number of parallels. In an article titled, “Fructose: metabolic, hedonic, and societal parallels with ethanol,” published in the Journal of the American Dietetic Association in 2010, Robert H. Lustig, MD broke new ground by identifying the great similarities between these two substances:

“Rates of fructose consumption continue to rise nationwide and have been linked to rising rates of obesity, type 2 diabetes, and metabolic syndrome. Because obesity has been equated with addiction, and because of their evolutionary commonalities, we chose to examine the metabolic, hedonic, and societal similarities between fructose and its fermentation byproduct ethanol. Elucidation of fructose metabolism in liver and fructose action in brain demonstrate three parallelisms with ethanol. First, hepatic fructose metabolism is similar to ethanol, as they both serve as substrates for de novo lipogenesis, and in the process both promote hepatic insulin resistance, dyslipidemia, and hepatic steatosis. Second, fructosylation of proteins with resultant superoxide formation can result in hepatic inflammation similar to acetaldehyde, an intermediary metabolite of ethanol. Lastly, by stimulating the “hedonic pathway” of the brain both directly and indirectly, fructose creates habituation, and possibly dependence; also paralleling ethanol.Thus, fructose induces alterations in both hepatic metabolism and central nervous system energy signaling, leading to a “vicious cycle” of excessive consumption and disease consistent with metabolic syndrome. On a societal level, the treatment of fructose as a commodity exhibits market similarities to ethanol. Analogous to ethanol, societal efforts to reduce fructose consumption will likely be necessary to combat the obesity epidemic.” [emphasis added]

While the parallel between fructose and alcohol consumption may seem strange, the intimate connection between what we eat and our psychological health is beginning to gain wider recognition, especially considering new research linking aggression to trans fatty acid consumption, episodes of acute wheat mania, and the widespread presence of opiates in common foods.

It may come as a surprise to many, but there is a fructose-opiate infatuation deeply embedded within mammalian biology, which has been the subject of scientific investigation since the late 80’s. A study published in the European Journal of Pharmacology in 1988 found that both glucose and fructose were capable of antagonizing morphine-induced pain killing effects, likely due to the direct opioid effects of these sugars or their metabolic byproducts on the central nervous system. In fact, the researchers found that fructose was more potent than glucose in accomplishing these effects.

Could the narcotic properties of fructose, or one of its metabolic byproducts, explain why we would consume such vast quantities of something so inherently harmful to our bodies? 

As it turns out, not only has fructose’s manifold toxic properties been studied, but researchers have also investigated what natural substances reduce fructose’s adverse effects.

GreenMedInfo contains research on 21 natural compounds with fructose toxicity attenuating action, including:

• Berberine
• Fish Oil
• Astaxanthin
• Bitter Melon
• Chlorella
• Coconut Water
• Garlic
• Ginger
• Holy Basil
• Quinoa
• Resveratrol
• Spirulina

To view them all, you can visit our Fructose-Induced Toxicity page.

Ultimately, avoiding fructose in any other than its naturally embedded form in the intelligent and infinitely complex structures of food, e.g. fruit, is ideal. Food cravings for sweets, after all, may conceal unmet emotional or spiritual needs, so sometimes it is best to search deeper within for the answers. Or, using natural non- or low-calorie sweeteners like xylitol or stevia may also take the edge off an intense sweet tooth.

But, beyond the increasingly obvious adverse effects of isolated fructose to human health, is the “hidden” damage that fructose does to environmental/planetary health. This is because fructose from HFCS is invariably produced from genetically modified (GM) corn, which requires massive environmental inputs of harmful pesticides, glyphosate, gene products with the ability to transfer horizontally, and other unsustainable practices. The “hidden tax” of fructose consumption is the accelerating, GM-mediated destruction of the biosphere; a biosphere, mind you, without which human health and human existence, is not possible.

*Fructose: derived from Latin fructus (“fruit”) + -ose (“sugar”).

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References

[i] Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep ;110(9):1307-21.

[ii] Antagonism of the morphine-induced locomotor activation of mice by fructose: comparison with other opiates and sugars, and sugar effects on brain morphine. Life Sci. 1991 ;49(10):727-34.

[iii] Antagonism of antinociception in mice by glucose and fructose: comparison of subcutaneous and intrathecal morphine. Eur J Pharmacol. 1988 Feb 9 ;146(2-3):337-40.

[iv] USDA Economic Research Service, Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005

[v] Packaging Digest, FDA rejects renaming of high-fructose corn syrup, 6/7/2012