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Brain Regeneration: Can Infrared Light Reverse Parkinson’s & Alzheimer’s?

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This article was written by Ali Le Vere at Greenmedinfo.com. It’s republished here with their permission. For more information from Greenmedinfo, you can sign up for the newsletter here.

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Contrary to conventional wisdom, brain regeneration is possible. One promising therapy that promotes neurogenesis and is effective in pre-clinical studies of Alzheimer’s and Parkinson’s is near infrared light therapy, and it may improve other mental illnesses and neurodegenerative disorders including dementia, stroke, ALS, and traumatic brain injury as well.

Alzheimer’s disease and Parkinson’s disease are the most common neurodegenerative disorders. The former is a type of dementia that occurs secondary to the accumulation of abnormal protein deposits in the brain, including β-amyloid plaques and intraneuronal neurofibrillary tangles made of tau protein (1). Upon neuroimaging studies, gross cerebral cortical atrophy is found, meaning that the part of the brain responsible for executive functions such as learning, memory, language, decision-making, and problem-solving progressively degenerates (1). In addition, gliosis, or brain inflammation, is a hallmark characteristic of Alzheimer’s (1).

One hypothesis that is championed proposes that Alzheimer’s occurs due to self-propagating, prion-like protein assemblies, which interfere with the function of nerve cells (2). An alternate theory is that these so-called proteinopathies occur secondary to a microvascular hemorrhage or brain bleed (3). The brain bleed is believed to be the result of age-induced degradation of cerebral capillaries, which creates neuron-killing protein plaques and tangles (3).

Dysfunction of mitochondria, the energy-generating powerhouses of the cell, is also implicated in Alzheimer’s, as reduced efficacy of these organelles creates oxidative stress-inducing reactive oxygen species, or free radicals, which lead to neuronal cell death (4). Whatever the cause, extensive death of brain cells occurs, which explains the cognitive deficits that occur with Alzheimer’s disease, in addition to symptoms such as impaired judgment, confusion, agitation, linguistic abnormalities, social withdrawal, and even hallucinations (1).

Parkinson’s disease, on the other hand, is characterized by progressive death of dopamine-producing neurons in a region of the brainstem called the substantial nigra, but it can extend to other brain areas such as the locus coeruleus, olfactory bulb, dorsal motor nucleus of the vagal nerve, and even the cortex in late stages (5). As a result, the primary manifestation is that dopamine deficiency appears in the basal ganglia, a set of nuclei embedded deep in the brain hemispheres that is responsible for motor control (6). This leads to the cardinal manifestation of Parkinson’s, namely, a movement disorder that includes bradykinesia or slow movement, loss of voluntary movement, muscular rigidity, and resting tremor (7).

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Not unlike what happens in Alzheimer’s, accumulation of abnormal intracellular protein aggregates known as Lewy bodies, composed of a protein called α-synuclein, is thought to be central to the pathogenesis of Parkinson’s disease (8). Like Alzheimer’s, mitochondrial dysfunction induced by genetic mutations, toxic agents, or damage to blood vessels is also considered to contribute to neuron cell death in Parkinson’s (9). Toxin exposure is especially implicated, as animal studies hint that development of Parkinson’s disease may occur as a byproduct of exposure to neurotoxins such as rotenone or paraquat (10). Impaired blood brain barrier function and damage to the endothelial cells of the vascular system, which line the interior surface of blood vessels, are also thought to play a role in Parkinson’s (10).

Overturning Old Notions of Neuroscience

The central dogma of neuroscience conceived of the central nervous system tissue as “perennial” after the doctrines of Giulio Bizzozero, the most prominent Italian histologist, who decreed that the lifelong cells of the nervous system were devoid of replicative potential (11). In other words, the perennial nature ascribed to the nerve cells of the brain and spinal cord meant that nerve cells were believed to be incapable of undergoing proliferation, or cell division, in the postnatal brain (11). While the early stage of in utero prenatal development known as embryogenesis permits massive neurogenesis, or the ability to create new nerve cells, the scientific consensus up until the end of the twentieth century held that neurogenesis was arrested after birth in mammals.

Santiago Ramon y Cajal, who led the charge in the neuroscience discipline in the later half of the nineteenth century onward and won a Nobel Prize for Medicine and Physiology, in fact stated that: “Once development was ended, the fonts of growth and regeneration of the axons and dendrites dried up irrevocably. In adult centers, the nerve paths are something fixed and immutable: everything may die, nothing may be regenerated” (11). Acknowledgment of the mere possibility of adult neurogenesis was hampered by the fact that scientists lacked the visualization techniques to detect neural stem cells, the precursors to new neurons and means by which neurogenesis occurs, and also did not have access to the molecular markers and microscopy required to observe cells in different cycle phases.

This view of nervous tissue as perennial was also reinforced by clinical observations that patients with chronic neurodegeneration, traumatic brain lesions, and cerebrovascular diseases do not experience functional recovery (11). Prevailing theories posited that adult neurogenesis was an evolutionary unlikelihood, since it would interfere with pre-existing neuronal connections and the fine-tuned electrochemical communication in the nervous system, as well as disrupt memory recall, which was believed to occur via stable neuronal circuits created and encoded during learning (11).

That brain cells are finite, and incapable of regeneration, painted a portrait of doom and gloom and inexorable debilitation for patients suffering from devastating neurodegenerative conditions. However, relatively recent discoveries have overturned these antiquated conceptions by revealing that the brain is plastic, or pliable, and that even neurons in adult higher vertebrates are capable of neurogenesis.

Scientists Discover Neural Regeneration is Possible

In the 1960s, these postulates of the old neurobiology were disproven when Joseph Altman and colleagues performed an experiment where radioactively labelled thymidine, one of the nucleotide base pairs that makes up DNA, was incorporated into a brain area called the dentate gyrus of the hippocampus and integrated into the genetic material of what was later confirmed via electron microscopy to be dividing neurons (12, 13). In essence, this illustrated that neurons were undergoing mitosis, a process of cell division where genetically identical daughter cells are created, and showed that adult neurogenesis is possible.

Another nail in the coffin of this antiquated perception of the nervous system was that neural stem cells, the multipotent, self-renewing progenitors from which new neurons arise, were found in the brains of adult mammals, and discovered to undergo expansion in their populations when prompted by signaling molecules called growth factors and morphogens (11). The multiplication and differentiation of neural stem cells, which are residents of the central nervous system, is essential for neurogenesis (14). Neural stem cells are capable of generating all of the cell types of the nervous system, including astrocytes, glial cells, and what are called oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system (11). Researchers Colucci-D’Amato and Bonita in fact state that, “To date neural stem cells have been isolated from nearly all areas of the embryonic brain and in a growing list of adult mammalian brain areas, including cerebellum and cortex” (11, p. 268).

Other advances, such as confocal microscopy and the identification of cellular markers which allowed the phenotype of cells to be characterized all culminated in the realization that neurogenesis occurs continuously in some brain area, such as the hippocampus and subventricolar zone (SVZ), the former of which is responsible for the formation and consolidation of memories (11). To date, neurogenesis has been shown to be influenced by various chemical, pharmacological, and environmental stimuli. For instance, work by researcher Fernando Nottebohm demonstrated the spontaneous replacement of neurons in the adult avian brain (15). In song birds such as canaries, which experience seasonal modification in their songs, new neurons are recruited into their neuronal circuitry in a way that may be dependent upon social and reproductive interactions, territorial defense, migratory patterns and food caching (15).

This all should serve as a beacon of hope for patients experiencing the ravages of neurodegenerative disease, as it may mean that epigenetics, or the way gene expression changes based on lifestyle factors, may lend itself to neurogenesis and the reversal of these scourges of mankind. For example, researchers state that an enriched environment, learning, exercise, exposure to different odorant molecules, and drugs such as antidepressants, steroids, and alcohol can all favorably or unfavorably impact neurogenesis  (11). These newfound revelations are being used in fact as an impetus to find cures for a laundry list of neurodegenerative diseases (11).

Novel Therapy Shown to Grow New Nerve Cells

Despite this research, the prevailing view of neurodegenerative diseases such as Alzheimer’s and Parkinson’s is that their underlying pathophysiology, a relentless progression of neuronal death, remains irreversible (10). Thus far, then, approaches have aimed to slow or stop neuronal cell death or to develop disease-modifying treatments that could stabilize the rate of neurodegeneration (10). One non-pharmacological therapy that may be able to actually regenerate brain cells, however, is light in the near infrared range, also known as low-level laser or light emitting diode (LED) therapy that utilizes wavelengths in the red to infrared spectrum.

Near infrared light therapy has the potential to “mitigate ubiquitous processes relating to cell damage and death,” and may have applications in conditions that “converge on common pathways of inflammation and oxidative stress” (10). This is demonstrated by the widespread efficacy of near infrared light therapy in improving conditions including traumatic brain injury, ischemic stroke, major depression, and age-related macular degeneration (10). In traumatic brain injury, for example, treatment with near infrared light improves social, interpersonal, and occupational functions, reduces symptoms of post-traumatic stress disorder (PTSD), and is helpful for sleep (16).

Because near infrared light treatment improves cognitive and emotional dimensions (17) and enhances short-term memory and measures of sustained attention (18), researchers have long suspected its potential for neuropsychological disorders. In a revolutionary publication, scientists propose that infrared light is superior to pharmacological standard of care for these debilitating conditions given its neuron-saving abilities (10).

For instance, in mouse models of traumatic brain injury, near infrared light increases levels of brain-derived neurotrophic factor (BDNF), a protein which helps dying nerve cells survive (19). In addition, infrared light both improves neurological performance and increases the numbers of neuroprogenitor cells, the precursors to new neurons, in areas of the brain such as the dentate gyrus of the hippocampus and the sub ventricular zone (20).

Near Infrared Light Therapy in Alzheimer’s and Parkinson’s

Although human trials have not been yet conducted in Alzheimer’s disease, mouse studies show that near infrared treatment reduces its characteristic proteinopathies, decreasing brain levels of β-amyloid plaques and neurofibrillary tangles of tau proteins, while also ameliorating cognitive deficits (10). Cellular energy production, as indicated by levels of ATP, were increased in these studies alongside bolstered mitochondrial function and (10). In transgenic mouse models of Alzheimer’s, application of non-thermal near infrared light reversed significant deficits in working memory and significantly improved cognitive performance (21).

In animal models of Parkinson’s, near infrared treatment has been shown to rescue dopaminergic neurons, the subset that degenerate in this condition, from death (10). In addition, near infrared light treatment corrects the abnormal firing activity of neurons in deep subthalamic brain regions that occurs in parkinsonian conditions (22). Various animal models of Parkinson’s disease shown improved motor control and locomotor activity, as measured by both mobility and velocity, after near infrared is applied (10).

In a macaque monkey model of Parkinson’s, an optical fiber device that administered near infrared to the midbrain largely prevented the development of clinical signs of Parkinson’s when the animals were injected with a chemical known to induce this disorder (23). It also preserved a greater number of dopaminergic nigral cells compared to the monkeys that had not received infrared treatment (23). Limited case reports in humans have shown that near infrared administered through an intranasal apparatus improves symptoms in the majority of Parkinson’s patients, and that its application to the back of the head and upper neck reduced signs of Parkinson’s in one patient (10). Other reports indicate that gait, speech, cognitive function, and freezing episodes were improved in late-stage Parkinson’s patients who undertook this therapy (24), but the study was low-quality (10).

Mechanism of Action: How Near Infrared Promotes Neurogenesis

The ways in which near infrared promotes neurogenesis are multi-fold. There is evidence that near infrared light exerts a hormetic effect, acting as an adaptive or positive stressor. Another example of a hormetic effect is that exhibited by phytonutrients in fruits and vegetables, which act as antioxidants by paradoxically stimulating oxidative damage via a pro-oxidant mechanism. This in turn up-regulates our endogenous antioxidant defense system. Similarly, near infrared light activates cellular stress response systems by targeting a key enzyme in the electron transport chain which is responsible for mitochondrial-based energy production called cytochrome c oxidase, an enzyme that is fundamental to the cellular bioenergetics of nerve cells (25).

By accepting light in the near infrared range of the electromagnetic spectrum, this enzyme induces a change in the electrochemical potential of the mitochondrial membrane, jump-starting production of the cellular energy currency called adenosine triphosphate (ATP) and causing a mild burst in the synthesis of reactive oxygen species (ROS) (10). As a result, downstream signaling pathways are triggered which induce reparative and neuroprotective mechanisms, including neurogenesis, the creation of new synapses, and brain-based antioxidant and metabolic effects (25).

Restoration of mitochondrial function in the endothelial cells lining cerebral blood vessels may also help neurons survive by repairing the blood-brain barrier and vascular network which is compromised in neurogenerative conditions (10). Impressively, “This modulation of multiple molecular systems appears capable of both conditioning neurons to resist future damage and accelerating repair of neurons damaged by a previous or continuing insult” (10).

On the other hand, the application of near infrared light has been shown to elicit systemic effects, possibly via circulating molecular factors (10). In other words, light in the near infrared spectrum applied to a local area elicits benefits in distal tissues remote from the initial site, perhaps by stimulating immune cells that have a neuroprotective role (10). Another way in which near infrared light activates global effects in the body is by up-regulating the production of signaling molecules known as anti-inflammatory cytokines, while down-regulating pro-inflammatory cytokines (26).

Near infrared also mobilizes tissue repair processes by improving the migration of white blood cells to wounds, increasing neovascularization, or the formation of new blood vessels, and facilitating formation of collagen (27). There is also evidence that near-infrared light exposure causes stem cells from the bone marrow to navigate to the site of damage and to release so-called trophic factors such as BDNF, which enhances nerve cell function and survival (28). Lastly, a system of communication between the mitochondria in the brain and the mitochondria in the tissues may be at play, so that application of near infrared light at a point in the body far from the brain can lead to neural regeneration (10).

Practical Application of Near Infrared Light Therapy

The key to mitigating the burden of chronic illness lies in physiological regeneration, which is emerging as a physiological inevitability, even in regions of the body where it was previously not thought possible. The ability to regenerate, secondary to normal biological processes of cellular erosion and decay, is programmed into our body in order for us to regain homeostasis.

So-called “photobiomodulation,” which includes near infrared light therapy, has limitless possible applications, and has even been shown to improve animal models of wound healing, heart attack, spinal cord injury, stroke, arthritis, familial amylotropic lateral sclerosis (FALS), diabetic ulcers, carpal tunnel syndrome, major depression, generalized anxiety disorder, frontotemporal dementia (29) and traumatic brain injury (27).

The biggest obstacle with infrared light therapy in neurodegenerative disease is targeting the zone of pathology, “when there are many intervening body tissues, namely skin, thick cranium, and meninges, and brain parenchyma,” since there is considerable dissipation of the signal across each millimeter of brain tissue (10). This is less problematic in Alzheimer’s, where the target regions are more superficial structures, but less easily rectified in the case of Parkinson’s, where there is significant distance from cranium to the brainstem where neurodegeneration takes place (10).

With Alzheimer’s, optimal delivery would be a near infrared light-emitting helmet worn over the entire cranium (10). Parkinson’s patients can achieve symptomatic relief when near infrared is applied in this fashion, as this would influence the abnormal neural circuitry in the cortex. However, to circumvent the problem of the sheer distance to the region of pathology in the brainstem, researchers propose that the minimally invasive surgical implantation of an optical fiber device near the brain parenchyma would be ideal, which would deliver therapeutic levels of near infrared (10). Until these options are commercially available, photobiomodulation devices or near infrared saunas may be a viable option, although human studies have not proved their efficacy.

Given its large margin of safety and lack of adverse effects, near infrared light therapy should be offered as an option for patients suffering from a myriad of chronic conditions, but is especially promising for neurodegenerative diseases including Alzheimer’s and Parkinson’s and may even have future use in multiple sclerosis. Near infrared therapy is superior to the mainstay drug treatments for these diseases since pre-clinical studies have demonstrated proof-of-concept that near infrared either arrests or slows the underlying pathology of these disease processes, and leads to the birth of new neurons, rather than merely mitigating symptoms (10).


References

1. Bird, T.D. (1998). Alzheimer disease overview. GeneReviews® [Internet]. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK1161/

2. Goedert, M. (2015). Alzheimer’s and Parkinson’s diseases: the prion concept in relation to assembled Aβ, tau, and α-synuclein. Science, 349, 1255555.

3. Stone, J. (2008). What initiates the formation of senile plaques? The origin of Alzheimer-like dementias in capillary haemorrhages. Medical Hypotheses, 71, 347–359.

4. Gonzalez-Lima, F., Barksdale B.R., & Rojas J.C. (2014). Mitochondrial respiration as a target for neuroprotection and cognitive enhancement. Biochemical Pharmacology, 88, 584–593. 10.1016/j.bcp.2013.11.010

5. Bergman, H., & Deuschl, G. (2002). Pathophysiology of Parkinson’s disease: from clinical neurology to basic neuroscience and back. Movement Disorders, 7(Suppl. 3), S28–S40.

6. Lanciego, J.L., Luquin, N., & Obeso, J.A. (2012). Functional Neuroanatomy of the Basal Ganglia. Cold Springs Harbor Perspectives in Medicine, 2(12), a009621.

7. De Virgilio, A. et al. (2016). Parkinson’s disease: Autoimmunity and neuroinflammation. Autoimmunity Reviews, 15(10), 1005-1011. doi: 10.1016/j.autrev.2016.07.022.

8. Gitler A.D. et al. (2009). Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity. Natural Genetics, 41, 308–315.

9. Exner, N. et al. (2012). Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences. EMBO Journal, 31, 3038–3062. 10.1038/emboj.2012.170

10. Johnstone, D.M. et al. (2015). Turning On Lights to Stop Neurodegeneration: The Potential of Near Infrared Light Therapy in Alzheimer’s and Parkinson’s Disease. Frontiers in Neuroscience, 9, 500. doi:  10.3389/fnins.2015.00500

11. Colucci-D’Amato, L., & Bonavita, V. (2006). The end of the central dogma of neurobiology: stem cells and neurogenesis in adult CNS. Neurological Science, 27(4), 266-270.

12. Altman, J. (1962). Are new neurons formed in the brains of adult mammals? Science, 135, 1127-1128.

13. Kaplan, M.S., & Hinds, J.W. (1977). Neurogenesis in the adult rat: electron microscopic analysis of light radioautographs. Science, 197, 1092-1094.

14. Martino, G. et al. (2011). Brain regeneration in physiology and pathology: the immune signature driving therapeutic plasticity of neural stem cells. Physiological Reviews, 91(4), 1281-1304.

15. Nottebohm, F. (2002). Why are some neurons replaced in adult brain? Journal of Neuroscience, 22(3), 624-628.

16. Naeser, M.A. et al. (2014). Significant improvements in cognitive performance post-transcranial, red/near-infrared light-emitting diode treatments in chronic, mild traumatic brain injury: open-protocol study. Journal of Neurotrauma, 31,(11), 1008-1017.  doi: 10.1089/neu.2013.3244.

17. Barrett, D.W., & Gonzalez-Lima, F. (2013). Transcranial infrared laser stimulation produces beneficial cognitive and emotional effects in humans. Neuroscience, 230, 13-23.  doi: 10.1016/j.neuroscience.2012.11.016.

18. Blanco, N.J., Maddox, W.T., & Gonzalez-Lima, F. (2015). Journal of Neuropsychology, 11(1),14-25. doi: 10.1111/jnp.12074.

19. Xuan, W. et al. (2013). Transcranial low-level laser therapy improves neurological performance in traumatic brain injury in mice: effect of treatment repetition regimen. PLoS ONE, 8, e53454.

20. Xuan, W. et al. (2014). Transcranial low-level laser therapy enhances learning, memory, and neuroprogenitor cells after traumatic brain injury in mice. Journal of Biomedical Optics, 191(10), 108003.

21. Michalikova, S. et al. (2008). Emotional responses and memory performance of middle-aged CD1 mice in a 3D maze: effects of low infrared light. Neurobiology of Learning and Memory, 89(4), 480-488.

22. Shaw, V.E. et al. (2012). Patterns of Cell Activity in the Subthalamic Region Associated with the Neuroprotective Action of Near-Infrared Light Treatment in MPTP-Treated Mice. Parkinsonian Disease, 2012, 29875. doi: 10.1155/2012/296875.

23. Darlot, F. et al. (2016). Near-infrared light is neuroprotective in a monkey model of Parkinson disease. Annals of Neurology, 79(1), 59-65. doi: 10.1002/ana.24542.

24. Maloney, R., Shanks, S., & Maloney J. (2010). The application of low-level laser therapy for the symptomatic care of late stage Parkinson’s disease: a non-controlled, non-randomized study. American Society of Laser Medicine and Surgery, 185.

25. Rojas, J.C., & Gonzalez-Lima, F. (2011). Low-level light therapy of the eye and brain. Eye and Brain, 3, 49–67.

26. Muili, K.A. et al. (2012). Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by photobiomodulation induced by 670 nm light. PLoS ONE, 7, e30655.

27. Chung, H. et al. (2012). The Nuts and Bolts of Low-level Laser (Light) Therapy. Annals of Biomedical Engineering, 40(2), 516-533.gma

28. Hou, S.T. et al. (2008). Permissive and Repulsive Cues and Signalling Pathways of Axonal Outgrowth and Regeneration. International Review of Cell and Molecular Biology, 267, 121-181.

29. Purushothuman, S. et al. (2013). The impact of near-infrared light on dopaminergic cell survival in a transgenic mouse model of parkinsonism. Brain Research, 1535, 61–70.

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Awareness

Long-Term Consequences of Mumps Vaccination: Many Unanswered Questions

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This is Part II of a two-part series on mumps. Part I discussed how mumps vaccination and the flawed mumps component of Merck’s MMR vaccine are fostering dangerous mumps outbreaks in adolescents and young adults.

It has been about five decades since the U.S. Food and Drug Administration (FDA) approved Merck’s first mumps vaccine. The company began launching combination MMR (measles, mumps and rubella) vaccines in the 1970s. Coincidentally—or not—an infertility crisis has been brewing over roughly the same time period, with dramatic declines in sperm counts and record-lowfertility levels. However, few investigators seem interested in assessing whether mumps outbreaks in highly vaccinated populations of teens and young adults could be having long-termeffects on fertility or other health indicators.

As described in Part I, childhood MMR vaccination has been an unmitigated disaster where mumps is concerned, deferring mumps infection to older ages and leaving adolescents and young adults vulnerable to serious reproductive complications. Public health reports show that the vast majority of mumps cases and outbreaks occur in youth who have been fully vaccinatedwith the prescribed two-dose MMR series, supporting a hypothesis of “waning immunity after the second dose.” FDA and Centers for Disease Control and Prevention (CDC) officials even admitthat mumps outbreaks in the post-vaccination era “typically involve young adults,” and that vaccination is failing to protect those who are college-age and above.

Myopically, many vaccine experts have called for a third MMR dose—or even “booster dosing throughout adulthood”—even though the FDA’s and CDC’s own research shows that MMR boosters in college-age youth barely last one year. As alleged in whistleblower lawsuits wending their way through the courts over the past eight years, Merck presented the FDA with a “falsely inflated efficacy rate” for the MMR’s mumps component, using animal antibodies and other fraudulent tactics to fool FDA—and the public—into believing that the vaccine was effective.

When infection arises after puberty, however, mumps is no laughing matter, presenting an increased risk of complications such as hearing loss, encephalitis and inflammation of the reproductive organs.

Mumps after puberty is no laughing matter

Around the time that the first mumps vaccine came on the market, the 1967 children’s classic The Great Brain humorously depicted mumps infection in childhood as a mere nuisance. The book’s young protagonist goes out of his way to intentionally infect himself with mumps so that he can beat his two brothers to the recovery finish line—and he experiences no adverse consequences other than his siblings’ annoyance.

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When infection arises after puberty, however, mumps is no laughing matter, presenting an increased risk of complications such as hearing loss, encephalitis and inflammation of the reproductive organs. About one in three postpubertal men with mumps develops orchitis(inflammation of the testes), which can damage sperm, affect testosterone production and contribute to subfertility and infertility. During a mumps outbreak in England in the mid-2000s, mumps orchitis accounted for 42% of all hospitalized mumps cases; the researchers attributed this outcome—which was the most common reason for hospitalization—to “the high attack rates in adolescents and young adults” that occurred “despite high coverage with two-dose MMR.” An analysis of a 2006 mumps outbreak in the U.S. reported that male patients were over three times more likely than female patients to experience complications, “due primarily to orchitis.”

An estimated 5% to 10% of postpubertal women will develop oophoritis (swelling of the ovaries) following mumps infection. Oophoritis is associated with premature menopause and infertility, but mumps-related oophoritis has garnered little notice.

Mumps infections are often asymptomatic or produce nonspecific symptoms such as fever, while cases of orchitis may present with no other mumps symptoms. Nonetheless, public health officials advise clinicians that orchitis is an instant cue to test for mumps virus, and testing often reveals elevated mumps antibodies. In a case report of MMR failure, British clinicians isolated a novel genetic strain of mumps virus from the patient’s semen two weeks after the onset of orchitis and found mumps RNA in the semen 40 days later; they also noted “the appearance of anti-sperm antibodies,” with “potential long-term adverse effects on the patient’s fertility.”

In 2017, researchers who reviewed 185 studies conducted in Western nations found that sperm counts had plummeted by 50% to 60% between 1973 and 2011—an average decrease of 1.4% annually. Commenting on this work, one analyst estimated that 20% to 30% of young men in Europe and North America have sperm concentrations associated with a reduced ability to father a child. Given estimates that as much as 40% of reproductive problems have to do with the male partner, there is agreement on the importance of “finding and eliminating [the] hidden culprits in the environment” that most researchers believe are to blame.

An estimated 5% to 10% of postpubertal women will develop oophoritis (swelling of the ovaries) following mumps infection. Oophoritis is associated with premature menopause and infertility, but mumps-related oophoritis has garnered little notice.

MMR’s and MMRV’s potential to impair fertility never studied

Merck has not evaluated either of its two MMR vaccines—the MMR-II and the MMR-plus-varicella (MMRV) vaccine—for their potential to impair fertility. Whether such testing would unearth direct effects on fertility (as appears to be possible with HPV vaccination in women) is thus unknown. However, mumps vaccination undeniably increases reproductive-age individuals’ risk of mumps infection and, in the process, increases the risk of fertility-altering complications. These facts alone should be attracting far more attention.

Unfortunately, because clinicians already tend to underdiagnose mumps infection and underestimate mumps complications, it is likely that they are failing to recognize possible vaccine-induced reproductive health consequences of mumps infection in their adolescent and young adult patients. In one university outbreak, “most physicians…did not suspect mumps,” and even when they became aware of the outbreak, “diagnosing mumps was not always straightforward.” Moreover, although differentiating between vaccine strains of mumps virus and wild types could provide valuable information, few clinicians have the capacity or inclination to perform testing of this type. A Japanese study of cerebrospinal fluid and saliva from patients with mumps complications found vaccine strain in nearly all of the samples and noted the information’s importance in helping determine whether the complications were vaccine-related.

Those who have sought to understand mumps vaccines’ poor performance point to a mixture of explanatory factors. These include waning immunity, the high population density and close quarters encountered in settings such as college campuses, incomplete vaccine-induced immunity to wild virus as well as viral evolution such that “the vaccine triggers a less potent reaction against today’s mumps viruses than those of 50 years ago.” However, some also quietly admit that individuals with “mild vaccine-modified disease” could be perpetuating the chain of transmission. This latter point ought to be raising questions about the logic and wisdom of administering further rounds of MMR boosters during outbreaks while ignoring the problems created by the doses already given.

… some individuals respond poorly to mumps vaccination and vaccine-induced antibody levels correlate poorly with protection from mumps infection, irrespective of the number of additional doses of mumps-containing vaccine they receive.

Most scientists appear to be either resigned to ongoing mumps outbreaks in vaccinated populations or actually accept periodic outbreaks as the cost of doing business. Publications by FDA and CDC researchers reveal these agencies’ awareness that some individuals respond poorly to mumps vaccination and that vaccine-induced antibody levels correlate poorly with protection from mumps infection, “irrespective of the number of additional doses of mumps-containing vaccine they receive.” Considering the effects on fertility, the generally abysmal track record of mumps vaccination and Merck’s fraudulent claims about efficacy, it is hard to fathom medical and public health experts’ complacency about current mumps vaccines and vaccine policies.


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Alternative News

Investigation Shows The MMR Vaccine Was Approved Based On Small Studies Showing Disturbing Results

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In Brief

  • The Facts:

    A FOIA request by Del Bigtree reveals that the 8 studies supporting the release of the MMR vaccine were only 6 weeks long, used only 800 children, and led to damaging respiratory and gastrointestinal illnesses to many of the children.

  • Reflect On:

    Are we ready to collectively deal with the implications of ongoing revelations of industry malfeasance with regards to vaccines that for some may require a shift in long-held beliefs?

Amidst a rash of efforts to bring forward mandatory vaccination in pockets of the United States is the recent move in New York City to declare a public health emergency Tuesday over a measles outbreak and order mandatory vaccinations in one neighborhood for people who may have been exposed to the virus.

Mayor Bill de Blasio announced the unusual order to address what he said was a measles “crisis” in Brooklyn’s Williamsburg section, where more than 250 people have gotten measles since September. The order applies to anyone living, working or going to school in four zip codes in the neighborhood. The declaration requires all unvaccinated people who may have been exposed to the virus to get the vaccine, including children over 6 months old. People who ignore the order could be fined $1,000.

Challenging Assumptions

This kind of invasive move gives rise to several serious questions, including challenging many of the assumptions that are necessarily made to justify such a move.

Assumption #1: People who may have been infected with the measles should get vaccinated immediately. De Blasio wants people who may have been infected with the measles to get vaccinated. The assumption here is that the vaccine would actually help someone who has the virus by preventing them from getting the measles or preventing them from spreading it to others. But this just doesn’t stand to reason. If someone is already infected, getting a measles vaccine will not prevent the outbreak. That’s not what a vaccine is designed for. And while the person is going through the 2-week period it takes for the vaccine to take hold, it’s quite possible that this will weaken the immune response to the actual measles infection the person has. Quarantining people suspected of being infected would be the sensible response, not vaccinating. If they happen to have the measles, no problem. Once they recover they will then be immune for life.

Assumption #2: The MMR Vaccine Can Create Herd Immunity. There is an article in the Huffington post entitled ‘I’m No Anti-Vaxxer, But the Measles Vaccine Can’t Prevent Outbreaks,’ in which Dr. Gregory Poland, who strongly advocates for vaccines, notes that outbreaks are often initiated and spread by people who have been fully vaccinated against the measles–over 50% in the case of a 2011 outbreak in Quebec. How is this possible? While this Quebec outbreak happened within a community that supposedly had achieved herd-immunity status of over 95% vaccinated, the facts are, as the article notes, that “9 per cent of children having two doses of the vaccine, as public health authorities now recommend, will have lost their immunity after just seven and a half years. As more time passes, more lose their immunity.” Therefore, herd immunity for measles is simply impossible to achieve with this vaccine.

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Assumption #3: The MMR Vaccine, in de Blasio’s words, is ‘safe, effective, and life-saving.’ The claim that the MMR vaccine is ‘life-saving’ does not stand up to simple statistics, as we detail in our article ‘Statistics Show The MMR Vaccine Kills More People Than The Measles Does.’ Whether it is effective, we have already seen that it is incapable of creating herd immunity, wanes over time, does not work at all for some people, and in some of the latest outbreaks the majority of people infected were fully vaccinated. Is it safe? This is the important question we cover in the next section.

The Studies That Stand Behind The Approval Of the MMR Vaccine

The pharmaceutical industry, as well as governmental regulatory bodies like the CDC and the FDA, assure the public that they take the safety of vaccines seriously, and that there is irrefutable science behind the notion that vaccines are safe in terms of the studies that their approval is based on.

However, a Freedom of Information Act request by Del Bigtree has revealed absolutely startling information about the studies that supported the approval of the MMR vaccines that have been injected into our children. To begin with, only 8 studies were conducted and the total combined number of children participating in the studies was only a little over 800! Furthermore, the studies only recorded symptoms for the first 6 weeks after the vaccines were given, unlike many other drug studies that follow symptoms for 5 years or more. And finally, the study revealed serious side-effects in those receiving the vaccine, including a highly significant number of participants who suffered upper respiratory illness and gastrointestinal illness, which has been linked to autism.

In our latest episode of The Collective Evolution Show on CETV, Joe, Arjun and I discussed New York’s mandatory vaccination order as well as Del Bigtree’s analysis of the MMR studies he received and the reason that Big Pharma not only does not want to do proper, large-scale studies on the safety of vaccines, but they also want to try to prevent other researchers like Dr. Christopher Exley from doing so as well.

You can watch the full episode of The Collective Evolution Show where we talk about this subject in more detail here.

You can go here to see the full episode of ‘The Highwire’ where Del Bigtree breaks down the MMR studies in question.

The Takeaway

The veils of illusion that have been masking the truth are lifting as our consciousness awakens. Transparency is coming, though how long it takes will depend on our continued efforts to dig for and spread the truth far and wide.

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Merck’s Julie Gerberding Wins Industry ‘Woman Of The Year’ Award For Putting Profits Ahead Of Human Health

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In Brief

  • The Facts:

    Julie Gerberding, the Healthcare Businesswomen’s Association 'Woman of the Year,' is a prime example of someone who has gone through the revolving door between government regulatory agencies and the corporations they are supposed to be regulating.

  • Reflect On:

    It is becoming clear that our authorities in government and business alike are making decisions purely for their own interests, in utter disregard for human safety and well-being. How does this realization play a role in our awakening?

If you are not already clear about how the Corporatocracy that we live in is able to consistently serve their own power and wealth interests at the expense of our heath, well-being and prosperity, then the case of Julie Gerberding should provide some excellent insight. Her career path makes her the poster child for people who want to succeed in the world by embracing the corrupt, deceitful system that is currently in place.

Here is the blueprint: first, become an expert in a very specific area through a good old fashioned Western education. Use the talent and intelligence you have been blessed with to move up the ranks in your chosen industry to gain a position of power within the highest government agency in your field. Work in close collaboration with the corporations you are supposed to be the watchdogs for, and display a particular talent to get away with murder, not only deflecting obvious conflicts of interest and preventing them from materializing into lawsuits, but also demonstrating a highly developed ability–and willingness–to garner public trust around the safety and effectiveness of the products being pushed by the corporations you are colluding with.

Julie Gerberding

Julie Gerberding completed her internship and residency in internal medicine at UCSF, where she also served as Chief Medical Resident before completing her fellowship in Clinical Pharmacology and Infectious Diseases. She earned an M.P.H. degree at the University of California, Berkeley in 1990.

Before becoming CDC Director and ATSDR Administrator, Gerberding was Acting Deputy Director of the National Center for Infectious Diseases (NCID). She joined CDC in 1998 as Director of the Division of Healthcare Quality Promotion, NCID, where she developed CDC’s patient safety initiatives and other programs to prevent infections, antimicrobial resistance, and medical errors in healthcare settings.

But it is perhaps her talent in knowing how to speak with quiet authority, and a persona that people felt they could trust, that not only helped her rise up in the ranks of the government’s regulatory bodies, but also made giants of the corporatocracy take notice and treat her as one of their own. Knowing how to appeal to people emotionally, with eloquence and persuasion, is something you cannot force, nor can you teach it. Some people just have that power. What they decide to do with it is another matter.

Less than a year after she resigned from her CDC post in in January 2009, she was hired as president of Merck’s vaccine division. Now we can look at the low-hanging fruit and remark that during her tenure at the CDC, Merck became the manufacturer of 14 of the 17 vaccines ‘recommended’ for children by the CDC, and 9 of the 10 vaccines ‘recommended’ for adults by the CDC. The conflict of interest here is beyond obvious, and one would be reasonable to assume that this appointment, which garnered over $5 million in stock options alone, amounted to payback for favors done to Merck while head of the CDC.

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But I believe Merck saw genuine value in the type of leadership Gerberding brought to the table: a cold and calculating devotion to the bottom line, covered over by a veneer of compassion-like-symptoms and a trustworthy tone of authority. In the pharmaceutical industry, these qualities are gold.

CNN Interview

During our bi-weekly broadcast on CETV, Joe Martino and I had a discussion about the ‘revolving door’ between government regulatory agencies and the corporations they serve. We look at statistics that would literally make your head spin about the hordes of people who have enjoyed the freedom to move from working on one side of the aisle to the other. Typically this pattern serves those willing to ‘play ball’ with corporate powers in their capacity as government regulators, to then be rewarded by the wealthy corporations with cushy jobs and board appointments.

In the case of Julie Gerberding, we dove deep into a CNN interview Gerberding did with Sanjay Gupta while she was at the CDC around the time that the Hannah Poling case was making headlines and getting widespread public attention. (Hannah Poling was the first child to receive money from the National Vaccine Injury Compensation Program for her vaccine injury; in essence, the government conceded that vaccines caused Hannah Poling’s autism). Big Pharma seemed to be in need of a reassuring voice directed at the public to prevent a massive exodus of parents from the growing vaccine schedules being lined up for their children.

Joe and I talked about the various techniques Gerberding uses to deftly move the conversation from a very vague ‘admission’ of what the government had conceded to assurances that all caring parents should continue to have their children vaccinated.

By some accounts, Julie Gerberding had a significant impact at this time in preventing a complete loss in confidence in vaccine safety, which would have been a major disaster for the pharmaceutical industry. Makes you wonder why she didn’t win the Healthcare Businesswomen’s Association ‘Woman of the Year’ award sooner.

The Takeaway

As difficult as it is for some of us to accept, the belief that those in authority have humanity’s best interests at heart has long run its course. It is an important part of our collective evolution that we realize we cannot count on our elected officials, corporate leaders, bureaucrats or other authority figures to make decisions that are in our best interests, because by and large we are seeing that they are only making decisions in their own interests, for the expansion and consolidation of their power. As individuals we must seek to become sovereigns, and as sovereigns to link together and awaken to our collective power to consciously create the type of world we really want to live in.

Help Support Collective Evolution

The demand for Collective Evolution's content is bigger than ever, except ad agencies and social media keep cutting our revenues. This is making it hard for us to continue.

In order to stay truly independent, we need your help. We are not going to put up paywalls on this website, as we want to get our info out far and wide. For as little as $3 a month, you can help keep CE alive!

SUPPORT CE HERE!

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