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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.

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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.

Dive Deeper

These days, it’s not just knowing information and facts that will create change, it’s changing ourselves, how we go about communicating, and re-assessing the underlying stories, ideas and beliefs that form our world. We have to practice these things if we truly want to change. At Collective Evolution and CETV, this is a big part of our mission.

Amongst 100's of hours of exclusive content, we have recently completed two short courses to help you become an effective changemaker, one called Profound Realization and the other called How To Do An Effective Media Detox.

Join CETV, engage with these courses and more here!

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Study: Weekly Use of Disinfectants Greatly Increases Your Risk of Fatal Lung Disease

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In Brief

  • The Facts:

    A 30-year study conducted by Harvard researchers and the French National Institute of Health and Medical Research found that people who use disinfectants once a week have a 22-32% increased chance of developing lung disease.

  • Reflect On:

    How reliable are regulatory agencies when it comes determining how safe the products we use for cleaning are for our health and environment? Did you know that there are a number of effective alternatives and products available out there?

Follow me on Instagram here. Make sure you follow Collective Evolution on Telegram as we have no idea how much longer we will be on Facebook.

What Happened: A 30-year study conducted by researchers at Harvard University alongside researchers at the French National Institute of Health and Medical Research (Inserm) found that regular use of bleach and other commonly used disinfectants can increase your chances of developing fatal lung disease. The study found that those who used these types of products just once a week had up to a 32% increased chance of developing the condition.

It’s called chronic obstructive pulmonary disease (COPD). Researchers looked at the incidence of the disease for the study in more than 55,000 nurses in the United States. Nurses were used for the study because they use disinfectants to clean surfaces on a regular basis. In this study population, 37 percent of nurses used disinfectants to clean surfaces on a weekly basis and 19 percent used them to clean medical instruments on a weekly basis.

In the UK alone, COPD is present approximately 1.2 million people. It includes various lung conditions like chronic bronchitis and emphysema. Obviously there are multiple factors that play a role, but according to this study, disinfectants are definitely one of them or at the very least, can’t be ruled out. Correlation may not mean causation but it’s safe to assume that breathing in these substances is not really safe, in my opinion, and can be detrimental to our health.

As far as deaths go, 25,000 people a year die from COPD in England. This number represents the third highest death rate from the disease. This study is thought to be the very first to identify such a link between COPD and specific cleaning products/chemicals known as “quaternary ammonium compounds (quats).”

To the best of our knowledge we are the first to report a link between disinfectants and COPD among healthcare workers, and to investigate specific chemicals that may underlie this association…Some of these disinfectants, such as bleach and quats, are frequently used in ordinary households, and the potential impact of domestic use of disinfectants on COPD development is unknown…Earlier studies have found a link between asthma and exposure to cleaning products and disinfectants at home, such as bleach and sprays, so it is important to investigate this further.- Inserm researcher Orianne Dumas (source)

The researchers analysed data from a mass study on female US nurses commenced by Harvard in 1989. In 2009, they looked at those who were still working as nurses who had no history of COPD and tracked them until May this year. During that period, 663 were diagnosed with the condition.

A follow up study published in 2019 examining more than 70,000 nurses came to the same conclusions.

We found that use of several specific disinfectants was associated with higher risk of COPD development; these included hypochlorite bleach (chlorine), hydrogen peroxide, alcohol, and quaternary ammonium compounds (commonly used for low-level disinfection of noncritical items, such as environmental surfaces) and glutaraldehyde (used for high-level disinfection). Several of these exposures often occurred concurrently, and disentangling the role of each product was challenging. When studying combinations of exposure to specific disinfectants, we found the highest risks of COPD incidence among nurses exposed to hypochlorite bleach or hydrogen peroxide and in those combining these exposures with exposure to aldehydes. Both the chemical properties of specific products and the greater number of products used could explain these elevated risks. Moreover, all of the agents that were associated with COPD incidence when evaluated separately have been described as airway irritants.

Why This Is Important: 

The everyday use of bleach currently has no specific health guidelines, and that’s very true with many other products as well. Cosmetics is a great example, that particular industry is not quite regulated as it should be, and products that do pass through federal health regulatory regulation and inspection are not always safe. Glyphosate is a great example, and there is a growing concern today among academics, journalists and everyday people regarding the close relationship between these regulatory agencies and the companies that manufacture these products. Sure they may work, but the case with many of these products is that there are alternatives that are just as effective and much more safer.

Whether it’s banking soda and vinegar, tea tree oil and lemons, or something else, the market and natural health stores are now filled with cleaning products that do not pose the same threat as mainstream conventional cleaning products. They’re not hard to find, all it takes is a simple internet search, or a trip to your local natural health food store. Many regular chains are also starting to carry more health and environmentally sound cleaning/disinfectant products as well. If you’re truly concerned and put effort into searching, you’ll have no problem finding these products.

Dive Deeper

These days, it’s not just knowing information and facts that will create change, it’s changing ourselves, how we go about communicating, and re-assessing the underlying stories, ideas and beliefs that form our world. We have to practice these things if we truly want to change. At Collective Evolution and CETV, this is a big part of our mission.

Amongst 100's of hours of exclusive content, we have recently completed two short courses to help you become an effective changemaker, one called Profound Realization and the other called How To Do An Effective Media Detox.

Join CETV, engage with these courses and more here!

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How Effective is The Covid-19 Vaccine?

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In Brief

  • The Facts:

    The 95% efficacy of the Pfizer vaccine is widely touted by the media and the medical establishment, but there are important questions to be asked about this claim.

  • Reflect On:

    Are we being given all information available from covid vaccine study to make informed decisions? Are the studies even being done in a way that represents what effects the vaccine may have on the whole population?

Are you going to decline the Covid-19 vaccine if it is offered to you? Why or why not? No matter how certain you are in your reasoning there will no doubt be someone else who feels exactly the opposite to you and will be just as certain of their position. We trust different sources of information, we have had different experiences with vaccines and we have different impressions of the threat of SARS-COV2 to us and our species.

I would suggest that those in the “vaccine cautionary” community would decline the vaccine based on their ideas around its potential risks. On the other hand, supporters of the vaccine are more likely to focus on its potential benefits. The debate has largely been centered around the disagreement people have about the risks. In this essay I will consider the uncertainty I and others have about its benefits.

Is the Medical Community biased about the Vaccine?

As a contributor to Collective Evolution I am well aware of the “cautionary” perspective on vaccinations and CDC directives. As a physician, I have a reasonable understanding of how those in the medical community regard the “best of what modern science has to offer”. I am part of a Physician group on social media where doctors can seek advice from each other around all matters Covid-19, from interesting cases to rare side effects to how to address special concerns raised by patients. It has been alarming to realize how unilateral the support of vaccination is in this community. 

I mean no disrespect to my medical colleagues. Many of those in this community have seen their patients die from this very real virus. They have had to struggle with the divergent directives coming from the CDC. They have had to work through many weeks where Personal Protective Equipment (PPE) was in short supply as their hospital wards rapidly reached capacity and overflowed. Now that the Pfizer and Moderna vaccines have met minimum requirements for efficacy under the Emergency Use Authorization (EUA), they are faced with yet another impediment to getting themselves and their patients through this pandemic: growing skepticism around the vaccine coming from the very same people they are endeavoring to help. Their frustration around the situation is understandable, but is it biasing them?

Before consenting to any intervention it is important to understand its relative risks and benefits. As I mentioned earlier, there has been much concern in the “vaccine cautionary” sphere about side-effects and deaths. Here I will take a closer look at what we know about the benefits of the vaccine based on Pfizer-Biontech’s  briefing document to the FDA’s Vaccines and Related Biological Products Advisory Committee. How confident can we be in the efficacy of the vaccine? Has the manufacturer done its due diligence in its analysis and in being transparent? These are the central questions that need to be answered.

Understanding False Positives and Negatives

There has been a lot of discussion about the rate of “false-positives” with regard to the Polymerase Chain Reaction (PCR) test for confirming infection with SARS-COV2. The PCR test can return a positive result even if only trace fragments of the virus are present. Fragments of the virus on a nasal swab is not necessarily representative of an active infection or transmissibility. Moreover the sensitivity of this test is dependent on the number of amplification cycles, or the cycle threshold (Ct), used.  The Ct is not standardized. It is not unreasonable to say that there will be a percentage of people who test positive that do not have the disease. Nevertheless, without a better test we as the public must treat all positive PCR tests as an indication of an infection. We must assume the test is right. The rate of false positives, whatever it is, is directly proportional to the overestimation of the prevalence of the disease. 

Here I would like to discuss the significance of “false-negatives”. These are people who get a negative PCR result but may still be infected. The rate of false negatives is directly proportional to the underestimation of disease prevalence. This aspect of the inaccuracy of our primary diagnostic test gets relatively little attention for practical reasons. If you are suffering symptoms consistent with Covid-19 but have a negative PCR test we assume that you have Covid-19 anyway. In other words, if someone is symptomatic we assume that the test is wrong, i.e. that it is a false-negative, and necessary measures are taken. We quarantine and isolate until we feel healthy again whether we have Covid-19 or not. 

Because we are in the midst of a pandemic we have no choice but to make these assumptions. We are responding appropriately given the limitations of the test. Because of the assumptions we are forced to make, we are exaggerating the prevalence of the disease and our response to it to some extent. It is the nature of the situation we are in.

How do we know that the Vaccine is 95% effective?

With this in mind I would like to discuss a post in the opinion blog of the British Medical Journal (BMJ) that appeared earlier this month. The author, Peter Doshi (PhD and Associate Editor at the BMJ), takes a rigorous look at the results reported by Pfizer regarding the efficacy of their mRNA vaccine. The success of their vaccine has been widely publicized to be 95%. Where exactly does this figure come from?

During the four weeks of observation (three weeks between 1st and 2nd dose followed by 7 days), 162 participants who received the placebo expressed symptoms of Covid-19 and tested positive by PCR. Compare that with only 8 in the group that received their experimental vaccine. The chance of getting Covid 19 after receiving the vaccine was about 20 times lower than if you got the placebo. This is the basis of the claim that their vaccine was 95% effective, well over the 50% threshold required for Emergency Use Authorization that allows their product to be deployed despite the fact that the two-year Phase III trial is still 20 months from completion.

How did Pfizer handle study participants in the “Suspected Covid-19” group?

It is less commonly known that of the nearly 38,000 participants in the Pfizer study, 3,410 fell into a group labeled “suspected Covid-19”. These are people who developed symptoms consistent with disease but tested negative by PCR. 1,594 of those in this group received the vaccine and 1,816 received the placebo. It should be quite clear that how we regard this much bigger group of symptomatic participants will have an enormous impact on the true efficacy of the vaccine. In other words, if we assume that the PCR test was accurate in all of these people and that they didn’t have Covid-19 and developed symptoms from another virus, the flu for example, then the vaccine would in fact be 95% effective as reported. On the other hand, if the PCR test was wrong every time and they all in fact had Covid-19, the efficacy of the vaccine would be much different: 1602 (1594 + 8) in the vaccine wing vs. 1978 (1816 + 162) in the placebo wing results in a vaccine efficacy of only 19%. 

The PCR test (like any test) can be wrong some of the time and right some of the time. No test is 100% accurate, however in this situation the accuracy of the PCR test has a very large impact on how we interpret the results of the vaccine trial. The true efficacy of the Pfizer vaccine can be known only if we know how many symptomatic people in each wing had Covid-19 despite testing negative by PCR.

It is likely that the percentage of false negatives are different in each arm. As the FDA briefing document on the Pfizer study and the BMJ piece correctly note, there should be fewer false negatives in the vaccine group. Why? It is because there is a greater chance of developing Covid-19 symptoms after receiving the vaccine compared to getting a placebo. Reactogenicity, or the acute response of the body to the vaccine, is common. Most of the acute inflammatory reaction to the vaccine occurs in the first seven days after receiving the vaccine. Looking more closely at the data, 409 patients in the vaccine group developed symptoms in the first seven days after inoculation. Compare this to 287 in the placebo group. If we assume that any participant who expressed symptoms in the first seven days must be suffering from the side effects of the vaccine or the placebo and not a new Covid-19 infection, the efficacy of the vaccine would still only be 29% if everyone else in that group was a false negative. This is admittedly a very large assumption but it is not outside the realm of possibility.

There are other more extreme possibilities. If all of the vaccinated participants who were suspected of Covid-19 truly did not have the disease and all of the unvaccinated (placebo) participants who were suspect did have the disease we would have a true miracle vaccine. Why? It would mean that only 8 people got the disease in the vaccinated group compared to 1978 in the placebo group. This would mean that the vaccine was approximately 99.6% effective. On the other hand, if all those who got vaccinated in the suspected group got Covid-19 and those who got the placebo didn’t, the vaccine would be not just ineffective, it would be dangerous.

Putting aside extreme and unlikely possibilities, the matter of the 3,412 “suspected Covid-19” participants and our assumptions about them still has very large implications. Let us say hypothetically that we as a nation decide to vaccinate our entire population with the Pfizer vaccine assuming that it has a 95% efficacy in preventing the disease. In other words, we are assuming that none of those “suspected” of having Covid-19 actually have the disease. This is in fact the assumption that the FDA is making when approving the use of the vaccine under the EUA. We can predict that within a month about 6.3% people will develop Covid-like symptoms from something other than vaccine reactogenicity or the disease itself. This is based on the number of participants who became symptomatic (from something other than reactogenicity) despite getting the vaccine and testing negative (1,185) divided by the total number who got the vaccine (18,801) = 0.063. That’s what happened in the study.

In a population of 300 million, we would expect roughly 19 million people to develop symptoms of Covid from something other than SARS-COV2 within a month. We can agree that we must be extremely confident about whether these 19 million people have the disease or not. Why would we assume they all don’t have Covid-19 when the vaccine trial itself considered them to be “suspected” of having it? We won’t. We shouldn’t, and practically speaking, we will be in the same situation we are in right now.

Pfizer either did not do or report additional testing that would have helped

The real issue here is that we shouldn’t be guessing about such important numbers. What do you suppose Pfizer did, knowing that this larger pool of symptomatic participants could have an enormous impact on the estimation of their vaccine’s efficacy? In my opinion, they should have tested everyone who developed symptoms for antibodies to help quantify the percentage of false negative PCR tests. If a participant felt like they were coming down with Covid-19 but had a negative PCR test, it seems clear that performing an antibody test would have offered additional clarity. This was either not done or not reported.

We must be careful when interpreting the power of a vaccine study. Although tens of thousands of people were enrolled, the only meaningful numbers with regard to efficacy have to do with those who contracted the disease during the period of observation. This is the only way to assess the efficacy of the vaccine. When Pfizer only considers participants that became symptomatic and tested positive we only have a group of 170 cases to cross compare.

The 3,410 people who became symptomatic but tested negative during the four weeks of observation would represent a much larger set of cohorts and would amplify the power of the study 20 fold if infection could be confirmed or ruled out through additional testing. In other words, the 3,410 symptomatic people should be the ones that Pfizer were hoping would emerge when they enrolled 37,000+ individuals in their study. I find this lapse in diligence suspicious and at the very least inexplicable, especially in light of the latitude they are granted under the EUA. The fact of the matter is that we do not know if this was done. Pfizer, per their own protocol, will not make this data available until the trial is completed 20 months from now. 

Why didn’t Pfizer look harder?

This forces us to ask some sobering questions. If Pfizer is required (or has agreed) to make all data available in two years, would they have conducted antibody tests on the “suspected Covid” group? If those results told a different story it would be quite damning, if not now, eventually. Their product would not be permitted for use under the EUA if a 50% efficacy requirement could not be met. On the other hand, if antibody tests were conducted and the results confirmed the impressive efficacy of the vaccine, why wouldn’t they have made the data available right now?

It should be clear that if Pfizer’s primary goal was to obtain approval under the EUA they would have had little incentive to do further testing to confirm their product’s efficacy. Why would they take the risk of seeking more information on 3,400 participants that could potentially overturn their results that were based on only 170 outcomes? This is where we must be very careful in our assessment of the situation. If you believe Pfizer and vaccine manufacturers are only out for profit, it would be easy to conclude that they are being manipulative. If you believe that these corporations are seeking to improve public health and safety you may grant them a lot of latitude here. To be truly objective we must ask if they have been scientific in their approach.

At the very least I feel that they have not been diligent, and their position hints at disingenuousness: Pfizer didn’t mention this group of participants in their 92 page report or in their publication in the New England Journal of Medicine. This group was only mentioned in two paragraphs of a 53 page briefing to the Vaccines and Related Biological Products Advisory Committee (VRBPAC) of the FDA submitted December 10, 2020. The FDA, an agency of the department of Health and Human Services that ostensibly serves to protect the public by ensuring the safety of drugs, biological products and medical devices, continues to remain silent around this issue.

The Take Away

The 95% efficacy of the Pfizer vaccine is widely touted by the media and the medical establishment. Why didn’t Pfizer test or report the testing of an enormously important group of participants in their trial? We can predict that without these additional tests deploying the vaccine will not change our behavior nor our attitude to this pandemic.

Dive Deeper

These days, it’s not just knowing information and facts that will create change, it’s changing ourselves, how we go about communicating, and re-assessing the underlying stories, ideas and beliefs that form our world. We have to practice these things if we truly want to change. At Collective Evolution and CETV, this is a big part of our mission.

Amongst 100's of hours of exclusive content, we have recently completed two short courses to help you become an effective changemaker, one called Profound Realization and the other called How To Do An Effective Media Detox.

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Alternative News

Norway Investigates 29 Deaths in Elderly Patients After Pfizer Covid-19 Vaccination

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In Brief

  • The Facts:

    Norway has registered a total of 29 deaths among people over the age of 75 who’ve had their first Covid-19 vaccination shot, raising questions over which groups to target in national inoculation programs.

  • Reflect On:

    Should freedom of choice always remain here? Should governments and private institutions not be allowed to mandate this vaccine in order to have access to certain rights and freedoms?

What Happened: 29 patients who were quite old and frail have died following their first dose of the Pfizer COVID-19 vaccination. As a result, Norwegian officials have since adjusted their advice on who should get the COVID-19 vaccine.

This doesn’t come as a surprise to many given the fact that the clinical trials were conducted with people who are healthy. Older and sick people with co-morbidities were not used in the trials, and people with severe allergies and other diseases that can make one more susceptible to vaccine injury were not used either. It can be confusing given the fact that vaccination is being encouraged for the elderly in nursing homes and those who are more vulnerable to COVID-19.

Steinar Madsen, medical director of the Norwegian Medicines Agency (NOMA), told the British Medical Journal (BMJ) that “There is no certain connection between these deaths and the vaccine.”

On the 15th of January it was 23 deaths, Bloomberg is now reporting that a total of 29 deaths among people over the age of 75 who’ve had their first COVID-19 shot. They point out that “Until Friday, Pfizer/BioNTech was the only vaccine available in Norway”, stating that the Norwegian Medicines Agency told them that as a result “all deaths are thus linked to this vaccine.”

“There are 13 deaths that have been assessed, and we are aware of another 16 deaths that are currently being assessed,” the agency said. All the reported deaths related to “elderly people with serious basic disorders,” it said. “Most people have experienced the expected side effects of the vaccine, such as nausea and vomiting, fever, local reactions at the injection site, and worsening of their underlying condition.”

Madsen also told the BMJ that,

There is a possibility that these common adverse reactions, that are not dangerous in fitter, younger patients and are not unusual with vaccines, may aggravate underlying disease in the elderly. We are not alarmed or worried about this, because these are very rare occurrences and they occurred in very frail patients with very serious disease. We are not asking for doctors to continue with vaccination, but to carry out extra evaluation of very sick people whose underlying condition might be aggravated by it. This evaluation includes discussing the risks and benefits of vaccination with the patient and their families to decide whether or not vaccination is the best course.

The BMJ article goes on to point out that the Paul Ehrlich Institute in Germany is also investigating 10 deaths shortly after COVID-19 vaccination, and closes with the following information:

In a statement, Pfizer said, “Pfizer and BioNTech are aware of reported deaths following administration of BNT162b2. We are working with NOMA to gather all the relevant information.

“Norwegian authorities have prioritised the immunisation of residents in nursing homes, most of whom are very elderly with underlying medical conditions and some of whom are terminally ill. NOMA confirm the number of incidents so far is not alarming, and in line with expectations. All reported deaths will be thoroughly evaluated by NOMA to determine if these incidents are related to the vaccine. The Norwegian government will also consider adjusting their vaccination instructions to take the patients’ health into more consideration.

“Our immediate thoughts are with the bereaved families.”

Vaccine Hesitancy is Growing Among Healthcare Workers: Vaccine hesitancy is growing all over the globe, one of the latest examples comes from Riverside County, California. It has a population of approximately 2.4 million, and about 50 percent of healthcare workers in the county are refusing to take the COVID-19 vaccine despite the fact that they have top priority and access to it.  At Providence Holy Cross Medical Center in Mission Hills, one in five frontline nurses and doctors have declined the shot. Roughly 20% to 40% of L.A. County’s frontline workers who were offered the vaccine did the same, according to county public health officials. You can read more about that story here.

Vaccine hesitancy among physicians and academics is nothing new. To illustrate this I often point to a conference held at the end of 2019 put on by the World Health Organization (WHO). At the conference, Dr. Heidi Larson a Professor of Anthropology and the Risk and Decision Scientist Director at the Vaccine Confidence Project Emphasized this point, having  stated,

The other thing that’s a trend, and an issue, is not just confidence in providers but confidence of health care providers. We have a very wobbly health professional frontline that is starting to question vaccines and the safety of vaccines. That’s a huge problem, because to this day any study I’ve seen…still, the most trusted person on any study I’ve seen globally is the health care provider.

A study published in the journal EbioMedicine  as far back as 2013 outlines this point, among many others.

Pfizer’s Questionable History:  Losing faith in “big pharma” does not come without good reason. For example, in 2010 Robert G. Evans, PhD, Centre for Health Services and Policy Research Emeritus Professor, Vancouver School of Economics, UBC, published a paper that’s accessible in PubMed titled “Tough on Crime? Pfizer and the CIHR.”

In it, he outlines the fact that,

Pfizer has been a “habitual offender,” persistently engaging in illegal and corrupt marketing practices, bribing physicians and suppressing adverse trial results. Since 2002 the company and its subsidiaries have been assessed $3 billion in criminal convictions, civil penalties and jury awards. The 2.3-billion settlement…set a new record for both criminal fines and total penalties. A link with Pfizer might well advance the commercialization of Canadian research.

Suppressing clinical trial results is something I’ve come across multiple times with several different medicines. Five years ago I wrote about how big pharma did not share adverse reactions people had and harmful results from their clinical trials for commonly used antidepressant drugs.

Even scientists from within federal these health regulatory agencies have been sounding the alarm. For example, a few years ago more than a dozen scientists from within the CDC put out an anonymous public statement detailing the influence corporations have on government policies. They were referred to as the  Spider Papers.

The Takeaway: Given the fact that everything is not black and white, especially when it comes to vaccine safety, do we really want to give government health agencies and/or private institutions the right to enforce mandatory vaccination requirements when their efficacy have been called into question? Should people have the freedom of choice? It’s a subject that has many people polarized in their beliefs, but at the end of the day the sharing of information, opinion and evidence should not be shut down, discouraged, ridiculed or censored.

In a day and age where more people are starting to see our planet in a completely different light, one which has more and more questioning the human experience and why we live the way we do it seems the ‘crack down’ on free thought gets tighter and tighter. Do we really want to live in a world where we lose the right to choose what we do with our own body, or one where certain rights and freedoms are taken away if we don’t comply? The next question is, what do we do about it? Those who are in a position to enforce these measures must, it seems, have a shift in consciousness and refuse to implement them. There doesn’t seem to be a clear cut answer, but there is no doubt that we are currently going through that possible process, we are living in it.

Dive Deeper

These days, it’s not just knowing information and facts that will create change, it’s changing ourselves, how we go about communicating, and re-assessing the underlying stories, ideas and beliefs that form our world. We have to practice these things if we truly want to change. At Collective Evolution and CETV, this is a big part of our mission.

Amongst 100's of hours of exclusive content, we have recently completed two short courses to help you become an effective changemaker, one called Profound Realization and the other called How To Do An Effective Media Detox.

Join CETV, engage with these courses and more here!

Continue Reading
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