Friday, July 31, 2015

Sugary drinks blamed over type 2 diabetes cases

PUBLISHED: 01:47 EST, 22 July 2015 | UPDATED: 01:47 EST, 22 July 2015
Drinking sugary drinks could be causing nearly 8,000 cases of type 2 diabetes a year, according to research.
A study led by the University of Cambridge found sugar-sweetened drinks could give rise to 1.8 million diabetes cases over 10 years in the United States and 79,000 in the UK.
Academics analysed studies carried out in both the US and UK as they had the most data available, and found sugar-sweetened beverages were consumed by 54.4% and 49.4% of people in each country respectively.

Sugary drinks could be behind thousands of cases of the condition every year, according to research
They concluded that regular consumption of sugar-sweetened beverages may be linked to 2-6% of type 2 diabetes cases in the UK, and 4-13% in the US. This was independent of individuals obesity status.
Sugar-sweetened beverages were defined as any sweetened beverages, including sugar-sweetened fruit juice, not presented as diet or non-caloric beverages.
Artificially sweetened beverages included low-caloric soft drinks, while fruit juice was defined as 100% fruit juice, or fruit juice assessed separately from fruit drinks.
Although artificially sweetened beverages and fruit juice also showed positive associations with incidence of type 2 diabetes, researchers said these findings were likely to involve bias.
However they added that both artificially sweetened beverages and fruit juice were unlikely to be healthy alternatives to sugar-sweetened beverages for the prevention of type 2 diabetes.
They said previous studies had found obese individuals tend to consume more sugar-sweetened and artificially sweetened beverages and less fruit juice than leaner people.
The study, which is published in the BMJ, pointed out that the studies analysed were observational, so no definitive conclusions can be drawn about cause and effect.
"Although more research on cause and effect needs to be carried out, this study indicates the potential health gains that may be achieved by reducing the consumption of sugar sweetened drinks," they wrote.
Meanwhile, a second study published in the BMJ found that a low birth weight combined with an unhealthy lifestyle in adulthood are jointly related to an increased risk of type 2 diabetes.
A team led by Harvard School of Public Health in the US tracked 150,000 men and women for 20 to 30 years, looking at f ive lifestyle factors - diet, smoking, physical activity, alcohol consumption, and body mass index (BMI).
Nearly 12,000 new cases of type 2 diabetes were found, with consistent associations found between low birth weight and unhealthy lifestyle.

Astrology/tarot July 31-Aug 7. Nuit Report with Aepril. Full moon in Aqu...

Thursday, July 30, 2015

Vitamin E – A Proven Alzheimer’s Breakthrough The prestigious Journal of the American Medical David Perlmutter, M.D.

Vitamin E – A Proven Alzheimer’s Breakthrough
The prestigious Journal of the American Medical Association welcomed in the new year by publishing what will surely become a landmark study. Researchers announced the results of a clinical trial of vitamin E in people with mild-to-moderate Alzheimer’s disease, and their findings may well revolutionize our approach to treating Alzheimer’s, a disease affecting more than 5.4 million Americans.
The study looked at the effect of dietary supplementation using 2,000 international units of non-prescription vitamin E daily in a large group of elderly Alzheimer’s patients, and compared their results over an average of around 2.3 years to similar patients who received a placebo, a pharmaceutical (memantine), or a combination of memantine along with vitamin E.
The best results were found in the patients who received the vitamin E alone. In these patients, the annual rate of decline in functional performance was slowed by approximately 20%. Functional performance includes important day-to-day tasks like preparing meals, bathing, shopping and eating.
While these results are far from representing a cure for Alzheimer’s, they do show that vitamin E did allow Alzheimer’s patients to get by with less help from caregivers and maintain their independence longer. This is in contrast to the findings in those who were given the Alzheimer’s drug memantine, either alone or in combination with vitamin E.
Vitamin E acts as an antioxidant, meaning it protects tissues against the damaging effects of chemicals called free radicals which are produced in the body as a normal part of metabolism. It has been shown in earlier research that there is an excess of free radical activity in the brains of Alzheimer’s patients. So researchers are focusing on vitamin E’s antioxidant activity as a possible explanation of its effectiveness in treating Alzheimer’s patients.
While the dosage of vitamin E used in this study far exceeds the government’s recommended dose for healthy adults (22.4 IU daily), no serious health consequences were reported in those just taking the vitamin E. In fact, the only serious problems in the study were reported in those who were given the pharmaceutical memantine.
As a practicing neurologist treating Alzheimer’s patients each day the results of this study are extremely encouraging. Vitamin E is widely available, doesn’t require a prescription, and is now proven to slow the progression of this devastating disease.

Vitamin E can interact with medications including the blood thinner warfarin, medications used in chemotherapy, and anti-inflammatory drugs. So it’s a good idea to check with your healthcare provider before starting vitamin E or any nutritional supplement.

Satsang with Magdi Thursday July 30 at 6pm EST (4pm CRT)

How Depression Affects Your Brain Structure


By Dr. Mercola
That depression can take a toll on your physical health is pretty well-recognized. Recent research has also found that it can actually cause changes in your brain.
Specifically, recurring depressive episodes reduce the size of your hippocampus — an area of your brain involved in forming emotions and memory — stressing the importance of early intervention, especially among teenagers.
Your memory isn't only restricted to remembering dates and passwords; it also plays an important role in developing and maintaining your sense of self.
When your hippocampus shrinks, it's not just your rote memory that is affected, behaviors associated with your sense of self are also altered, and a smaller hippocampus equates to a general loss of emotional and behavioral function.
The good news is the damage is likely reversible, but to do that, you have to actually do something about your situation.
Chronic Depression Can Damage Your Brain
Using brain magnetic resonance imaging (MRI) data of nearly 8,930 people from around the world, an international team of researchers found that those who suffered recurring bouts of depression also had a smaller hippocampus.1,2,3
This applied to about 65 percent of all depressed participants.  Those who were experiencing their first depressive episode did not show evidence of shrinkage, suggesting it's the repetitive recurrence that causes the hippocampus to shrink.
Those who showed hippocampal shrinkage also reported getting depressed earlier than the others, typically before the age of 21.
Previous studies have noted that depressed people tend to have a smaller hippocampus, but it was not known whether this was a predisposing factor, or a result of the illness.
This study reveals the answer: Depression comes first; the brain damage follows...  According to co-author Professor Ian Hickie:4
"[The] more episodes of depression a person had, the greater the reduction in hippocampus size. So recurrent or persistent depression does more harm to the hippocampus the more you leave it untreated.
This largely settles the question of what comes first: the smaller hippocampus or the depression? The damage to the brain comes from recurrent illness...
Other studies have demonstrated reversibility, and the hippocampus is one of the unique areas of the brain that rapidly generates new connections between cells, and what are lost here are connections between cells rather than the cells themselves.
Treating depression effectively does not just mean medicines. If you are unemployed, for example, and then sit in a room doing nothing as a result, this can shrink the hippocampus. So social interventions are just as important, and treatments such as fish oils are also thought to be neuro-protective."
The Inflammatory Roots of Depression
Contrary to popular belief, depression is not likely caused by unbalanced brain chemicals; however there are a number of other biological factors that appear to be highly significant. Chronic inflammation is one such factor.5
Scientists have also found that your mental health can be adversely impacted by factors such as vitamin D deficiency and/or unbalanced gut flora — both of which, incidentally, play a role in keeping inflammation in check, which is really what the remedy to depression is all about.
As discussed in an article by Dr. Kelly Brogan, depressive symptoms can be viewed as downstream manifestations of inflammation.
"The source itself may be singularly or multiply-focused as stress, dietary and toxic exposures, and infection... [I]nflammation appears to be a highly relevant determinant of depressive symptoms such as flat mood, slowed thinking, avoidance, alterations in perception, and metabolic changes,"6 she writes.
Certain biomarkers, such as cytokines in your blood and inflammatory messengers like CRP, IL-1, IL-6, and TNF-alpha, show promise as potential new diagnostic tools, as they're "predictive7 and linearly8 correlative" with depression.
For example, researchers have found that melancholic depression, bipolar disorder, and postpartum depression are associated with elevated levels of cytokines in combination with decreased cortisol sensitivity (cortisol is both a stress hormone and a buffer against inflammation).9
As explained by Dr. Brogan:
"Once triggered in the body, these inflammatory agents transfer information to the nervous system, typically through stimulation of major nerves such as the vagus, which connects10 the gut and brain. 
Specialized cells called microglia in the brain represent the brain's immune hubs and are activated in inflammatory states.
In activated microglia, an enzyme called IDO (indoleamine 2 3-dioxygenase) has been shown11 to direct tryptophan away from the production of serotonin and melatonin and towards the production of an NMDA agonist called quinolinic acid that may be responsible for symptoms of anxiety and agitation.
These are just some of the changes that may conspire to let your brain in on what your body may know is wrong."
Sugar Is One of the Most Inflammatory Ingredients in Your Diet
It's virtually impossible to address inflammation without noting the role of sugar, found in ample supply in most processed foods.
Besides promoting chronic inflammation, refined sugar intake can also exert a toxic effect by contributing to insulin and leptin resistance and impaired signaling, which play a significant role in your mental health.
Sugar also suppresses activity of a key growth hormone called BDNF (brain derived neurotrophic factor), which promotes healthy brain neurons. BDNF levels are critically low in both depression and schizophrenia, which animal models suggest might actually be causative.
In 2004, the British psychiatric researcher Malcolm Peet published a provocative cross-cultural analysis of the relationship between diet and mental illness.12 His primary finding was a strong link between high sugar consumption and the risk of both depression and schizophrenia.
Another study13 published in 2007 found that inflammation may be more than just another risk factor for depression. It may in fact be the risk factor that underlies all others. According to the researchers:
"The old paradigm described inflammation as simply one of many risk factors for depression. The new paradigm is based on more recent research that has indicated that physical and psychological stressors increase inflammation.
These recent studies constitute an important shift in the depression paradigm: inflammation is not simply a risk factor; it is the risk factor that underlies all the others.
Moreover, inflammation explains why psychosocial, behavioral and physical risk factors increase the risk of depression. This is true for depression in general and for postpartum depression in particular."
Eating Real Food May Be Key for Successful Treatment of Depression
The evidence clearly indicates that your diet plays a key role in your mental health, for better or worse. So if you're struggling with depression, mood swings, or feel yourself sliding into "the blues," I strongly advise you to look at what you're eating. The key is to eat real food, ideally organic (to avoid chemical exposures) and locally grown (for maximum freshness).
Also make sure to eat plenty of traditionally cultured and fermented foods, which will help nourish beneficial bacteria in your gut. Good examples include fermented vegetables of all kinds, including sauerkraut and kimchi, kombucha (a fermented drink), as well as fiber-rich prebiotic foods like jicama (Mexican yam).
Optimizing your gut flora appears to be absolutely crucial for good mental health, which is understandable when you consider that gut bacteria actually manufacture neurochemicals such as dopamine and serotonin, along with vitamins that are important for brain health. In fact, you have a greater concentration of serotonin in your gut than in your brain.
I recommend avoiding all types of processed foods, including certified organic ones, as processed foods are no longer "alive." What you're looking for is whole, unadulterated foods, with which to cook from scratch (or eat raw). Processed foods are simply loaded with ingredients known to alter your gut flora and promote inflammation, thereby inviting depression. This includes:
  • Added sugar and high fructose corn syrup
  • Genetically engineered (GE) ingredients (primarily corn, soy, and sugar beets) which, besides their own unknown health risks, also tend to be heavily contaminated with glyphosate—a Class 2A carcinogen that can also damage your gut microbiome and has been linked to antibiotic-resistance. Most conventional (non-GE) wheat is also treated with toxic glyphosate prior to harvesting.
  • By altering the balance of your gut flora, pesticides and herbicides also disrupt the production of essential amino acids like tryptophan, a serotonin precursor, and promote production of p-cresol, a compound that interferes with metabolism of other environmental chemicals, thereby increasing your vulnerability to their toxic effects.
  • Artificial sweeteners, along with thousands of food additives, most of which have never been tested for safety
  • Chemicals in the food packaging, such as bisphenol-A (BPA), bisphenol-S (BPS), and phthalates, which can migrate into the food
  • Trans fats
Exercise Effectively Combats Depression and Helps Rebuild Your Hippocampus
Recent research has shown clear links between inactivity and depression. Women who sat for more than seven hours a day were found to have a 47 percent higher risk of depression than women who sat for four hours or less per day. Those who didn't participate in any physical activity at all had a 99 percent higher risk of developing depression than women who exercised. Indeed, exercise is perhaps one of the most effective yet underutilized treatments for depression.

Studies have shown its efficiency typically surpasses that of antidepressant drugs. One of the ways exercise promotes mental health is by normalizing insulin resistance and boosting natural "feel good" hormones and neurotransmitters associated with mood control, including endorphins, serotonin, dopamine, glutamate, and GABA. 
It also helps rid your body of stress chemicals that can lead to depression, and while depression can shrink your hippocampus, exercise has been shown to increase the volume of gray matter in the hippocampal region of the brain. It also promotes neurogenesis, i.e. your brain's ability to adapt and grow new brain cells. While sugar suppresses brain derived neurotrophic factor (BDNF), thereby raising your risk of depression, exercise boosts it. 
Exercise initially stimulates the production of a protein called FNDC5, which in turn triggers the production of BDNF. BDNF is a remarkable rejuvenator in several respects. In your brain, it not only preserves existing brain cells, it also activates brain stem cells to convert into new neurons, and effectively makes your brain grow larger. Research14 confirming this includes a study by Kirk Erickson, PhD, in which seniors aged 60 to 80 who walked 30 to 45 minutes, three days per week for one year, increased the volume of their hippocampus by two percent.
Meditation Also Alters Your Brain in Beneficial Ways
Meditation is another underutilized tool to optimize mental health. Not only is it helpful for stress relief and gaining greater self awareness (if not a more spiritual perspective of life's ups and downs), it too has been shown to alter the structures of your brain for the better. As reported by Forbes:15
"The practice appears to have an amazing variety of neurological benefits – from changes in grey matter volume to reduced activity in the 'me' centers of the brain to enhanced connectivity between brain regions...
Skeptics, of course, may ask what good are a few brain changes if the psychological effects aren't simultaneously being illustrated? Luckily, there's good evidence for those as well, with studies reporting that meditation helps relieve our subjective levels of anxiety and depression, and improve attention, concentration, and overall psychological well-being."
With regards to depression specifically, a 2014 meta analysis16 of 47 studies concluded that mindfulness meditation can be helpful. While the overall effect size17 was "moderate" at 0.3, Forbes rightfully points out that this is identical to the effect size for antidepressants, which is also 0.3, and the go-to solution in most cases of depression. Like exercise, mindfulness meditation has also been shown to increase cortical thickness in the hippocampus, and brain areas involved in the regulation of emotions and self-referential thought processes.18
Shrinkage of the amygdala has also been noted. In this case, less cell volume in a brain center can be a blessing, as the amygdala controls the subjective perception of fear, anxiety, and stress.
People suffering with anxiety disorders tend to produce too much serotonin in the amygdala, which is why serotonin-boosting drugs like SSRIs can worsen depression and anxiety in some people. Previous studies have also revealed that increased nerve activity in the amygdala is part of the underlying mechanism that produces anxiety. Basically, those with anxiety disorders have an over-active fear center, and meditation may help dampen this over-activity.
Key Strategies to Overcome Depression
Two key strategies for overcoming depression have already been addressed above: diet (trading in the processed foods for real food, with an emphasis on fermented foods to optimize your gut flora), and exercise. Optimizing your vitamin D level by getting appropriate sun exposure (or taking a vitamin D3 supplement with vitamin K2) is another key strategy not to be overlooked. In one previous study, people with the lowest levels of vitamin D were 11 times more prone to be depressed than those who had normal levels.
Considering the fact that vitamin D deficiency is typically the norm rather than the exception, and has been implicated in both psychiatric and neurological disorders, getting your vitamin D level checked and addressing any deficiency is a crucial step.
There's no doubt in my mind that if you fail to address the root of your depression, you could be left floundering and struggling with ineffective and potentially toxic band-aids for a long time. Your diet does play a large part in your mental health, so please address the impact processed foods might be having.
Also be sure to support optimal brain functioning with essential fats. This includes healthy saturated fats like avocados, butter made from raw grass-fed organic milk, raw dairy, organic pastured egg yolks, coconuts and coconut oil, unheated organic nut oils, raw nuts, and grass-fed meats. I also recommend supplementing your diet with a high-quality, animal-based omega-3 fat, like krill oil. This may be the single most important nutrient to battle depression.
Last but not least, add some effective stress-busting strategies to your toolbox. Ultimately, depression is a sign that your body and your life are out of balance. One way to return balance to your life is by addressing stress. Meditation can be helpful, as discussed above. When weather permits, get outside for a walk. But in addition to that, I also recommend using a system that can help you address emotional issues that you may not even be consciously aware of.
For this, my favorite is Emotional Freedom Technique (EFT). Recent research has shown that EFT significantly increases positive emotions, such as hope and enjoyment, and decreases negative emotional states.  EFT is particularly powerful for treating stress and anxiety because it specifically targets your amygdala and hippocampus, which are the parts of your brain that help you decide whether or not something is a threat.19,20

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Although you can learn the basics of EFT on your own, if you have a serious mental disorder or depression, I highly recommend consulting a qualified EFT practitioner.21 For serious or complex issue you need a qualified health care professional that is trained in EFT to help guide you through the process, as it typically takes years of training to develop the skill to tap on and relieve deep-seated, significant issues.

Happy Birthday!!!

Wednesday, July 29, 2015

Reversal of cognitive decline: A novel therapeutic program
Online ISSN: 1945-4589

AGING, Vol 6, No 9 , pp 707-717
PDF version     |    Abstract

Dale E. Bredesen1, 2
1 Mary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095;
2 Buck Institute for Research on Aging, Novato, CA 94945.
Key words:
Alzheimer's, dementia, mild cognitive impairment, neurobehavioral disorders, neuroinflammation, neurodegeneration, systems biology
9/15/14; Accepted: 9/26/14; Published: 9/27/14
This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer's disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND). The first 10 patients who have utilized this program include patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI). Nine of the 10 displayed subjective or objective improvement in cognition beginning within 3-6 months, with the one failure being a patient with very late stage AD. Six of the patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. Improvements have been sustained, and at this time the longest patient follow-up is two and one-half years from initial treatment, with sustained and marked improvement. These results suggest that a larger, more extensive trial of this therapeutic program is warranted. The results also suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes. Furthermore, given the failure of monotherapeutics in AD to date, the results raise the possibility that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system.
Magnitude of the problem
Cognitive decline is a major concern of the aging population, and Alzheimer's disease is the major cause of age-related cognitive decline, with approximately 5.4 million American patients and 30 million affected globally [1]. In the absence of effective prevention and treatment, the prospects for the future are of great concern, with 13 million Americans and 160 million globally projected for 2050, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer's disease prevalence is on the rise, which makes the need to develop effective prevention and treatment increasingly pressing. Recent estimates suggest that AD has become the third leading cause of death in the United States [2], behind cardiovascular disease and cancer. Furthermore, it has been pointed out recently that women are at the epicenter of the Alzheimer's epidemic, with 65% of patients and 60% of caregivers being women [3]. Indeed, a woman's chance of developing AD is now greater than her chance of developing breast cancer [4].
Failure of monotherapeutics
Neurodegenerative disease therapeutics has been, arguably, the field of greatest failure of biomedical therapeutics development. Patients with acute illnesses such as infectious diseases, or with other chronic illnesses, such as cardiovascular disease, osteoporosis, human immunodeficiency virus infection, and even cancer, have access to more effective therapeutic options than do patients with AD or other neurodegenerative diseases such as Lewy body dementia, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. In the case of Alzheimer's disease, there is not a single therapeutic that exerts anything beyond a marginal, unsustained symptomatic effect, with little or no effect on disease progression. Furthermore, in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one.
Therapeutic success for other chronic illnesses such as cardiovascular disease, cancer, and HIV, has been improved through the use of combination therapies [5]. In the case of AD and its predecessors, mild cognitive impairment (MCI) and subjective cognitive impairment (SCI), comprehensive combination therapies have not been explored. However, the past few decades of genetic and biochemical research have revealed an extensive network of molecular interactions involved in AD pathogenesis, suggesting that a network-based therapeutics approach, rather than a single target-based approach, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer's disease.
Preclinical studies
Extensive preclinical studies from numerous laboratories have identified multiple pathogenetic targets for potential intervention. These include, in addition to amyloid-β (Aβ) oligomers and tau, inflammatory mediators, apolipoproteins and lipid metabolism factors, hormonal mediators, trophic factors and their receptors, calcium regulatory pathways, axoplasmic transport machinery, neurotransmitters and their receptors, prion protein, and a host of other potential targets. However, one of the drawbacks of these preclinical studies is that many have implicated single pathways, and shown large effects of targeting one pathway, whereas in human studies, such approaches have not been borne out. There are several possible inferences from such discrepant results: first, it is possible that it will be necessary to target multiple pathways simultaneously in order to effect an improvement in symptoms and pathophysiology. Second, it is possible that targeting a single pathway will be sufficient, but that earlier intervention will be required. Third, it is possible that all of these seemingly disparate pathways will converge on a single critical pathway, so that either a single targeted therapy or a multi-component, multi-targeted approach may be effective. And fourth, of course it is possible that neither of these two types of approaches will be sufficient. It is worth noting, however, that it is possible that addressing multiple targets within the network underlying AD pathophysiology may be successful even when each target is affected in a relatively modest way; in other words, the effects of the various targets may be additive, multiplicative, or otherwise synergistic.
Based on a combination of in vitro and in vivo studies, we have advanced a model in which AD results from an imbalance in endogenous plasticity signaling (Fig. 1), [5-9], and in which the β-amyloid precursor protein (APP) is a mediator of such plasticity-related signaling. Thus the model suggests that AD is analogous to other chronic illnesses such as cancer, osteoporosis, and atherosclerosis. In the case of osteoporosis, osteoblastic signaling is chronically exceeded by osteoclastic signaling, resulting in an age-associated chronic illness featuring loss of bone. By analogy, in Alzheimer's disease, there is a fundamental, age-associated imbalance between the dynamically opposed physiological processes that mediate plasticity, i.e., between synaptoblastic and synaptoclastic activity. This signaling involves physiological mediators of synaptic development, maintenance, repair, and remodeling, including APP, its derivative peptides, ApoE, and tau, and is modulated by all of the many disparate factors associated with Alzheimer's disease. Furthermore, just as for neoplasia, positive feedback selects and amplifies the disease process; however, whereas in oncogenesis, the positive feedback occurs at the cellular level, in Alzheimer's disease, the positive feedback occurs at the molecular species level, in the form of prionic loops [5, 8, 9].

Figure 1. Alternative processing of, and signaling by, APP. [5].
In support of this model, the four peptides derived from the amyloidogenic processing of β-amyloid precursor protein (APP)—sAPPβ, Aβ, Jcasp, and C31—have been shown to mediate neurite retraction, synaptic inhibition, caspase activation, and programmed cell death [6, 10-12]; whereas, in contrast, the two peptides derived from the non-amyloidogenic processing of APP—sAPPα and αCTF—mediate neurite extension, and inhibit Aβ production, caspase activation, and programmed cell death [13-15]. Thus APP appears to function as a molecular switch, mediating plasticity-related processes, and AD is associated, whether causally or incidentally, with an increase in the ratio of the neurite-retractive peptides to the neurite-extending peptides. Reducing this ratio, whether by affecting BACE (β-site APP cleaving enzyme) or other cleavage of APP, appears to mitigate the AD severity [7, 16, 17].
Of particular interest for the development of a therapeutic program whose goal is to correct the hypothesized chronic synaptoblastic:synaptoclastic imbalance is the feedback mechanism: whereas homeostatic (negative) feedback is utilized by biological systems with single goal outcomes (e.g., serum pH) and no requirement for amplification, prionic loop (positive) feedback is utilized by biological systems with multi-goal outcomes and a requirement for rapid amplification (e.g., thrombus formation or, potentially, synapse modulation), and such systems therefore function as molecular switches [9]. In these latter systems, the positive feedback feature of the systems dictates that the molecular mediators involved, or a subset thereof, beget more of themselves, or enhance their own activities. Thus such amplifying systems are prionic, with the degree of infectivity depending on the stability of the molecular species involved. In the case of APP signaling, binding of a trophic ligand such as netrin-1 increases the production of sAPPα [18], which inhibits BACE cleavage [19], with the complementary fragment, αCTF, inhibiting γ-secretase cleavage [14]; thus cleavage at the α-site produces fragments that inhibit cleavage at the β-site and γ-site rather than feeding back to reduce α-site cleavage. Similarly, cleavage at the β-site and γ-site to produce Aβ feeds back positively to increase APP-C31 production [20], thus favoring the pro-AD, anti-trophic processing of APP. Moreover, Aβ itself has been shown to exhibit prionic properties [21], although the mechanism by which it does so has not been clarified.
Thus APP processing displays positive feedback, and therefore APP and its derivative peptides function as a molecular switch. This has critical implications for therapeutic development, since it offers a mechanism by which a threshold effect occurs. We have taken advantage of this phenomenon to develop drug candidates that increase the anti-AD, trophic APP signaling, while reducing the pro-AD, anti-trophic APP signaling [22] and enhancing cognition [23].
We have found that the manipulation of the plasticity balance that is mediated or reflected by the APP-derivative peptide balance (Fig. 1), whether genetically or pharmacologically, leads to predictable effects on learning and memory. Mutation of the caspase site at Asp664 inhibits the synaptic loss, memory deficits, and dentate gyral atrophy that otherwise occurs in the PDAPP transgenic mouse model of AD [7, 17, 24-26]. Furthermore, knock-in studies of a wild type mouse D664A support the notion that APP is indeed involved fundamentally in plasticity. (Kane, et al, unpublished data, 2014)
Systems biology and systems therapeutics of AD
The transgenic mouse studies suggest that APP signaling can be manipulated to inhibit AD pathophysiology. However, the mouse models feature mutations in APP or other familial AD-related genes such as presenilin-1, whereas the large majority of patients with AD suffer from sporadic AD, without an APP or PS1 mutation (although the majority do express the ε4 allele of ApoE). Given the many inputs to the APP signaling balance in humans (e.g., estrogen, netrin-1, Aβ, etc.), and the minimal success with each of many potentially therapeutic agents (e.g., estrogen, melatonin, exercise, vitamin D, curcumin, Ashwagandha, etc.), the pathobiology of AD dictates a system or program rather than a single targeted agent. Successes with other chronic illnesses such as cardiovascular disease, neoplasia, and HIV support the efficacy of multiple-component systems. My colleague and I have recently described such a system for AD [5]. The basic tenets for such a comprehensive therapeutic system are the following: 1) Just as for other chronic illnesses such as atherosclerotic cardiovascular disease, the goal is not simply to normalize metabolic parameters, but rather to optimize them. As an example, a serum homocysteine level of 12 μmol/l is considered to be within normal limits, but is well documented to be suboptimal [27]. Similar arguments can be made for many other metabolic parameters.
2) Based on the hypothesis that AD results from an imbalance in an extensive plasticity network, the therapy should address as many of the network components as possible, with the idea that a combination may create an effect that is more than the sum of the effects of many monotherapeutics [5].
3) Just as for other chronic illnesses such as osteoporosis, cancer, and cardiovascular disease, the underlying network features a threshold effect, such that, once enough of the network components have been impacted, the pathogenetic process would be halted or reversed. Therefore, even though it is not expected that most patients will be able to follow every single step of the protocol, as long as enough steps are followed to exceed the threshold, that should be sufficient.
4) The approach is personalized, based on the contributory laboratory values affecting the plasticity network; and is computationally intensive, since many physiological data points are analyzed, interdependent network-component status is assessed, and many interventions are prioritized to determine the therapeutic program.
5) The program is iterative, so that there is continued optimization over time.
6) For each network component, the goal is to address it in as physiological a way, and as far upstream, as possible.
Patient one: history
A 67-year-old woman presented with two years of progressive memory loss. She held a demanding job that involved preparing analytical reports and traveling widely, but found herself no longer able to analyze data or prepare the reports, and therefore was forced to consider quitting her job. She noted that when she would read, by the time she reached the bottom of a page she would have to start at the top once again, since she was unable to remember the material she had just read. She was no longer able to remember numbers, and had to write down even 4-digit numbers to remember them. She also began to have trouble navigating on the road: even on familiar roads, she would become lost trying to figure out where to enter or exit the road. She also noticed that she would mix up the names of her pets, and forget where the light switches were in her home of years.
Her mother had developed similar progressive cognitive decline beginning in her early 60s, had become severely demented, entered a nursing home, and died at approximately 80 years of age. When the patient consulted her physician about her problems, she was told that she had the same problem her mother had had, and that there was nothing he could do about it. He wrote "memory problems" in her chart, and therefore the patient was turned down in her application for long-term care.
After being informed that she had the same problem as her mother had had, she recalled the many years of her mother's decline in a nursing home. Knowing that there was still no effective treatment and subsequently losing the ability to purchase long-term care, she decided to commit suicide. She called a friend to commiserate, who suggested that she get on a plane and visit, and then referred her for evaluation.
She began System 1.0 (Table 1), and was able to adhere to some but not all of the protocol components. Nonetheless, after three months she noted that all of her symptoms had abated: she was able to navigate without problems, remember telephone numbers without difficulty, prepare reports and do all of her work without difficulty, read and retain information, and, overall, she became asymptomatic. She noted that her memory was now better than it had been in many years. On one occasion, she developed an acute viral illness, discontinued the program, and noticed a decline, which reversed when she reinstated the program. Two and one-half years later, now age 70, she remains asymptomatic and continues to work full-time.
Patient one: therapeutic program
As noted above, and following an extended discussion of the components of the therapeutic program, the patient began on some but not all of the system: (1) she eliminated all simple carbohydrates, leading to a weight loss of 20 pounds; (2) she eliminated gluten and processed food from her diet, and increased vegetables, fruits, and non-farmed fish; (3) in order to reduce stress, she began yoga, and ultimately became a yoga instructor; (4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day; [5] she took melatonin 0.5mg po qhs; (6) she increased her sleep from 4-5 hours per night to 7-8 hours per night; (7) she took methylcobalamin 1mg each day; (8) she took vitamin D3 2000IU each day; (9) she took fish oil 2000mg each day; (10) she took CoQ10 200mg each day; (11) she optimized her oral hygiene using an electric flosser and electric toothbrush; (12) following discussion with her primary care provider, she reinstated HRT (hormone replacement therapy) that had been discontinued following the WHI report in 2002; (13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime; (14) she exercised for a minimum of 30 minutes, 4-6 days per week.
Table 1. Therapeutic System 1.0
Rationale and References
Optimize diet: minimize simple CHO, minimize inflammation.
Patients given choice of several low glycemic, low inflammatory, low grain diets.
Minimize inflammation, minimize insulin resistance.
Enhance autophagy, ketogenesis
Fast 12 hr each night, including 3 hr prior to bedtime.
Reduce insulin levels, reduce Aβ.
Reduce stress
Personalized—yoga or meditation or music, etc.
Reduction of cortisol, CRF, stress axis.
Optimize sleep
8 hr sleep per night; melatonin 0.5mg po qhs; Trp 500mg po 3x/wk if awakening. Exclude sleep apnea.
30-60' per day, 4-6 days/wk
[37, 38]
Brain stimulation
Posit or related
Homocysteine <7 p="">
Me-B12, MTHF, P5P; TMG if necessary
Serum B12 >500
CRP <1 .0="" a="">1.5
Anti-inflammatory diet; curcumin; DHA/EPA; optimize hygiene
Critical role of inflammation in AD
Fasting insulin <7 hgba1c="" p="">
Diet as above
Type II diabetes-AD relationship
Hormone balance
Optimize fT3, fT4, E2, T, progesterone, pregnenolone, cortisol
[5, 42]
GI health
Repair if needed; prebiotics and probiotics
Avoid inflammation, autoimmunity
Reduction of Aβ
Curcumin, Ashwagandha
Cognitive enhancement
Bacopa monniera, MgT
[46, 47]
25OH-D3 = 50-100ng/ml
Vitamins D3, K2
Increase NGF
H. erinaceus or ALCAR
[49, 50]
Provide synaptic structural components
Citicoline, DHA
Optimize antioxidants
Mixed tocopherols and tocotrienols, Se, blueberries, NAC, ascorbate, α-lipoic acid
Optimize Zn:fCu ratio
Depends on values obtained
Ensure nocturnal oxygenation
Exclude or treat sleep apnea
Optimize mitochondrial function
CoQ or ubiquinol, α-lipoic acid, PQQ, NAC, ALCAR, Se, Zn, resveratrol, ascorbate, thiamine
Increase focus
Pantothenic acid
Acetylcholine synthesis requirement
Increase SirT1 function
Exclude heavy metal toxicity
Evaluate Hg, Pb, Cd; chelate if indicated
CNS effects of heavy metals
MCT effects
Coconut oil or Axona
CHO, carbohydrates; Hg, mercury; Pb, lead; Cd, cadmium; MCT, medium chain triglycerides; PQQ, polyquinoline quinone; NAC, N-acetyl cysteine; CoQ, coenzyme Q; ALCAR, acetyl-L-carnitine; DHA, docosahexaenoic acid; MgT, magnesium threonate; fT3, free triiodothyronine; fT4, free thyroxine; E2, estradiol; T, testosterone; Me-B12, methylcobalamin; MTHF, methyltetrahydrofolate; P5P, pyridoxal-5-phosphate; TMG, trimethylglycine; Trp, tryptophan
Patient two: history
A 69-year-old entrepreneur and professional man presented with 11 years of slowly progressive memory loss, which had accelerated over the past one or two years. In 2002, at the age of 58, he had been unable to recall the combination of the lock on his locker, and he felt that this was out of the ordinary for him. In 2003, he had FDG-PET (fluoro-deoxyglucose positron emission tomography), which was read as showing a pattern typical for early Alzheimer's disease, with reduced glucose utilization in the parietotemporal cortices bilaterally and left > right temporal lobes, but preserved utilization in the frontal lobes, occipital cortices, and basal ganglia. In 2003, 2007, and 2013, he had quantitative neuropsychological testing, which showed a reduction in CVLT (California Verbal Learning Test) from 84%ile to 1%ile, a Stroop color test at 16%ile, and auditory delayed memory at 13%ile. In 2013, he was found to be heterozygous for ApoE4 (3/4). He noted that he had progressive difficulty recognizing the faces at work (prosopagnosia), and had to have his assistants prompt him with the daily schedule. He also recalled an event during which he was several chapters into a book before he finally realized that it was a book he had read previously. In addition, he lost an ability he had had for most of his life: the ability to add columns of numbers rapidly in his head.
He had a homocysteine of 18 μmol/l, CRP <0 .5mg="" 0.58miu="" 1.27ng="" 1.3="" 120mcg="" 14mcg="" 165mg="" 24.9.="" 25-oh="" 25mg="" 28ng="" 3.02pg="" 47="" 5.4="" 610ng="" 64="" 6ng="" 78mcg="" 92="" a1c="" albumin:globulin="" am="" and="" bmi="" ceru-loplasmin="" cholecalciferol="" cholesterol="" copper="" cortisol="" dl="" free="" hdl="" hemoglobin="" l="" ldl="" lipitor="" ml="" of="" on="" p="" pregnenolone="" ratio="" serum="" t3="" t4="" testosterone="" triglyceride="" tsh="" zinc="">
He began on the therapeutic program, and after six months, his wife, co-workers, and he all noted improvement. He lost 10 pounds. He was able to recognize faces at work unlike before, was able to remember his daily schedule, and was able to function at work without difficulty. He was also noted to be quicker with his responses. His life-long ability to add columns of numbers rapidly in his head, which he had lost during his progressive cognitive decline, returned. His wife pointed out that, although he had clearly shown improvement, the more striking effect was that he had been accelerating in his decline over the prior year or two, and this had been completely halted.
Patient two: therapeutic program
The patient began on the following parts of the overall therapeutic system: (1) he fasted for a minimum of three hours between dinner and bedtime, and for a minimum of 12 hours between dinner and breakfast; (2) he eliminated simple carbohydrates and processed foods from his diet; (3) he increased consumption of vegetables and fruits, and limited consumption of fish to non-farmed, and meat to occasional grass-fed beef or organic chicken; (4) he took probiotics; (5) he took coconut oil i tsp bid; (6) he exercised strenuously, swimming 3-4 times per week, cycling twice per week, and running once per week; (7) he took melatonin 0.5mg po qhs, and tried to sleep as close to 8 hours per night as his schedule would allow; (8) he took herbs Bacopa monniera 250mg, Ashwagandha 500mg, and turmeric 400mg each day; (9) he took methylcobalamin 1mg, methyltetrahydrofolate 0.8mg, and pyridoxine-5-phosphate 50mg each day; (10) he took citicoline 500mg po bid; (11) he took vitamin C 1g per day, vitamin D3 5000IU per day, vitamin E 400IU per day, CoQ10 200mg per day, Zn picolinate 50mg per day, and α-lipoic acid 100mg per day; (12) he took DHA (docosahexaenoic acid) 320mg and EPA (eicosapentaenoic acid) 180mg per day.
Patient three: history
A 55-year-old attorney suffered progressively severe memory loss for four years. She accidentally left the stove on when she left her home on multiple occasions, and then returned, horrified to see that she had left it on once again. She would forget meetings, and agree to multiple meetings at the same time. Because of an inability to remember anything after a delay, she would record conversations, and she carried an iPad on which she took copious notes (but then forgot the password to unlock her iPad). She had been trying to learn Spanish as part of her job, but was unable to remember virtually anything new. She was unable to perform her job, and she sat her children down to explain to them that they could no longer take advantage of her poor memory, that instead they must understand that her memory loss was a serious problem. Her children noted that she frequently became lost in mid-sentence, that she was slow with responses, and that she frequently asked if they had followed up on something she thought she had asked them to do, when in fact she had never asked them to do the tasks to which she referred.
Her homocysteine was 9.8μmol/l, CRP 0.16mg/l, 25-OH cholecalciferol 46ng/ml, hemoglobin A1c 5.3%, pregnenolone 84ng/dl, DHEA 169ng/dl, estradiol 275pg/ml, progesterone 0.4ng/ml, insulin 2.7μIU/ml, AM cortisol 16.3mcg/dl, free T3 3.02pg/ml, free T4 1.32ng/l, and TSH 2.04mIU/l.
After five months on the therapeutic program, she noted that she no longer needed her iPad for notes, and no longer needed to record conversations. She was able to work once again, was able to learn Spanish, and began to learn a new legal specialty. Her children noted that she no longer became lost in mid-sentence, no longer thought she had asked them to do something that she had not asked, and answered their questions with normal rapidity and memory.
Patient three: therapeutic program
She began on the following parts of the therapeutic system: (1) she fasted for a minimum of three hours between dinner and bedtime, and for a minimum of 12 hours between dinner and breakfast; (2) she eliminated simple carbohydrates and processed foods from her diet; (3) she increased consumption of vegetables and fruits, limited consumption of fish to non-farmed, and did not eat meat; (4) she exercised 4-5 times per week; (5) she took melatonin 0.5mg po qhs, and tried to sleep as close to 8 hours per night as her schedule would allow; (6) she tried to reduce stress in her life with meditation and relaxation; (7) she took methylcobalamin 1mg 4x/wk and pyridoxine-5-phosphate 20mg each day; (8) she took citicoline 200mg each day; (9) she took vitamin D3 2000IU per day and CoQ10 200mg per day; (10) she took DHA 700mg and EPA 500mg bid; (11) her primary care provider prescribed bioidentical estradiol with estriol (BIEST), and progesterone; (12) her primary care provider worked with her to reduce her bupropion from 150mg per day to 150mg 3x/wk.
Table 2. Summary of patients treated with the therapeutic system described
History, evaluation
67F 3/3
2yr memory ?; FH+
Normal x 2.5 yrs; working
69M 4/3
12yr memory ⇓; FDG-PET+, NPsych+
Early AD
"Clearly improved;" working
70M 4/3
4yr memory ⇓; NPsych+, failed MemTrax
Improved; MemTrax passed
75M 3/3
1yr memory ⇓
Improved; working
75F C677T
1yr memory ⇓
aMCI/early AD
55F 3/3
4yr memory ⇓
aMCI/early AD
Normal; working
72M 3/3
7yr memory ⇓
Improved; working
55M 4/3
2yr memory ⇓
Normal; working
63F 4/3
FH dementia, mild memory ⇓
Normal, negative amyloid PET; working
60F 4/3
4yr rapid decline; MoCA 6, amyloid PET+
Late AD
F, female; M, male; 3/3, ApoE 3/3; 4/3, ApoE 4/3; C677T, the C677T mutation in methylene tetrahydrofolate reductase (MTHFR); FH, family history; aMCI, amnestic mild cognitive impairment; SCI, subjective cognitive impairment; FDG-PET+, fluorodeoxyglucose positron emission tomography interpreted as typical of Alzheimer?s disease; amyloid PET+, amyloid PET scan read as abnormal, indicative of amyloid accumulation; NPsych+, quantitative neuropsychology tests showing abnormalities typical of AD; MoCA, Montreal Cognitive Assessment; MemTrax, an iPhone application that quantitates memory.
All 10 patients are summarized in Table 2.
Results from the 10 patients reported here suggest that memory loss in patients with subjective cognitive impairment, mild cognitive impairment, and at least the early phase of Alzheimer's disease, may be reversed, and improvement sustained, with the therapeutic program described here. This is the first such demonstration. However, at the current time the results are anecdotal, and therefore a more extensive, controlled clinical trial is warranted.
The results reported here are compatible with the notion that metabolic status represents a crucial, and readily manipulable, determinant of plasticity, and in particular of the abnormal balance of plasticity exhibited in SCI, MCI, and early AD. Furthermore, whereas the normalization of a single metabolic parameter, such as vitamin D3, may exert only a modest effect on pathogenesis, the optimization of a comprehensive set of parameters, which together form a functional network, may have a much more significant effect on pathogenesis and thus on function.
The therapeutic system described in this report derives from basic studies of the role of APP signaling and proteolysis in plasticity, and the imbalance in this receptor proteolysis that reproducibly occurs in Alzheimer's disease. There are numerous physiological parameters that feed into this balance, such as hormones [28, 29], trophic factors [18], glucose metabolism [30], inflammatory mediators [31], ApoE genetic status [32] sleep-related factors [33], exercise-related factors [34], and many others; therefore, the therapeutic system is designed to reverse the self-reinforcing (i.e., prionic) signaling imbalance that we have hypothesized to mediate Alzheimer's disease pathophysiology [8].
One potentially critical result from the study is the impact of the therapeutic program on the ability of the various patients to work effectively. Six of the 10 patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. One additional patient had not had difficulty at work at the time of presentation, and has continued to work without difficulty. The other three patients had not worked for years, and did not begin again after treatment. The improvement in function that is required to work effectively after struggling due to cognitive decline is an important outcome of any successful therapeutic system, and is ultimately more critical to the patients than biomarker effects or test performance.
It is recognized that the system described here is an initial system, one that is likely to benefit from optimization. The system is designed to address multiple key pathogenetic mechanisms, but most of the key pathogenetic mechanisms are suboptimally affected by this initial system. This highlights multiple potential therapeutic targets, and optimizing the therapeutics for each of these targets is the goal of ongoing research and development.
It is noteworthy that the major side effect of this therapeutic system is improved health and optimal BMI (body mass index), a result in stark contrast to monopharmaceutical treatments. However, the program is not easy to follow, and none of the patients followed the entire protocol. The significant diet and lifestyle changes, and multiple pills required each day, were the two most common complaints of the patients. However, these complaints were mitigated by the fact that all of the patients had previously been made aware, either through their physicians or the media, that their prognosis was poor and their cognitive decline essentially untreatable.
One potentially important application of the therapeutic program described herein is that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system. Combination therapeutics have proven successful in multiple chronic illnesses, such as HIV and cancer [5].
The positive results reported here are perhaps not surprising given that therapeutic programs have proven more effective than monotherapeutics in multiple chronic illnesses, such as atherosclerotic cardiovascular disease, HIV, and cancer [5, 35]. Indeed, chronic illnesses may be more amenable to therapeutic systems than to monotherapeutics. However, the current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer's disease, and how long improvement can be sustained.
In summary:
•A novel, comprehensive, and personalized therapeutic system is described that is based on the underlying pathogenesis of Alzheimer's disease. The basic tenets for the development of this system are also described.
•Of the first 10 patients who utilized this program, including patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI), nine showed subjective or objective improvement.
•One potentially important outcome is that all six of the patients whose cognitive decline had a major impact on job performance were able to return to work or continue working without difficulty.
•These anecdotal results suggest the need for a controlled clinical trial of the therapeutic program.
I am grateful for support from the NIH (AG16570, AG034427 and AG036975), the Mary S. Easton Center for Alzheimer's Disease Research at UCLA, the Douglas and Ellen Rosenberg Foundation, the Stephen D. Bechtel, Jr. Foundation, the Joseph Drown Foundation, the Alzheimer's Association, the Accelerate Fund, the Buck Institute and Marin Community Foundation, the Michael and Catherine Podell Fund, Mr. Craig Johnson, and Ms. Michaela Hoag. I thank Dr. David Jones, Dr. Rammohan Rao, and Dr. Varghese John for discussions, and Rowena Abulencia for preparing the manuscript.
Conflict of interest statement
The author of this manuscript declares no conflict of interest.

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Lyme Disease on the Rise As Tick Epidemic Spreads Across the US

July 29, 2015 | 125,968 views

By Dr. Mercola
According to the Centers for Disease Control and Prevention (CDC),1 an estimated 300,000 Americans are diagnosed with Lyme disease each year, and the prevalence is rising.
Since national surveillance began in 1982, the number of annual Lyme cases reported has increased nearly 25-fold.2 The disease is also spreading out geographically.3
Between 1993 and 1997, 43 counties across the US had a high incidence of Lyme disease. By 2012, the number of hotspots had skyrocketed to 182. As reported by Time Magazine:4
“‘Lyme disease is not only becoming more rampant in its normal hotspot of the northeast United States, it’s spreading across the country,’ a new report5 from the Centers for Disease Control and Prevention warns.
 ‘Over time, the number of counties identified as having high incidence of Lyme disease in the northeastern states increased more than 320 percent,’ researchers write...
They also note that the disease is appearing in states where it has never been recorded before. One big reason why Lyme disease is spiking, according to the CDC report: climate change.”6
Eliminating Predators Have Allowed Lyme Disease to Spread and Become More Prevalent
While deer usually gets the blame for spreading tick-borne disease, rodents are actually the primary threat. According to Richard Ostfeld, a disease ecologist at a Lyme disease research center:7
“The resurgence of deer population is an overblown factor. Our research suggests that white-footed mice are more important numerically. Basically, mice are a fantastic host for both the tick and [the bacteria that causes Lyme].”
Ticks are not born with the Lyme spirochetes. It picks up the bacteria when feeding on an infected host.8 Ostfeld’s research indicates that white-footed mice infect 75-95 percent of larval ticks that feed on them, while deer only infect about one percent.
Urban sprawl and hunting has eliminated many of the mice’s natural predators, allowing populations to grow, and with them comes infected ticks. This year, ticks are epidemic in certain areas of the US, including Illinois.
The CDC has identified high-risk counties in 17 states, including Connecticut, Massachusetts, New Hampshire, Maine, Vermont, Pennsylvania, Virginia, New York, Iowa, Michigan, and Minnesota.
What Is Lyme Disease?
Lyme disease refers to illnesses transferred by biting or blood-sucking insects. The bacterium responsible for Lyme infection is Borrelia burgdorferi, 9 a “cousin” to the spirochete bacterium that causes syphilis.
Many still attribute transmission of Lyme disease exclusively to ticks (in the US, the black-legged deer tick, Ixodes scapularis; in Europe, the castor bean tick, I. ricinus.).10
But according to Dr. Dietrich Klinghardt — one the leading authorities on Lyme disease — the bacteria can also be spread by other biting or blood-sucking insects, including mosquitoes, spiders, fleas, and mites.
Common side effects of tick bites include an itchy “bull’s eye” rash, pain, fever, and inflammation.
However, you don’t have to get the hallmark “bull’s eye” as this rash occurs only in about half of those infected, so absence of such a rash does not exclude the possibility of a tick bite. Symptoms of Lyme disease typically start out with:
  • Unrelenting fatigue
  • Recurring fever
  • Headaches / migraines
  • Achy muscles and/or joints
If left untreated, the disease may progress to muscle spasms, loss of motor coordination, and even intermittent paralysis, meningitis, or heart problems. For a more complete list of symptoms, refer to the Tick-Borne Disease Alliance.11 has also created a printable Symptom Checklist.12
The B. burgdorferi spirocheteis shaped like a corkscrew, which allows it to burrow into and hide in a variety of your body’s tissues. It can also live intracellularly (inside your cells), which allows it to evade antibiotics.
For this reason, some doctors recommend giving antibiotics along with Plaquenil in order to change the intracellular pH.13 The organisms can also take up residence in biofilms, or in an encoated “cyst” form.
All of these different morphologies and clever evasion capabilities explain why Lyme infection can cause such wide-ranging multisystem involvement and why treatment is so difficult.
This also explains why recurrence of symptoms can still occur after standard antibiotic protocols. Complicating matters further, ticks can also infect you with a number of other disease-causing organisms, such as Bartonella, Rickettsia, Ehrlichia, and Babesia.
These organisms can travel with Borrelia burgdorferi (the causative agent of Lyme) and each organism causes a different set of symptoms. According to Dr. Klinghardt, many Lyme patients have one or more of these co-infections, which may or may not respond to any given treatment.
The Lyme bacterium has yet another stealthy survival mechanism. While most bacteria need iron to survive, the Lyme bacterium has adapted to survive without iron, using manganese instead.
This allows it to evade your body’s natural immune system defenses that destroy pathogens by cutting off their iron supply.14
Why Lab Tests Are Unreliable for Diagnosing Lyme Disease

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The simplest presentation of Lyme disease is the orthopedic forms, which typically affect the larger joints. When the microbes and the associated immune reactions are situated in the connective tissue, the infection presents as a “vague, dispersed pain,” which oftentimes ends up being misdiagnosed as fibromyalgia by conventional doctors. In fact, Lyme disease is notoriously difficult to diagnose, and doctors quite often get it wrong.15
Lyme is known as “the great imitator,” as it can mimic many other disorders, including multiple sclerosis (MS), arthritis, chronic fatigue syndrome, fibromyalgia, ALS, ADHD, and Alzheimer’s disease.16 When nothing unusual shows up on blood tests, some patients are even told their problems are “all in their head,” and may be referred to a psychologist.  
One of the reasons blood tests are so unreliable as indicators of Lyme infection is that the spirochete is capable of infecting your white blood cells. Lab tests rely on the normal function of these cells to produce the antibodies they measure. If your white cells are infected, they will not respond to an infection appropriately. Interestingly, the worse your Borrelia infection is, the less likely it will show up on a blood test.
In order for Lyme tests to be useful, you actually have to be treated first. Once your immune system begins to respond normally, only then will the antibodies show up on a blood test. This is called the “Lyme Paradox” — you have to be treated before a proper diagnosis can be made.
I recommend the specialized lab called IGeneX because they test for more outer surface proteins (bands), and can often detect Lyme while standard blood tests cannot. IGeneX also tests for a few strains of co-infections such as Babesia and Erhlichia. That said, a negative on the IGeneX test for these co-infections does not necessarily mean you are not infected, as there are many more strains than tests can currently detect.
The Controversy over Treatment for Chronic Lyme
While most doctors now acknowledge that Lyme disease is real, controversy still remains over whether or not Lyme can persist and become chronic — and if so, whether extended, long-term treatment with antibiotics is effective.17 Doctors who belong to the Infectious Disease Society of America (IDSA) do not believe in chronic Lyme and typically will not treat a Lyme patient beyond four weeks.
Doctors belonging to the International Lyme and Associated Diseases Society18 (ILADS), on the other hand, do believe Lyme can persist and are willing to treat you beyond the four- week period. Insurance companies typically will not pay for extended use of antibiotics though, as they follow the guidelines of the IDSA.
Personally, I find it baffling that physicians would deny the possibility of ongoing infection when these organisms are known to operate by stealth, and are capable of evading detection and most standard treatment protocols. I can tell you first hand, from my experience with my girlfriend Erin who was diagnosed with Lyme disease in 2013 after suffering from a range of hard-to-pin-down symptoms for 14 years, chronic Lyme does exist.
The good news is that no matter how long you’ve had it, there is hope for a full recovery. A new Lyme research center attached to the rheumatology division at Hopkins Bayview Medical Center has also been created, specifically to investigate chronic Lyme. As reported by BDN Maine News:19
“Dr. John Aucott, a leading Lyme researcher tapped to direct the Lyme Disease Clinical Research Center... said his new affiliation with Hopkins will bring fresh attention, and resources, to the issue. He and others will look to determine if the infection is hiding or, as he hypothesizes, is developing into a new disorder, possibly an autoimmune one like rheumatoid arthritis. He and others will explore if there is a genetic component, an underlying condition or other bacteria or viruses involved.”
Treatment Recommendations

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Total Video Length: 1:35:03

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I personally do not believe that long-term antibiotic treatment is a wise choice for most chronic Lyme sufferers. I recommend exhausting every natural alternative before resorting to long-term antibiotics as it will seriously impair your gut microbiome. They also leave you open to yeast or fungal co-infections, which are already common in the disease.
Eliminating the beneficial bacteria in your gut with antibiotics will also seriously impair your natural immune function, and may raise your risk of antibiotic-resistant infection, which could be life-threatening. A gentler solution to conventional antibiotics is the Nutramedix line of herbal antimicrobials. This was developed by one of my alternative medicine mentors, Dr. Lee Cowden, and is often termed the “Cowden Protocol.” 
It is not thought to cause resistance because this protocol cycles various herbal antimicrobials. The use of antifungals like fluconazole and nystatin may be appropriate and helpful when a secondary yeast infection is present. Ideally, you would focus on boosting your immune function with a healthy diet and antioxidants such as astaxanthin. A compounded drug called low-dose naltrexone (LDN), known to help your body fight harder, may also be beneficial. 
Below is a summary of Dr. Dietrich Klinghardt’s basic treatment strategies. For more comprehensive details on his full treatment protocol, please see this previous article: “Dr. Klinghardt's Treatment of Lyme Disease.” You can also visit Dr. Klinghardt’s website,20 where he posts his more current treatment protocols and recipes. In summary, there are five basic steps to his protocol:
  1. Evaluation of all external factors. External factors include electrosmog, EMF, microwave radiation from wireless technologies, and molds. (For more information on mold, see Ritchie Shoemaker’s website21).
  2. Remediation and mitigation of external factors. Once external factors have been assessed, they're remediated and mitigated. (Please refer to our previous article on mold remediation.) To mitigate microwave radiation, Dr. Klinghardt recommends shielding the outside of your home with a graphite paint called Y Shield. Inside, he uses a special silver-coated cloth for your curtains. Patients are instructed to remove all cordless telephones and turn off all the fuses at night, until they have recovered from Lyme disease.
  3. Addressing emotional issues. Emotional components of the disease are addressed using Energy Psychology tools, including psychokinesiology (PK), which is similar to the Emotional Freedom Technique (EFT), but more refined and advanced.
  4. Addressing parasitic, bacterial, and viral infections. Dr. Klinghardt addresses the parasites first, followed by the bacteria and the viruses. "The Klinghardt Antimicrobial Cocktail," which includes wormwood (artemisinin), phospholipids, vitamin C, and various herbs, is an integral part of this treatment. He addresses viral infections with Viressence (by BioPure), which is a tincture of Native American herbs.
  5. Addressing other lifestyle factors. Nutritional considerations and supplements are addressed.
Nutritional Supplements That May Be Useful in the Treatment of Lyme Disease
The following table lists a number of nutritional supplements found to be useful in the treatment of Lyme disease by those embracing natural methods.
Probiotics to improve immunity and restore microflora during and after antibiotics
Curcumin is helpful at reducing neurological toxins and brain swelling
Astaxanthin to neutralize toxins, improve vision, and relieve joint pain, common in Lyme
Whey protein concentrate may help with nutrition, often poor in Lyme patients who don’t feel well enough to eat properly
Grapefruit seed extract may treat the cyst form of Borrelia
Krill oil to reduce inflammation
Cilantro as a natural chelator for heavy metals
Serrapeptase helps to break biofilms
Resveratrol may treat Bartonella, a co-infection and also helps detoxification
GABA and melatonin to help with insomnia
Artemisinin and Andrographis, two herbs that may treat Babesia, a common co-infection
CoQ10 to support cardiac health and reduce muscle pain and brain fog
Quercetin reduces histamine (often high in Lyme)
Transfer factors can help boost immune function
Additional Resources
  • International Lyme and Associated Disease Society (ILADS)
  • Tick-Borne Disease Alliance (TBDA). Under the “Diagnosing TBDS” tab, you can find a listing of medical professionals knowledgeable in the treatment of Lyme
  • Lyme Disease Association, Inc.
  • Lyme disease expert Joseph J. Burrascano, MD, wrote what is essentially a manual for managing Lyme disease, entitled: Advanced Topics in Lyme Disease, which is worth adding to your resource files. Realize that his treatment focus is long-term antibiotics, which I believe should not be your first choice. Nevertheless, there is some good information there.
  • UNDER OUR SKIN. This film has changed the landscape of the Lyme epidemic, bringing unprecedented awareness in an engaging and accessible way. UNDER OUR SKIN exposes a hidden story of medical and scientific malfeasance and neglect. As official case numbers explode and hundreds of thousands of people around the world go undiagnosed or misdiagnosed, the film is as relevant and timely as ever.
Prevention 101
Considering how difficult it is to diagnose and treat Lyme disease, I strongly recommend taking preventive measures22 to prevent infection in the first place. This includes the following recommendations:
  • Avoid tick-infested areas, such as leaf piles around trees. Walk in the middle of trails, and avoid brushing against long grasses path edgings. Don’t sit on logs or wooden stumps.
  • Wear light-colored long pants and long sleeves, to make it easier to see the ticks.
  • Tuck your pants into socks, and wear closed shoes and a hat — especially if venturing out into wooded areas. Also tuck your shirt into your pants.
  • Ticks, especially nymphal ticks, are very tiny, so do a thorough tick check upon returning inside, and keep checking for several days following exposure. Also check your bedding for several days following exposure. Ticks must typically remain attached for at least 24 hours for the Lyme disease bacteria to be transmitted into your blood stream, so early removal is important.
  • If you have Japanese barberry on your property, you may want to consider getting rid of it. As noted in a recent Forbes article:23
  • “This popular shrub has pretty red color and is easy to grow — so much so that it is invasive, choking off native plants in its path. Deer favor native shrubs, leaving the thorny barberry alone.
    And the microclimate around the barberry also favors the tick’s reproduction and that of the white footed mouse, an intermediate host in the transmission cycle, resulting in an aptly described ‘tick nursery.’ So rid your property of barberry and go with native plants as much as possible.”
I do not recommend using chemical insect repellants directly on your skin as this will introduce toxins directly into your body. If you use them, spray them on the outside of your clothes, and avoid inhaling the spray fumes. The Environmental Protection Agency (EPA) has a list24 indicating the hourly protection limits for various repellents. Also beware of using toxic insect repellants on your pets. Misuse of Spot-On flea and tick products can be lethal. For safer alternatives, see Dr. Karen Becker’s recommendations.
If you find that a tick has latched on, it’s very important to remove it properly. For detailed instructions, please see’s Tick Removal page.25 Once removed, make sure you save the tick so that it can be tested for presence of pathogenic organisms.