Lower High Blood Pressure With More Potassium-Rich Foods, Less Sugar

Posted on April 24, 2017 by Mimi Castellanos

http://articles.mercola.com/sites/articles/archive/2017/04/24/potassium-rich-foods-lower-blood-pressure.aspx

By Dr. Mercola

Americans struggle with high levels of certain diseases like cardiovascular disease and related high blood pressure. In fact, the World Health Organization ranks this malady, also known as hypertension, as playing the leading role in heart disease.1

Conventional medicine says eating too much sodium is one cause of high blood pressure, but more studies are revealing that it’s actually an imbalance between your sodium intake and your potassium levels that may be the problem. According to one study:

“Findings suggest that public health efforts directed toward increasing consumption of K+ [potassium]-rich natural foods would reduce BP [blood pressure]and, thus, cardiovascular and kidney disease.”2

Potassium deficiency, known as hypokalemia, can be so serious that it could be fatal. One sign that you may be deficient is high blood pressure, but other things to look for include:

  • Fatigue
  • Muscle weakness
  • Abdominal pain and cramps
  • Abnormal heart rhythms
  • Muscle paralysis

Potassium: The ‘Good Salt’

There are a few facts about potassium that few people are aware of. First, it’s an essential mineral, but another thing to note is that, as an electrolyte, it plays a crucial role in regard to your blood pressure.

In spite of loads of studies and reports to the contrary, the fact is that it’s the balance between salt and potassium that will balance the health of your cells, not lowering your salt intake, unless of course, you’re talking about processed table salt.

Foods With High Potassium Content Help Lower Blood Pressure Levels

People with higher intakes of potassium tend to have lower blood pressure levels, so finding the foods to eat that contain it will definitely be good for you. For a good balance of potassium to sodium in your diet, eat fresh, whole, potassium-rich foods. I recommend:

Swiss chard Avocado Spinach Crimini mushrooms
Broccoli Brussels sprouts Celery Romaine lettuce

A passionate reader asked me to add this to my post about Brussel sprouts. https://www.jenreviews.com/brussels-sprouts/. This is a great and informative post with some science and recipes on Brussels sprouts.  My hubby likes them so we eat them a lot.

Additionally, Authority Nutrition3 notes other foods with high potassium content, such as leafy greens, tomatoes and sweet potatoes, wild-caught Alaskan sockeye salmon, melons, bananas, oranges and apricots. Fruits should be eaten in moderation, however, due to the fructose content.

Besides significantly lowering your blood pressure, pomegranate juice may protect your cells from negative effects like premature aging.

It’s also high in antioxidant polyphenols to cut your cancer and heart disease risks, and more antioxidants from tannins, anthocyanins and ellagic acid than green tea and red wine, Prevent Disease adds.4

Fruit polyphenols have been shown to have such a positive influence on potentially fatal heart-related issues that related research may even help change recommendations on what fruits are most beneficial to consume for optimal cardiovascular protection, one study concluded.5

A Florida study6 reported that 1 cup of blueberries a day may lower blood pressure and relax arteries. Around 50 hypertensive women were given either 22 grams of freeze-dried blueberry powder or a placebo powder to eat, with the result that the first group, on average, had a 7 mmHg drop in systolic blood pressure.

Raw grass fed yogurt is rich in probiotics, which helps keep blood pressure at balanced levels.

A review of several studies7 found that probiotics may benefit this area of your health naturally because they help optimize your cholesterol and lower blood sugar levels. And small amounts of dark chocolate provide flavonoids that cause blood vessels to dilate.8

Lifestyle Changes You Can Make to Lower Your Blood Pressure

Most people will say they want to live a “healthy” life, but it’s usually small, day-to-day decisions that make the difference in the long run. Blood pressure affects your body in a systemic way. If you struggle to maintain healthy levels, you may want to take a good look at your diet.

Conventional wisdom usually tells you to limit your salt intake, but the most impactful way to do the job is to cut down on sugar. As “bad” as salt is touted to be, sugar is far worse.

While you probably already know that processed foods are far too high in refined sodium, it’s refined sugar that’s the real culprit in the high incidence of high blood pressure and, consequently, the trickle-down effect of diseases that all too often follow along behind, such as metabolic syndrome, atherosclerosis, stroke and heart attack.

More and more studies indicate that sugar can be implicated in high blood pressure levels.9 In fact, one study shows that women who drank just one soda per day had higher levels that those who drank less than that.10

Researchers at the University of California–San Francisco and Touro University California conducted a study11 published in the journal Obesity that looked at the effects of limiting sugar intake. The study subjects were 43 children between the ages of 9 and 18 years.

For nine days, all the children ate meals, snacks and beverages with reduced sugar; however, they were allowed to eat fruit. Their fasting blood sugar levels, glucose tolerance and blood pressure were recorded before each meal.

All of them were given the same amounts of protein, fat and carbohydrates as before, including hot dogs, chips and pizza, but added sugar was replaced with bagels and cereal. In fact, sugar went from 28 percent to 10 percent. Carbs and fructose were reduced from 12 percent to 4 percent.

What Happens When Children Are Given Less Sugar to Eat?

Before long, the diet proved successful, as the scientists noted decreased blood pressure, improved cholesterol and improved liver function. Fasting blood glucose levels fell five points, while insulin levels dropped by a third.

This is particularly astonishing since the added sugar was replaced with bagels and cereal, which are far from healthy. Imagine if it had been replaced with vegetables or healthy fats! Lead author Robert Lustig stated:

“This study definitively shows that sugar is metabolically harmful not because of its calories or its effects on weight; rather sugar is metabolically harmful because it’s sugar.

(The study indicates) that sugar contributes to metabolic syndrome, and is the strongest evidence to date that the negative effects of sugar are not because of calories or obesity.”12

The Epoch Times quoted senior study author Jean-Marc Schwarz:

“These findings support the idea that it is essential for parents to evaluate sugar intake and to be mindful of the health effects of what their children are consuming. When we took the sugar out, the kids started responding to their satiety [fullness] cues.

They told us it felt like so much more food, even though they were consuming the same number of calories as before, just with significantly less sugar. Some said we were overwhelming them with food.”13

Active African-Americans Are Less Apt to Develop High Blood Pressure

Certain factors make high blood pressure more prevalent in some people than in others. One study based in Jackson, Mississippi, showed that African-Americans are less apt to develop high blood pressure if they’re physically active on a daily basis.

Further, study subjects who reported engaging in the ideal amounts of moderate to vigorous physical activity were about 24 percent less likely to have high blood pressure years later in comparison to those who didn’t.

As it happens, African-Americans have the highest blood pressure rates of any racial or ethnic group in the U.S., making heart attack, stroke and kidney disease risks more prevalent, and even early death. Unfortunately, the odds are high for this demographic. Dr. Keith Diaz of Columbia University Medical Center in New York explained:

“If you’re African-American, your odds of developing hypertension [are] pretty high. If you’re worried about hypertension or high blood pressure, one of the things you can do to prevent it is physical activity and exercise.”14

None of the 1,311 participants in the study had high blood pressure when they started it between 2000 and 2004. They were checked again between 2005 and 2008, and again between 2009 and 2013. Half them were monitored for at least eight years.

The upshot? Those getting 150 minutes of moderate-intensity exercise per week, or at least 75 minutes of vigorous exercise — specifically from programmed physical activity as opposed to household tasks —  were 24 percent less likely to have developed high blood pressure than people who didn’t.

How to Lower Your Blood Pressure Naturally

Most doctors charged with helping their patients with high blood pressure issues will hand their patients a pharmaceutical prescription, but there are remedies for this condition that cost far less, financially, physically, overall time consumed and long-term effects combined. Time15 and Authority Nutrition listed several, including:

  • Breathe. Mindfully slowing the breaths you take and breathing more slowly helps you relax, and relaxing helps improve your heart rate, makes your arteries more flexible and lowers your blood pressure, naturally.
  • Relax. Stress does more to negatively affect your body than you can imagine. Bouts of anger or stress, triggering your “fight or flight” hormones, can literally increase your risk of developing heart-related issues. Try the Emotional Freedom Techniques (EFT) and other natural methods to calm and soothe your mind.
  • Curb the coffee and alcohol. While there are studies that contend that moderate alcohol intake can provide heart benefits, overdoing it can raise your blood pressure, as well as cause subsequent health problems. Caffeine can also be a culprit, and it may come from drinking soda. Give it a rest — literally.
  • Walk and exercise regularly. Your heart is strengthened and pumps blood more efficiently, lowering arterial pressure. Just 150 minutes of moderate exercise like walking or 75 minutes of strenuous exercise such as high-intensity interval training (HIIT) can improve both.16
  • Lose weight. Even losing 5 percent of your total weight can significantly lower your blood pressure,17 and the effect is even greater when you exercise.18

 

 

Posted in Most Recent | Leave a comment

Commentary on two recent papers on GcMAF

Posted on April 13, 2017 by Mimi Castellanos

 Commentary on two recent papers on GcMAF

Marco Ruggiero, MD, PhD

Get this on PDF

Two important papers on GcMAF have been published in the past few days in peer-reviewed journals.

The paper by Borges and Rehder of the School of Molecular Sciences and of the Biodesign Institute at Arizona State University, Tempe, AZ, USA, clari es the chemical structure of the protein moiety of GcMAF, and represents a signifcant improvement in our understanding of the concepts and significance of GcMAF and nagalase. (Glycan structure of Gc Protein-Derived Macrophage Activating Factor as revealed by mass spec- trometry. Borges CR, Rehder DS. Arch Biochem Biophys. 2016 Aug 5. pii: S0003-9861(16)30278-8. doi: 10.1016/j. abb.2016.08.006).

It is interesting to notice that the paper by Borges and Rehder was published almost simultaneously with our latest paper on GcMAF (Medical Hypotheses 94 (2016) 126–131), and, although none of us was aware of each other’s imminent publication, the two papers are fully consistent with each other as they shed a new light on the interpretation of the results that have accumulated over the course of the past twenty years on GcMAF.

It is worth remembering that Borges and Rehder had published another important paper on the subject a few years ago, where they demonstrated that there is no lack of GcMAF precursor in cancer patients, as opposed to the prevailing theory of those days (Protein Sci. 2009 Oct;18(10):2036-42. doi: 10.1002/pro.214. Glycosylation status of vitamin D binding protein in cancer patients. Rehder DS, Nelson RW, Borges CR). Thus, according to the original theory rst proposed by Yamamoto, nagalase would “destroy” the precursor of Gc- MAF and, therefore, cancer patients would be unable to produce endogenous GcMAF: because of this, Gc- MAF had to be administered from the outside (Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF. Yamamoto N, Suyama H, Yamamoto N. Transl Oncol. 2008 Jul;1(2):65– 72).

Borges et al. demonstrated that this was not the case and cancer patients have plenty of their own GcMAF.

In the study of 2009 Borges et al. wrote: “The presence of relatively abundant quantities (5–10 mg/L or 100–200 nM) of what might nominally be considered GcMAF (i.e., DBP modi ed by a single terminal Gal- NAc residue) in cancer patient serum … present a paradox in which cancer patients with relatively high cir- culating concentrations of GcMAF can effectively be treated with trace quantities of (exogenous) GcMAF”.

This observation seems to indicate that there is no shortage of endogenous GcMAF production in cancer patients and, therefore, that GcMAF is not responsible for “protection” against the development of cancer.

Such a concept is further corroborated by the study of the cancer risk in individuals harboring the Gc2 alle- le only (Gc2 homozygotes) of the Gc protein. These individuals are unable to glycosylate the Gc protein on threonine 420 due to its substitution by lysine.

Thus, there is no N-acetylgalactosamine (GalNAc) in position 420. In other words, Gc2 homozygotes are unable to produce one single molecule of GcMAF but, despite this fact, the risk of cancer in these individu- als is decreased rather than increased as one would have expected given the absence of bona de GcMAF (Abbas S, Linseisen J, Slanger T, et al.: The Gc2 allele of the vitamin D binding protein is associated with a decrea- sed postmenopausal breast cancer risk, independent of the vitamin D status. Cancer Epidemiol Biomarkers Prev, 2008, 17: 1339-1343.). It should be noticed that this inconsistency refers to breast cancer that is one of the types of cancer where GcMAF had proven effective in vitro, and in vivo.

In the paper published a few days ago, Borges and Rehder further confirm these observations using carefully designed mass spectrometry methods, and highlight two important points that lend credit to our most recent hypothesis on the nature of GcMAF (Medical Hypotheses 94 (2016) 126–131).

  1. Nagalase does not affect the Gc protein, that is the precursor of GcMAF and, therefore, elevated nagalase levels do not correspond to reduced production of GcMAF. At variance with previous assumptions, Borges and Rehder demonstrate that nagalase is not endowed with endo-glycosi- dase activity and, therefore, cannot degrade the Gc protein. This carefully conducted observation explains the reason why cancer patients have elevated levels of endogenous GcMAF despite elevate serum nagalase activity.
  2. Beta-galactosidase, one of the enzymes used to (theoretically) convert the inactive Gc-protein into the active GcMAF by removing the galactose from the threonine 420 and exposing the GalNAc, does not work on the Gc-protein and does not remove the galactose; this means that the procedures to produce GcMAF by removal of galactose using beta-gaalcotsidase are, in actuality, ineffective. According to this observation, enzymatic treatment of purified Gc protein, or of serum, does not yield GcMAF but only a desialidated Gc protein where the GalNAc is still “covered” by galactose. According to the original theory proposed by Yamamoto, such a Gc protein with galactose still attached to GalNAc should be devoid of macrophage stimulating activity.

The results published a few days ago by Borges and Rehder are fully consistent with those published in 2010 by a Danish group using mass spectrometry, demonstrating that the three sugars on the Gc protein are arranged in a linear fashion (threonine 420-GalNAc-galactose-sialic acid) and, therefore, beta-galac- tosidase cannot work since it is not endowed with endo-glycosidase activity (Biochim Biophys Acta. 2010 Apr;1804(4):909-17. doi: 10.1016/j.bbapap.2009.12.022. Epub 2010 Jan 13. The glycosylation and characteriz- ation of the candidate Gc macrophage activating factor. Ravnsborg T1, Olsen DT, Thysen AH, Christiansen M, Houen G, Højrup P).

The lack of effect of the beta-galactosidase also forces to reconsider the interpretation of the results reported by the researchers from the University of Tokushima and from the Saisei Mirai Clinic of Japan, who demonstrated anti-cancer effects obtained by treating the Gc protein only with beta-galactosidase (Anti- tumor effect of degalactosylated gc-globulin on orthotopic grafted lung cancer in mice. Hirota K, Nakagawa Y, Takeuchi R, Uto Y, Hori H, Onizuka S, Terada H. Anticancer Res. 2013 Jul;33(7):2911-5. β-Galactosidase treatment is a common rst-stage modi cation of the three major subtypes of Gc protein to GcMAF. Uto Y, Yamamoto S, Mukai H, Ishiyama N, Takeuchi R, Nakagawa Y, Hirota K, Terada H, Onizuka S, Hori H. Anticancer Res. 2012 Jun;32(6):2359-64).

Quite obviously, treatment with beta-galactosidase alone did not produce any bona de GcMAF and, therefore, the observed anti-cancer effects have to be ascribed to some other mechanism or some other molecules.

The two most recent papers published on GcMAF may thus help reconcile several contradicting observations that have accumulated over the years. Such inconsistencies and contradictions are:

  1. The procedure to produce GcMAF using enzymatic treatment of purified Gc protein or serum using beta-galactosidase does not produce one single molecule of bona de GcMAF.
  2. Cancer patients who were successfully treated with what was thought to be GcMAF, but in actuality was not, had plenty of their own GcMAF, a quantity that was far higher than the trace amounts of the desialidated Gc-protein that was administered thinking it was GcMAF. Although the levels of GcMAF in autistic patients has never been determined, the inability of nagalase to reduce the production of GcMAF leads to conclude that also autistic children with elevated nagalase had normal level of endogenous GcMAF. Nevertherless they were successfully treated with desialidated Gc-protein that was administered thinking it was GcMAF.
  3. These inconsistencies notwithstanding, it is a fact that “GcMAF” (between quotation marks since now we know that it was not bona de GcMAF) has proven effective in vitro and in vivo, and the laboratory and clinical data obtained with “GcMAF” have been repeatedly and independently confirmed.

These contradictions and inconsistencies may all be solved if we consider the hypothesis put forward our most recent paper in Medical Hypotheses; a hypothesis that reconciles the apparently contradicting observations quoted above. In other words, we do not dispute the validity of any of results of the papers thus far published on GcMAF; in our opinion, it is their interpretation that needs to be revisited at the light of the most recent publications.

Our concept, that has been defined by Borges as “interesting and plausible” at the light of their own most recent results, is that the Gc protein, whether with one, two or three sugars, or with any sugar moiety as in the case of the Gc2 homozygotes, plays a little role, if any, in the activation of macrophages or in any of the other biological and clinical effects that we and others have described for what we thought was “GcMAF”. According to our hypothesis, it is a glycosaminoglycan that binds to the Gc protein, chondroitin sulfate, in conjunction with vitamin D and oleic acid bound to the Gc protein, that is responsible for the effects attributed to the “GcMAF”. The Gc protein, deglycosylated or not, at most is a carrier for chondroitin sulfate, vitamin D and oleic acid.

Our new interpretation also explains the well acknowledged fact that treatment with “GcMAF” leads to reduction of nagalase levels in patients with different diseases, and leads to reconsider the role of nagalase as a marker.

Thus, nagalase cannot be considered a marker of immunodeficiency since its elevated levels do not correspond to decreased levels of endogenous GcMAF and, more importantly, elevated levels of nagalase have never been associated with any deficiency of the immune system. For example, autistic subjects have levels of nagalase higher than those of many cancer patients and nevertheless they are not immune deficient in the least.

However, nagalase seems to be a very reliable marker of chronic inflammation regardless of the causes that are responsible for in ammation (J Proteome Res. 2015 Aug 7;14(8):3123-35). This would explain the reason why nagalase is elevated in diseases that have nothing in common but chronic inflammation such as cancer and autism.

In the case of cancer, it is of particular importance to notice that in ammation in itself plays a major role in the progression of the disease and it is, in and by itself, a predictor of negative prognosis as we have de- monstrated in 2012 (Fabris et al. American Journal of Immunology, 2012, 8 (3), 65-70).

If we consider that the biological and clinical effects that had been attributed to GcMAF are indeed to be ascribed to a multimolecular complex made of chondroitin sulfate, vitamin D and oleic acid, with the Gc protein playing a minor role if any, then it makes full sense these three molecules decrease nagalase, since they are very well known to have anti-inflammatory properties. It is also worth mentioning that chondroitin sulfate, vitamin D and oleic acid also show immune-stimulatory, anticancer and neuroprotective pro- perties that are superimposable to the biological and clinical properties thus far attributed to GcMAF.

Therefore, nagalase could be interpreted as a marker of chronic inflammation and evaluation of serum nagalase levels could be useful in monitoring the effectiveness of immunotherapies regardless of the under- lying disease. In this respect, nagalase measurement would have an advantage over specific markers such as tumor markers, since its variations would be useful in a much broader range of conditions.

In conclusion, the almost simultaneous publication of the papers by Borges and Rehder and by our research group opens a completely new perspective in the field of immunotherapy and GcMAF research, and helps solving the inconsistencies and contradictions that have characterized this field in the recent past.

dr. reinwald healthcare gmbh+co kg
Friedrich-Luber-Straße 29 Tel. +49 (0)9128 73977-0 Mail shop@drreinwald.com DE 90592 Schwarzenbruck, Germany Fax +49 (0)9128 73977-29 Web www.drreinwald.com

Posted in Most Recent | 2 Comments

BravoCoop seeks to establish a Private Membership Association

Posted on April 10, 2017 by Mimi Castellanos

Private Membership Association

Home Private Membership Association

1st and 14th Amendment Private Medical Association for Unlicensed or Licensed Medical Practitioners

In reviewing medical email solicitations, newsletters and other medical publications over the years, we at ProAdvocate Group are more than ever convinced than ever that there are numerous proven therapies/treatments outside of mainstream medicine that are providing relief and/or  cures for a wide variety of afflictions and diseases.

Unfortunately, there are untold numbers of alternative healthcare practitioners — I am sure you know several—who possess these therapies and treatments but are unable to effectively advertise, market, and practice their craft in the public domain because of the heavy hand of state or federal boards, regulators, law enforcement agencies and others who police any public unlicensed medical practice. 

What are the Benefits of a 1st and 14th Amendment Private Medical Membership for Unlicensed or Licensed Medical Practitioners?

  1. Eliminate Illegal Investigations and Sanctions by any Licensing Board.
  2. Practice Medicine in your chosen area without paying outrageous malpractice insurance premiums – LESS RISK OF MALPRACTICE LAWSUITS AND CLAIMS.
  3. Practice Medicine without the burden of strict compliance with the Federal Laws dealing with the protection of the public and HIPPA Laws.
  4. Maintain privacy of business and financial affairs.
  5. Practice alternative medical modalities without fear of discrimination and sanctions.

And most of all ……..

  1. Maintain more freedom and control of your chosen profession.

This letter is to inform you that there are real solutions to your present and future potential problems in practicing alternative medicine and ProAdvocate Group can be part of that solution. As you know, many of your fellow practitioners are being harassed, investigated and sanctioned by medical boards, law enforcement agencies and attorney generals in many states. They, of course, believe a great service is being performed in the name of “protection of the public.”

The solution to the problem is to change the public patient or client relationship into a private contract member relationship within your own Private Medical Membership Association (PMA).

There are four (4) categories under which a PMA may apply:

  1. Unlicensed Medical Practitioners and Medical Researchers
  2. Licensed Practitioners under Attack for Alternative Medicine
  3. Former Licensed Practitioners
  4. Licensed or Unlicensed Medical Practitioners who need to operate in two or more or all of the 50 States.

And this is why they apply:   under the First and Fourteenth Amendments of the U.S. Constitution and equivalent provisions of your own State Constitution, you have the right to associate with fellow members and offer benefits and services that are outside of the jurisdiction, venue and authority of State and/or Federal agencies. What would be considered a criminal act outside the association (e.g., unauthorized practice of medicine) would be perfectly legal within a private association.

This right of association is not absolute. The U.S. Supreme Court has ruled in many cases that the State cannot interfere with private association activities unless the private members are being subjected to a clear danger of substantial evil that would shock a person’s moral and common sense. For example, if the private members are becoming seriously ill or injured or dying due to the so-called benefits and services of the association, then outside State and/or Federal agencies can intervene.

However, if there is no “substantial evil” resulting from the association, and the benefits and services of the private association are merely controversial, unpopular, unconventional, or lack proper endorsements and approvals, the U.S. Supreme Court again has ruled overwhelmingly that a freedom of assembly and association cannot be violated. The law is clear and our legal association has successfully fought the battles in the legal association arena for over thirty (30) years. We also have the experience of setting up Private Medical Membership Associations for practitioners for nearly ten (10) years with no interference or problems with State and/or Federal authorities to date.

ProAdvocate Group is a private membership association whose primary objective is to assist our members with establishing their respective Private Medical Membership Associations. We use the protection of the Right to Associate provided by the First Amendment to the United States Constitution to form private membership self-help associations that are (a) not open to the public, (b) do not affect a public interest, (c) and whose activities are or are not inherently benign enough to exempt them from regulation by the states’ policing powers when services are not offered to the public.

If a group of persons wishes to avail themselves of the benefits of holistic or alternative health and wellness techniques (such as herbs, homeopathic, massage and body-work, magnetics, ozone, acupuncture, nutrition, UV light, polarity and energy manipulation and numerous other systems, etc.,) they can now do so within the confines of a bona fide membership association. They can now provide these services and activities that would otherwise be regulated pursuant to various licensing acts under state policing powers when done with members of the public.

ProAdvocate Group also offers a conference in which we give the “Book, Chapter and Verse” of the law concerning licensing and the states’ policing powers, and all the seminal U.S. Supreme Court decisions.  We will prove this is the safest way for a licensed (or unlicensed) physician to get involved with many “natural alternative treatments” outside the auspices of his/her licensed practice without being exposed to the threat of discipline from respective licensing boards. As a bonus, this seminar also gives an in-depth education on licensing board disciplinary actions that no attorney would ever dare give you.

As a licensed or unlicensed health or medical practitioner, you can experience the same peace of mind and legal protection to practice your chosen area or calling without interference or sanctions. However, if one continues to operate as an unlicensed practitioner or offer services of holistic or alternative health and wellness techniques to the public, he or she could be subject to sanctions and made an example of how the state is “protecting the public.” If this were to occur, then you would have no defense and would not prevail, even if you could afford to pay huge legal fees. We have seen this many times within your field of work, and that is why we are here to help.

We welcome you to check out the benefits as a Private Medical Association with no financial risk on your part.  Please call us at 214-387-0821 for more information or you may write to the address on this web site.

Posted in Most Recent | Leave a comment

Fecal Microbiota Transplantation and the Brain Microbiota in Neurological Diseases

Posted on April 9, 2017 by Mimi Castellanos

Clinical Endoscopy.pdf

Posted in Most Recent | Leave a comment

Clinical Observation of a Novel, Complementary, Immunotherapeutic Approach based on Ketogenic Diet, Chondroitin Sulfate, Vitamin D3, Oleic Acid and a Fermented Milk and Colostrum Product

Posted on April 9, 2017 by Mimi Castellanos

Clinical Experience Am J Immunol-2

Posted in Most Recent | Tagged , , | 18 Comments

Gc Protein-Derived Macrophage Activating Factor (GcMAF) and Autism: Do Clinical Results Require a Novel Interpretation?

Posted on April 9, 2017 by Mimi Castellanos

Editorial Am J Immunol-2

Posted in Most Recent | Leave a comment

A Beginner’s Guide to the Ketogenic Diet: An Effective Way of Optimizing Your Health

Posted on April 5, 2017 by Mimi Castellanos

http://articles.mercola.com/ketogenic-diet.aspx?utm_source=dnl&utm_medium=email&utm_content=secon&utm_campaign=20170405Z1_UCM&et_cid=DM140146&et_rid=1956589587

 

Many Americans suffer from various chronic diseases such as diabetes and obesity, and the main culprit is usually the food they eat. The standard American diet contains excessive amounts of protein and carbohydrates, neither of which is good for your health because it eventually causes you to develop insulin and leptin resistance.

As a result, you gain excess weight, develop inflammation and become prone to cellular damage.

To avoid this problem, significant changes in your diet are necessary, and the best way is inducing your body into a state of nutritional ketosis, a condition where your body burns fat as its primary fuel instead of sugar. In order to reach nutritional ketosis, you must follow a ketogenic diet. But what exactly is a ketogenic diet?

This guide will tell you everything you need to know about a ketogenic diet — how you can apply it to your lifestyle and what positives you can reap from it.

The Various Benefits of the Ketogenic Diet

A ketogenic diet is a dietary approach that focuses on minimal carbohydrates, moderate amounts of protein and high healthy fat consumption — the three keys to achieving nutritional ketosis. In fact, it’s what I recommend for most people who would like to optimize their health.

There are many reasons why you should try a ketogenic diet. It can be very beneficial for people suffering from chronic conditions, or for people who would simply like to be healthier than their current state. You’ll be excited to know that a ketogenic diet can help with the following:

• Weight loss

If you’re trying to lose weight, then a ketogenic diet is one of the best ways to do it, because it helps access your body fat so that it can be shed. Obese people in particular can benefit from this method.

In one study, obese test subjects were given a low-carb ketogenic diet and a low-fat diet. After 24 weeks, researchers noted that the low-carb group lost more weight (9.4 kilograms) compared to the low-fat group (4.8 kilograms).1

Even my own body was able to feel the benefits of following a ketogenic diet. I was able to drop my weight from 180 to 164 pounds, despite eating 2,500 to 3,000 calories per day. Since then, I have increased my consumption to 3,500 to 4,000 calories just to maintain my ideal weight.

• Anti-inflammatory

The human body can use sugar and fat as fuel sources. However, the latter is preferred because it is a cleaner, healthier fuel, as it releases far fewer reactive oxygen species (ROS) and secondary free radicals.

By eliminating sugar from your daily food consumption, you’re decreasing your risk of developing chronic inflammation throughout your body.

• Lowering risk of cancer

One exciting discovery about the ketogenic diet is how it can help prevent cancer. Dominic D’Agostino, Ph.D., an assistant professor at the University of South Florida, recently made headway on how the ketogenic diet can help impact this dreaded disease.

D’Agostino explains that all of your cells (including cancer cells) use glucose as fuel. However, cancer cells do not have metabolic flexibility and cannot adapt to using ketones as energy, which your regular cells can. Once your body enters a state of nutritional ketosis, the cancer cells starve to death.

• Increasing muscle mass

Jeff Volek, Ph.D, is a registered dietitian specializing on how a high-fat, low-carb diet can affect health and athletic performance. In one of his books, he states that ketones have a similar structure to branched-chain amino acids that can be useful for building muscle mass.

Ketones spare these amino acids, leaving higher levels of them around, which can help promote muscle mass.

• Reducing Appetite

Constant hunger can cause you to consume more calories than you can burn, which can eventually lead to weight gain. A ketogenic diet can help you avoid this problem because reducing carbohydrate consumption can reduce hunger symptoms.

In one study, participants who were given a low-carbohydrate diet had reduced appetites, helping them lose weight easier.2

• Lowering Insulin Levels

When you consume carbs, they are broken down into sugars in your body. In turn, this causes your blood sugar levels to rise and leads to a spike in your insulin.

Over time, you may develop insulin resistance, which can progress to type 2 diabetes. By altering your diet to a ketogenic approach, you can reduce your risk of developing type 2 diabetes.

In a study published in Nutrition & Metabolism, researchers noted that diabetics who ate low-carbohydrate ketogenic diets were able to significantly reduce their dependency on diabetes medication, and may even reverse it eventually.3

Different Types of Ketogenic Diets You Can Try

There are several variations of the ketogenic diet based on specific needs:4

• Standard Ketogenic Diet (SKD)

SKD is the type I typically recommend for most people, because it is very effective. It focuses on high consumption of healthy fats (70 percent of your diet), moderate protein (25 percent) and very little carbohydrates (5 percent).5

Keep in mind that there’s no set limit to the fat, because energy requirements vary from person to person, depending on their daily physical activities.

However, majority of your calories still need to come from fats, and you still need to limit your consumption of carbohydrates and protein for it to become a standard ketogenic diet.6

• Targeted Ketogenic Diet (TKD)

TKD is generally geared towards fitness enthusiasts. In this approach, you eat the entirety of your allocated carbs for the day in one meal, 30 to 60 minutes before exercise. The idea here is to use the energy provided by the carbs effectively before it disrupts ketosis.7

If you’re following this approach, I recommend that you eat carbs that are easily digestible with a high glycemic index to avoid upsetting your stomach. Then, when you’re done exercising, increase your intake of protein to help with muscle recovery, then continue consuming your fats afterwards.8

• Cyclic Ketogenic Diet (CKD)

Whereas TKD is focused on fitness enthusiasts, CKD is focused more on athletes and bodybuilders. In CKD, you cycle between a normal ketogenic diet, followed by a set number of days of high carb consumption, also known as “carb-loading.”9

The idea here is to take advantage of the carbohydrates to replenish the glycogen lost from your muscles during athletic activity or working out.10

If you’re a high-level athlete or bodybuilder, CKD may be a viable method for you. It usually consists of five days of SKD, followed by two days of carb-loading. During the ketogenic cycle, carb consumption is around 50 grams, but when you get to the carb-loading cycle, the amount jumps to 450 to 600 grams. Again, this method isn’t recommended for most people who do not have a high rate of physical activity.11

• High-Protein Ketogenic Diet

This method is a variant of the SKD. In a high-protein diet, you increase the ratio of protein consumption to 10 percent and reduce your healthy fat consumption by 10 percent. In a study involving obese men that tried this method, researchers noted that it helped reduce their hunger and lowered their food intake significantly, resulting in weight loss.12 If you’re overweight or obese, this may help you at first, then you can transition to SKD after you normalize your weight.

• Restricted Ketogenic Diet

As mentioned earlier, a ketogenic diet can be an effective weapon against cancer. To do this, you need to be on a restricted ketogenic diet. By restricting your carbohydrate and calorie intake, your body loses glycogen and starts producing ketones that your healthy cells can use as energy. Because cancer cells cannot use these ketones, they starve to death.13

A 2010 study helps back up this claim. A 65-year old woman who was suffering from glioblastoma multiforme (GBM), an aggressive type of brain cancer, was put into a restricted ketogenic diet that started with water fasting and then proceeded to consume 600 calories a day only. After two months, her weight decreased and the ketones in her body elevated.

Furthermore, there was no discernable brain tumor tissue detected using magnetic resonance (MRI) or fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging scans.14

Put Away These Foods Before Going on a Ketogenic Diet

Before coming up with an actual ketogenic diet food list, it’s important to take a look at what you’re eating first and take out anything that’s unhealthy. This means that you have to remove sugars, starches, packaged and processed foods from your diet, because a ketogenic diet focuses on eating real, whole food.

Furthermore, avoid drinking milk because it contains the carbohydrate galactose — drinking just one glass can basically eat up your entire carb allotment for the day. In addition, avoiding milk helps lactose-intolerant people to implement the ketogenic diet. Many other products should be avoided, such as hydrogenated vegetable oils (canola, sunflower, etc.), peanut butter, soy products and sodas. They may be low on carbohydrates, but they are unhealthy and can wreak havoc on your health.

The Ideal Foods to Eat for a Ketogenic Diet

So now that you’ve taken out all the unhealthy food sources, what’s the next step? When it comes to the core of an actual ketogenic diet, remember that you need to consume only a moderate amount of protein, or about one-half gram per pound of lean body mass, each day. In addition, carbohydrates must be minimized and high-quality fats increased to serve as your new fuel source.

To ease yourself into a ketogenic diet meal plan, I usually recommend adding C8 medium-chain triglyceride (MCT) oil into your food. It’s typically more expensive than other types of MCT oil, but I prefer it more because it converts into ketones more effectively. You can start with 1 teaspoon per day, then gradually increase your consumption to 2 to 3 tablespoons per day.

If your stomach does not agree with MCT oil, you can try MCT powder, which is easier on your stomach. The table below provides a good overview of other foods rich in high-quality healthy fats:

Coconut oil Animal-based omega-3 fats from healthy sources such as wild-caught Alaskan salmon, sardines, anchovies and krill Olives and olive oil (make sure they are third-party certified because most olive oils are diluted with vegetable oils)
Raw, grass fed butter Raw nuts, such as macadamia, almonds and pecans Various seeds such as pumpkin, sesame, cumin and hemp
Avocados Grass fed meats Lard and/or tallow
Ghee (clarified butter) Raw cacao butter Organic pastured eggs

When building your ketogenic diet meal plan, it’s important to stick to green leafy vegetables because they are rich in fiber, antioxidants and various nutrients. Your best choices include broccoli, spinach, parsley, Brussels sprouts and zucchini.

While fruits are generally healthy for you, majority of them should be are avoided in a ketogenic diet because of their high amounts of sugar. However, certain berries are safe to eat in moderate quantities, such as blackberry, blueberry and cranberry, because they are rich in antioxidants that can support your health.

As for beverages, there are several you can choose from. The most important is water, but you may also drink organic black coffee (without any sweeteners or milk), which is rich in antioxidants. Coconut milk can be consumed as well, as well as herbal teas because they are rich in various antioxidants and nutrients. If you want a more extensive list, Paleo Flourish Magazine has recommendations that encompass various food groups.15

Ketogenic Recipes You Can Try

It may look like there are plenty of foods not allowed when following a ketogenic diet, but there are actually many recipes that you can cook that adhere this method. Here are three ketogenic recipes that I personally use in my daily routine:

Dr. Mercola’s Chocolate Fat Bomb Recipe

Ingredients:

  • 1 Tbsp. of black sesame seeds
  • 1 Tbsp. of flax seeds
  • 1 Tbsp. of black cumin seeds
  • 1 Tbsp. of pumpkin seeds
  • 1 Tbsp. of organic psyllium
  • 1 Tbsp. of chia seeds
  • 1 scoop of Dr. Mercola’s Organic Greens
  • 1 tsp. of calcium from ground-pastured eggshells
  • 1/2 ounce of cocoa butter
  • 1 whole avocado
  • 1 to 2 Tbsp. of medium-chain triglyceride (MCT) oil
  • 1 drop of Stevia
  • Filtered water

Procedure:

  1. Let the black sesame, flax, pumpkin and black cumin seeds soak overnight (roughly 14 hours) in a mixing bowl.
  2. Mix the remaining ingredients.
  3. Pour water to desired consistency — it can range from a liquid to pudding texture.
  4. Using an immersion blender, blend for two to five minutes for desired consistency.

Dr. Mercola’s Keto Salad Recipe

Ingredients:

  • 2 ounces of ground organic lamb
  • 1/3 red onion
  • 1 whole avocado
  • 2 to 4 ounces of sunflower seed sprouts
  • 1 to 2 Tbsp. of Dr. Mercola’s coconut oil
  • 6 pieces of anchovies (packed in salt, not oil)
  • A handful of oregano to your desired flavor (cut finely)
  • 2 to 4 ounces of fennel bulb and/or leaves
  • 2 sprigs of rosemary (chopped finely)
  • 100 grams of red pepper
  • A handful of Malabar spinach
  • 1 habanero pepper (chopped)
  • 1 Tbsp. of salmon fish roe
  • 2 to 3 ounces of grass-fed pastured butter
  • 3 ounces of fermented vegetables
  • 4 to 7 shakes of Dr. Mercola’s Himalayan salt
  • 10 to 20 of shakes ground pepper (depending on your preference)

Procedure:

  1. Gently heat the coconut oil in a frying pan.
  2. Add onions and ground organic lamb at very low heat for 20 to 25 minutes.
  3. In a separate bowl, cut and mix the remaining ingredients.
  4. After 25 minutes, add the onions to the salad and then mix it well.
  5. Rinse salt off the anchovies and soak them for five minutes.
  6. Split each anchovy into three pieces and add to the salad.
  7. Add the organic lamb to the salad.

Dr. Mercola’s Macadamia Nut Fudge Recipe

Ingredients:

  • 300 grams of cocoa butter
  • 200 grams of Dr. Mercola’s coconut oil
  • 200 grams of raw, organic-pastured butter
  • 300 grams of macadamia nuts
  • 8 full droppers of stevia (you can use Luo Han as a substitute)
  • 1 teaspoon Dr. Mercola’s organic vanilla extract

Procedure:

  1. Mix the butters and oils under low heat for three to five minutes.
  2. Once the mixture cools, add the stevia and the vanilla extract.
  3. Pour the fudge into 8-ounce wide ball jars.
  4. Spread the nuts evenly across all jars.
  5. Refrigerate until the fudge reaches the desired consistency

This recipe makes eight servings.

The Side Effects of a Ketogenic Diet

Starting a ketogenic diet can help optimize your health tremendously in many ways. But like any major dietary changes, it can have several undesirable (but not alarming) side effects, such as:

Bad Breath: Once you start on a ketogenic diet, you may notice that your breath will have an undesirable odor due to the increased acetone levels in your body.

Acetone is a ketone produced during ketosis, which is expelled in your urine and partly your breath.

On a positive note, detecting acetone in your breath is a good indicator that your ketogenic diet is working.16 You can brush your teeth and/or rinse your mouth with coconut oil to help remove the bad breath.

Short-Term Fatigue: You may begin to feel fatigue at the start of a ketogenic diet. It’s actually one of the main reasons why many people choose not to continue with this approach long before they can enjoy the benefits.17

The reason why you get tired at the start is your body is adapting from using carbohydrates for energy to healthy fats.

The transition doesn’t happen overnight, and it may take you anywhere between seven to 30 days before your body achieves full ketosis.18

Frequent Urination: During the first few days of implementing a ketogenic diet, you may notice that you’re using the bathroom more often. That’s because your body is dumping the glycogen in your liver and muscles as urine.

Furthermore, as the insulin level in your blood begins to drop, excess sodium is expelled in the form of urine as well.19

Digestive Problems: A huge shift into any dieting method can increase your risk of digestive problems, and the ketogenic diet is no exception.

Constipation is commonly reported among those who are starting out on a ketogenic diet, but it may disappear in a few weeks once your body gets used to the healthier food you’re eating.20

Sugar Cravings: You may develop intense sugar cravings as your body switches from sugar to fat for fuel. However, I encourage you not to give in to temptation.

You can practice various relaxation method such as the Emotional Freedom Techniques or yoga to take your mind away from sugary foods.21

Hair Loss: You may notice that more strands of hair getting stuck on your brush during the first few days of your ketogenic diet.

Don’t worry because this is not a big cause of concern, since hair loss can result from any major dietary changes in general. It will stop once your body achieves ketosis.22

Going into nutritional ketosis by following a ketogenic diet is one of the most radical but highly beneficial lifestyle changes you can make to improve your health. As with most dietary changes, always remember to listen to your body. If you feel any side effects other than the ones listed above, then necessary adjustments may be needed to your food intake.

Frequently Asked Questions About the Ketogenic Diet

Q: How do I go into nutritional ketosis?

A: To enter into a state of nutritional ketosis, take a look at what you’re currently eating and remove any unhealthy items such as sugary drinks and processed foods. The next step is to consume whole, organic foods that are high in healthy fats, has moderate protein and only minimal carbohydrates.

Q: How long does it take to get into ketosis?

A: Each person reacts differently to a ketogenic diet. You may experience a few side effects in the first seven to 30 days, such as constipation, fatigue and urination. But once your body normalizes, you will start feeling the benefits.

Q: How many carbs can I consume to be in a state of ketosis?

A: It’s generally recommended that only 5 percent of your daily diet is allocated to carbohydrates because if you consume more than that, your body gets thrown off ketosis. However, this is only for SKD, or the standard ketogenic diet. If you’re an athlete or a bodybuilder, you can consume more carbs without affecting ketosis by following a targeted ketogenic diet (TKD) or a cyclic ketogenic diet (CKD).

Q: How long does it take before ketosis shows results?

A: The results of ketosis can be felt as early as the first week when your body begins to dump water and carbohydrates, but the weight loss will only be minor.23 As time goes on, your body will begin to consistently shed excess fat, provided you stick to your ketogenic program.24

 

 

 

Posted in Most Recent | Leave a comment

Conquer fatigue, keep your brain bright with nutrition

Posted on April 1, 2017 by Mimi Castellanos

These are the things I sent to my kids in their apartment to keep their nutrition up.  I needed something that would never go bad, that was easy to get at, tasty and picked them up.

Here is what I found on amazon

 

Premium Collagen Peptides (16oz) | Certified Paleo Friendly, Non-Gmo and Gluten Free – Unflavored and Easy to Mix
NitroGreens 240 Grams – Biotics
Healthworks Goji Berries Raw Organic, 1lb
Foods Alive Gold Flax Seed Oil, Artisan Cold-Pressed, Organic, 16oz
Magic Bullet NutriBullet 12-Piece High-Speed Blender/Mixer System
Pea Protein (84% Protein) from Germany by Anthony’s (2lb), Certified Gluten-Free

I also bought freeze dried fruit for flavor and interest

also coconut water for electrolites and to avoid tap water
don’t forget the bravo… at www.bravocoop.com
the bravo is a yogurt which brightens the body, turns on the immune system and provides lots of power to the body
and brain.
One of my mentors said,  “Its always the brain”.  Keep it strong with what it needs.  Low sugars, high oils and specific
really good nutrients.
I make a product called Brain Power which has gotten great results.
also, clean the liver. liver and brain are super related.
I use 10 day cleanses:
Garden of life – the perfect cleanse
Garden of Life – raw cleanse
Mostly eat tons of vegetable for minerals and fibers (this can be sources outside the home or in)
I gave the kids supplements with
oils
minerals and vitamins for blood type (lots of them  several times per day)
hydration supplement. oh yeah.
more greens and more greens.
brain power
more calcium/magnesium
B Vitamins for coping with methylation
This is a start..
You have to get the appeal and motivation.
they don’t get it that it helps them cope.
they are just hungry and its better than cereal and coffee.
Posted in Most Recent | Leave a comment

The family pictures from Christmas 2016

Posted on January 12, 2017 by Mimi Castellanos

christmas-letter-2016

Posted in Most Recent | 211 Comments

Parkinson’s – Another Look – Lawrence Broxmeyer, MD

Posted on November 22, 2016 by Mimi Castellanos

the book is here:

https://www.evernote.com/shard/s99/sh/542c807a-9a4d-4e84-9991-0ad5cf5bbae2/2c04119e814ec6f04231bd14265f3c57

Medical Hypotheses (2002) 59(4), 373–377 a 2002 Elsevier Science Ltd. All rights reserved.

doi: 10.1016/S0306-9877(02)00188-3, available online at http://www.idealibrary.com

Parkinson’s: another look

L. Broxmeyer

Med-America Research, Whitestone, New York, USA

Summary Recent studies in the Parkinson’s literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson’s disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson’s by finding serologic evidence in 20 of 20 Parkinson’s patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis. Parkinson’s: another look is a theoretical article which presents compelling, well-documented evidence for an infectious cause for Parkinson’s disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels. a 2002 Elsevier Science Ltd. All rights reserved.

BACKGROUND

Recent studies in the Parkinson’s literature have cited a tuberculosis-like germ called Nocardia as being respon- sible for Parkinson’s disease (1,2) on several occasions confirmed serologically in the blood. Kohbata seemingly cemented a relationship between Nocardia and Parkin- son’s by finding serologic evidence in 20 of 20 Parkin- son’s patients, acknowledging that blood tests for the Nocardia and the Mycobacteia such as tuberculosis often cross-react, as they belong to the same order – Actino- mycetales (3). Besides this difficulty in differentiation, a well-used medical school text of microbiology points out that even among experts, different observers may clas- sify the same strain as Nocardia or Mycobacteium tuberculosis (4). To add to existing difficulties, both or- ganism’s can be acid-fast, a property long used to iden- tify M. tuberculosis. Atlas also mentions still another Actinomycetales/corynebacteria as equally hard to pick out from the others. Diptheria is a corynebacteia which Martyn found linked to Parkinson’s (5). But even before this, diptheria’s role in PD peppered the Index Medicus

Received 21 May 2001 Accepted 31 October 2001

Correspondence to: Lawrence Broxmeyer MD, Med-America Research, 148-14A Eleventh Avenue, Whitestone, New York 11357, USA.

for decades. By 1994 Gao proved through the use of mycobacterial heat shock proteins against the blood of two Parkinson’s patients that mycobacteria were some- how linked to Parkinson’s (6). All of this has occurred in a setting in which not only do twin studies cast a doubtful aura regarding Parkinson’s as hereditary (7,8) but other seemingly environmental causes are so diverse as to boggle the mind, unless it is recognized that many of these factors affect the disposition of the germ that actually causes Parkinson’s to multiply, thrive and at- tack the dopaminergic nerve centers in the brain.

By 1934, Burn of Yale had identified a Gram-positive bacillus from the bloodstream of three infants that died from Parkinson causing Von Economo’s encephalitis (9). This pathogen, in its sluggish motility and resemblance to Listeria monocytogenes, bore an eerie resemblance to an organism which with advanced stains was found to be acid-fast by a network of post-World War II female M.D.’s and PhD’s (10), some of whom consistently found the germ in Wilson’s disease, a primary cause of Parkinson’s in the young (11). It had evolved as a cross between the mycobacteria and the nocardia as a result of viral phage transfer between the two species (10,12). Furthermore, the important Parkinson’s DATATOP study (13) unwittingly settled upon an agent from a class originally designed to cure tuberculosis, an MAO in- hibitor called Deprenyl (14). And recently Fuente-Agu- ado (15), Kurasawa (16), Mital and Sarkari (17), Otaki

373

374 Broxmeyer

(18) and Solanki (19) all cured symptomatic Parkinson’s using anti-tuberculous medications.

HISTORICAL AND OTHER PARALLELS

Parkinson’s and tuberculosis share many common threads. Both came into force and were linked with the great Industrial Revolution. The substantia nigra was established as important to Parkinson’s through a tu- berculous attack on an autopsied patient (20). Both share a common preferential site of attack, the convexity or underside of the brain were the substantia and basal ganglia lie. Parkinson’s last great epidemic, Von Eco- nomo’s Encephalitis was, according to Hall, almost in- distinguishable from T.B. (21). And Duvoisin all but ruled out any of the suspected viruses implicated at the time (22). Even in AIDS, often associated with Parkin- son’s, mycobacteria such as tuberculosis have been re- ported as the most common central nervous pathogen in HIV-infected people (23). Many of the patients with both Parkinson’s and T.B. share the common denominator of a chronic wasting disease, a cachexic eating away of the flesh. Finally both are primarily diseases of older people with a male preference.

EPIDEMIOLOGICAL CONSIDERATIONS

Guam sits in the southernmost Marianas, within the Asian Pacific Rim. Regions in the world where T.B. is most prevalent lie within that rim. It soon became rec- ognized that Guam had a relatively high number of neurodegenerative diseases in its midst – among them a Parkinson-dementia complex which melded classical Parkinson’s often preceded by memory impairment (24). Parkinson’s and ALS alone affect 10% of Guam’s natives. This, in America would be equal to approximately 27 million Americans affected, a nightmarish scenario. Leprosy was once common in the Mariana’s, but now is rare (25). To this day, there is no explanation as to why leprosy disappeared from the Mariana’s, but T.B. men- ingitis, common, remained.

At first, investigators thought it was only Guam’s in- digenous natives, called the Chamorros that were af- fected by these neurodegenerative diseases. But since Magellan’s Spanish claim to and discovery of the Mari- ana’s, the Island’s demographics where changing, rap- idly. By the 18th century, Filipino immigration created a situation where approximately 1 out of 5 Chamorros were direct descendants from Filipino–Chamorro un- ions. Soon it was discerned that after a mean lapse of two decades, Filipino’s were also contracting PD–Dementia on Guam. Or, were they importing it from the Philip- pines (26)? The question seemed impenetrable to Garr- uto until further epidemiologic studies were done back

in the Philippines. A recent study published in JAMAlists Filipino immigrants to the U.S. as having the highest case rates for tuberculosis among foreign-born persons, second only to immigrants from Mexico (27). Mulder acknowledged that T.B. is a leading cause of death on Guam and that T.B. meningitis was not infrequently seen in its hospitals (28).

Lessell’s study on the febrile seizures that accompany neurodegenerative disease concluded that the over- whelming majority of these occurred in the setting of upper respiratory tract infection (29). This does not support known viruses carried by insects. Hirano and Malamud’s 17 post-mortems on Parkinson–Dementia Complex showed two that presented with pulmonary tuberculosis (30), while several others had ‘pneumonia’ which in turn could have been caused by cryptic tu- bercular disease. But even in this study of general pathologic findings, most of the 17 cases presented with neuropathic changes duplicated in the literature of tu- berculous meningoencephalitis.

SMOKE SCREENS

Since James Parkinson wrote Essays on the Shaking Palsy, a mind-boggling number of causes and ‘risk factors’: infectious, pharmacologic, industrial and degenerative, have been implicated to cause the disease he first doc- umented. In few cases has doctor/medical researcher James Young’s warning been more applicable:

Sixty years ago, to claim that the specific disease tu- berculosis of the lungs had a multiplicity of direct causes was in keeping with the knowledge of the period. Thus it was believed that the inflammation of a bronchitis, the irritation of the inhaled frag- ments of stone with which this mason worked, etc. were each one a ‘direct’ cause of pulmonary tu- berculosis, and that there were many other causes as well – for example heredity, unhealthy environ- ment, etc. Time has shown that the greatly different direct irritants and the other indirect agencies oper- ate in one common way – by increasing cell and tis- sue susceptibility to the one common factor, the tubercle bacillus. In many other cases the history of medical progress has shown that, where several causes have been advanced to account for a dis- ease, these have proved to be nothing more than factors preceding, and predisposing to, the single common agent (31).

James Young, 1924

As Jancovic relates, if Parkinson’s was from a genetic cause, it would cluster primarily within at-risk gene lin- eage, but this, in general, has not been the case (32). In the meantime studies of twins, in which twins from a

Medical Hypotheses (2002) 59(4), 373–377

a 2002 Elsevier Science Ltd. All rights reserved.

single egg show no higher incidence of Parkinson’s than those from two eggs, also argue against a genetic basis for Parkinson’s (8).

Furthermore, most of the single-gene mutations found more commonly in Parkinson’s code for meta- bolic enzymes. But Merrill, Geier and Petricciani induced human cells to initiate enzyme synthesis through in- fectious (bacterial) gene change (33). This validated Morse and Lederberg’s earlier work which showed that the genetic code is universal and that genetic changes in human cells could come about by bacteria and their phage viruses within.

Inside disease-causing bacteria are viruses called ‘phages’. It has long been known that not only do bac- teria such as mycobacteria get infected with these phage viruses, but that there is an invisible war, called ‘lysog- eny’ going on, in which bacteria use phages as viral weapons. Lysogeny is where one colony of bacteria sets out to destroy another by launching its tadpole-shaped phages towards its victim. If phages do not kill, they can genetically alter, creating new and dangerous germs for mankind to cope with. Furthermore, Mankiewicz, col- laborating with Jackson established that phages inside mycobacteria such as tuberculosis could induce cyto- pathogenic changes in healthy mammalian tissue (12). Meanwhile, Lwoff and early phage workers showed how the phages inside Mankiewicz’s mycobacteria could be activated by a host of chemical and other agents (34), some of them pesticide-like, explaining how the prolif- eration of different agents felt to cause Parkinson’s could have occurred – by chasing phages with a cytopatho- genic capability for human target tissue out of an exist- ing bacterial infection.

In so far as those who would link the well-known risk factor of rural living to increased chemical exposure as a cause, Jancovic notes this could just as easily reflect exposure to an infectious agent (32). The Actinomyce- tales including the nocardia and mycobacteria are soil born worldwide and include Mycobacteria kansii.

Gorell documents that prolonged occupational ex- posure to copper, manganese and iron are all associated with Parkinson’s (35). But David, an expert on myco- bacteria, points out that mycobacterial cell mass can be greatly increased in the lab by adding any of these agents to existing culture medium (36).

On a biochemical level, oxidative stress has been mentioned as contributing to Parkinson’s. The substan- tia nigra is under triple jeopardy from oxidant stress injury. In the body tyrosine is first converted to dop- amine, itself highly toxic to catecholamine cells (37). Dopamine in turn is metabolized to hydrogen peroxide and free radical byproducts, which again can damage cell components of substantia (38). In addition, neuro- melanin, found in the substantia’s pigmented neurons,

contains large amounts of iron (39) which as has been mentioned is a significant growth factor for mycobacte- ria (36). Dopamine-derived hydrogen peroxide reacts with this iron, generating extremely neurotoxic free hydroxyl radicals. In 1991, Ben-Shacher and Youdin, by intranigral iron injections induced Parkinson’s in rats (40).

Just how much of what’s been documented in PD is secondary to mycobacterial intermediate metabolism is open to question. But mycobacteria are strict aerobes and oxygen must be available as the final electron ac- ceptor. Three distinct respiratory chains have been de- scribed, one of which leads to the formation of hydrogen peroxide. The disposal of accumulated hydrogen per- oxide is then accomplished by two iron–porphyrin en- zymes, catalase and peroxidase, which occur in all mycobacteria and the products of which release their own free oxygen radicals (36).

In addition, mycobacteria synthesize their own tyro- sine, precursor to dopamine in humans (36), and a pos- sible source of ‘oxidant stress overload’ as individual generations of mycobacteria are replaced during an en- suing infection.

Also, how much dead mycobacteria, who’s lipid content can amount to 40% of their dry weight (41), account for the higher levels of lipid peroxidation seen in the Parkinson’s substantia (42), is open to interpretation, as is whether the increased level of iron found in Par- kinson’s substantia (43) couldn’t at least be in part due to mycobacterial iron porphyrin release.

Pathologically in Parkinson’s there is an accumula- tion of melanin-containing nerve cells brain the in stem, chiefly in the substantia nigra and the locus coeruleus (44). Melanin may be formed biologically in vitro by oxidation of tyrosine or tryptophan, both of which are aromatic amino acids manufactured by the mycobacte- ria (36).

CONCLUSION

It might have been coincidental that both Mycobacteria tuberculosis and Parkinson’s came in to force and were linked with the great Industrial Revolution. Or fortuitous that Blocq and Marinesco established through tubercu- loma attack that the substantia was important to Par- kinson’s (20). It could be considered incidental that the preferential site of attack of tuberculosis meningoen- cephalitis is the convexity of the brain, where it covers the substantia, the basal ganglia and has ready access to the cranial nerves. Perhaps even coincidental that Von Economo’s encephalitis, which caused Parkinson’s reg- ularly, was, according to Hall and the ARNMD almost indistinguishable from CNS T.B. (21,45). It might be considered a fluke that Deprenyl (Eldopril) a Parkinson’s

a 2002 Elsevier Science Ltd. All rights reserved.

Medical Hypotheses (2002) 59(4), 373–377

Parkinson’s: another look 375

376 Broxmeyer

mainstay, comes from a class, the MAO inhibitors orig- inally designed to cure tuberculosis (14). Or circum- stantial that clinical and epidemiologic studies have peppered Parkinson’s literature for decades linking tu- berculosis-like germs: including nocardia, corynebacte- ria (diptheria) and the mycobacteria – not only easily confused by seasoned bacteriologists (4) but which also cross-react under serological identification (3). It might be considered adventitious that Burn isolated a germ (9) with an eerie resemblance to Jackson and Livingston’s (10, 11) mycobacteria/nocardia cross in three Von Eco- nomo’s infants at autopsy; or that Jackson found acid- fast forms in Burn’s bacillus that she implicated as causing Wilson’s disease (11), dominant cause of Par- kinson’s in the young. It might be considered insignifi- cant that tuberculosis-like Nocardia has a specific affinity for substantia nigral neurons (1) and that the most convincing Parkinson’s animal model to date happened when Beaman injected nocardia into mice (2). It might seem random that Kohbata & Shimokawa ce- mented a relationship by blood serology between no- cardia and mycobacteria in 20 of 20 Parkinson’s patients (3) or that Gao linked Parkinson’s to mycobacteria in blood through diagnostic heat shock proteins (6). It could be considered anecdotal that Mital and Sarkari (17), Otaki (18), Fuente-Aguado (15), Solanki and Ku- rasawa (19) all independently cured Parkinson’s with anti-tuberculosis therapy. It could be called inconse- quential that in AIDS-related Parkinson’s, sometimes listed as the most common cause of infectious Parkin- son’s, that Berenguer reported mycobacteria as the most common CNS pathogen in HIV infected people (23). It could be considered coincidental that Guam, where T.B. meningitis runs rampant, hosts an epidemic number of neurologic disorders, including Parkinson’s–Dementia (24). It might seem that there is a lack of essential con- nection between the post-traumatic Parkinson’s, say of an ex-boxer, and the fact that such trauma could also have caused a long-standing infection, such as tubercles in the brain, planted even decades before, to discharge bacilli into the meningeal spaces (46), reactivating a long quiescent disease from one punch too many. And it might seem unrelated that occupational exposure to copper, manganese and iron(35) are all not only associ- ated with parkinsonism but the very substances which act as mycobacterial growth factors in the laboratory (36).

And it might seem chance that the triple jeopardy of oxidative stress under which the substantia sits, namely catecholamine toxic dopamine, derived from tyrosine; hydrogen peroxide and free radical byproducts: all of which can damage the substantia (38) are also manu- factured by mycobacterial intermediary metabolism and cell-respiration (36).

It might be considered random that many Parkin- son’s victims show the same cachexic wasting away that has long typified consumption – or that the do- paminergic neuron loss McGear found as an active Parkinson’s process, even after death (47), is just the sort of chronic process that so characterizes a disease like tuberculosis, which often begins in youth or childhood.

It could be considered incidental that tuberculosis and Parkinson’s are presently considered diseases of the older population with more men than woman affected.

But in the end, and taken together, there are just too many coincidences in an ever-growing list to just casu- ally dismiss.

In conclusion, the preponderance of convincing evi- dence, as we near the bicentennial of James Parkinson’s original Essay points to a chronic infectious cause, not viral and most likely of the family Actinomycetales – ei- ther mycobacterial or a tuberculosis-like mycobacterial/ nocardial cross. Clinical trials await.

REFERENCES

1. Kohbata S., Beaman B. L. L-Dopa-responsive movement disorder caused by Nocardia Asteroides localized in the brains of mice. Infect Immunit 1991; 59: 181–191.

2. Beaman B. L., Beaman L., Kjelstrom J. A. Bacteria and neurodegeneration. In: D. Caino (ed). Neurodegenerative Diseases. Orlando, FL: W.B. Saunders, 1994: 319–338.

3. Kohbata S., Shimokawa K. Circulating antibody to nocardia in the serum of patient’s with Parkinson’s disease. Adv Neurol 1993; 60: 355–357.

4. Atlas R. Microbiology: Fundamentals and Applications, 2nd Edn. New York: Macmillan, 1988.

5. Martyn C. N., Osmond C. Parkinson’s disease and the environment in early life. J Neurol Sci 1995; 132: 201–206.

6. Gao Y. L., Raine C. S. Humoral response to hsp 65 in multiple sclerosis and other neurologic conditions. Neurology 1994; 44: 941–945.

7. Lux W. E., Kurtzke J. F. Is Parkinson’s disease acquired? Evidence from a geographic comparison with multiple sclerosis. Neurology 1987; 37: 471–487.

8. Betemps E. J., Buncher C. R. Birthplace as a risk factor in motor neurons disease and Parkinson’s disease. Int J Epidemiol 1993; 22(5): 898–904.

9. Burn C. G. Unidentified gram positive bacillus associated with meningo-encephalitis. Proc Soc Exp Biol Med 1934; 31: 1095.

10. Livingston V. A specific type of organism cultivated from malignancy: bacteriology and proposed classification. Annal N Y Acad Sci 1970; 174: 636–654.

11. Jackson E. A. A specific type of microorganism isolated from animal and human cancer: bacteriology of the organism. Growth 1954; 18: 37–51.

12. Mankiewicz E. Bacteriophages that lyse mycobacteria and corynebacteria, and show cytopathogenic effect on tissue cultures of renal cells of cercopithecus aethiops. Can Med Assoc J 1955; 92: 31–33.

13. DATATOP Parkinson’s Study Group. Ann Neurol. 1996; 39: 29–45.

Medical Hypotheses (2002) 59(4), 373–377

a 2002 Elsevier Science Ltd. All rights reserved.

  1. Hardman I. G., Gilman A. G. Goodman & Gillman’s The Pharmacologic Basis of Therapeutics, 9th Edn. New York: McGraw Hill, 1996.
  2. de la Fuente-Aguado J., Bordon J. Parkinsonism in an HIV- infected patient with hypodense cerebral lesion. Tubercle and Lung Disease 1996; 77: 191–192.

31. Young J. M. D. A new outlook on cancer: irritation and infection. Br Med J 1925;(Jan 10).

32. Jancovic J., Tolosa E. Parkinson’s Disease and Movement Disorders. Baltimore: Williams and Wilkins, 1998.

33. Merril C. R., Geier M. R., Petricciani J. C. Bacterial virus gene expression in human cells. Nature 1971; 233: 398–

16. Kurasawa T., Ikeda T., Inoue T. Pulmonary infection with 400.

mycobacterium kansasii presenting as solitary nodule shadow in the left anterior basal segment. Japan J Thorac Dis 1997; 35(2): 215–219.

  1. Mital O. P., Sarkari N. B., Singh R. P. Parkinsonian symptoms in T.B.M. (a case report). J Assoc Phys India 1974; 22(8): 629–631.
  2. Otaki M., Ichikawa Y., Oizumi K. KEKKAKU 1994; 69(7): 491–495.
  3. Solanki S. V., Kothari V. R. Parkinsonian Syndrome. J Indian Med Assoc 1977; 68(12): 255–257.
  4. Blocq P., Marinesco G. Tremblement Parkinsonian hemiplegique symtomatique D’une tumeur Du pedoncule cerebral. Compt Pendus Hebo Madair Seances Et Memoir De La Societe Paris 1893: 105–111.
  5. Hall A. J. Epidemic Encephalitis (Encephalitis Lethargicas). Bristol: John Wright and Sons Ltd, 1924.
  6. Duvoisin R. C., Yahr M. D. Encephalitis and Parkinsonism. Arch Neurol 1965; 12: 227.
  7. Berenguer J., Moreno S. Tuberculous meningitis in patients infected with the human immunodeficiency virus. New Engl Med 1992; 326(10): 668.
  8. Elizan T. S. Amyotrophic lateral sclerosis and Parkinsonism– Dementia complex: a study in mon-Chamorros of the Mariana and Caroline Islands. Arch Neurol 1966; 14: 347– 355.
  9. Mulder D. W., Kurland L. T. Neurologic diseases on Island of Guam. US Armed Forces Med J 1954; 5: 1724–1739.
  10. Garruto R. M. Amyotrophic lateral sclerosis and Parkinson– Dementia among Filipino Migrants to Guam. Ann Neurol 1981; 10: 341–350.
  11. Talbot E. A., Moore M. Tuberculosis among foreign-born persons in the United States 1993–1998. JAMA 2000; 284(22): 2894–2900.
  12. Mulder D. W., Kurland L. T. Neurologic diseases on Island of Guam. US Armed Forces Med J 1954; 5: 1724–1739.
  13. Lessell S. Seizure in a Guamanian village. Arch Neurol 1962; 7: 37–44.
  14. Hirano A. Parkinson–Dementia complex, an endemic disease on the island of Guam. Brain: J Neurol 1961; 84: 662–679.

34. Lwoff A. (Karl Taylor Compton Lecturers): Biologic Order. Cambridge, MA: The MIT Press, 1962.

35. Gorell J. M., Johnson C. C. Occupational exposures to metals as risk factors for Parkinson’s disease. Neurology 1997; 48: 650–658.

36. David H. L. Bacteriology of the Mycobacterioses. US Department of Health Education and Welfare. Public Health Service, Center for Disease Control, Atlanta, March, 1976.

37. Hastings T. G., Lewis D. A. Role of oxidation in the neurotoxic effects of intrastriatal dopa mine injections. Proc Natl Acad Sci USA 1966; 93: 1956–1961.

38. Cross C. E. Oxygen radicals and human disease. Ann Int Med 1987; 107: 526–545.

39. Zecca L., Pietra R. Iron and other metals in neuromelanin, substantia nigra and putamen in human brain. J Neurochem 1994; 62: 1097–1101.

40. Ben-Shacher D., Youdim M. B. Internigral iron injection induces behavioral and biochemical Parkinsonism in rats. J Neurochem 1991; 57: 2133–2135.

41. Anderson R. J., Yale J. Biol Med 1943; 15: 311.
42. Jenner P., Dexter D. T. Oxidative stress as a cause of nigral cell death in Parkinson’s disease and incidental Lewy body

disease. Ann Neurol 1992; 32(Suppl): S82–S87.
43. Softic E., Paulus W. Selective increase of iron in substantia

nigra zona compacta of Parkinsonian brains. J Neurochem

1991; 56: 978–982.
44. Jablonski S. Jablonski’s Dictionary of Syndromes and

Eponymic Diseases. Malabar, FL: Krieger Publishing

Company, 1991.
45. ARNMD (An Investigation by The Association for Research

in Nervous and Mental Disorders). Acute Epidemic Encephalitis (Lethargica Encephalitis). New York: Paul B. Hoebner, 1922.

46. Rom W. N., Garay S. M. Tuberculosis. New York: Little Brown and Company, 1998.

47. McGeer P. L., Ragaki S. Rate of cell death in Parkinsonism indicates active neuropathological process. Ann Neurol 1988; 24: 574–576.

a 2002 Elsevier Science Ltd. All rights reserved.

Medical Hypotheses (2002) 59(4), 373–377

 

 

Posted in Most Recent | 1,115 Comments