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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

Cancer is Now the Leading Cause of Death

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In Brief

  • The Facts:

    Cancer has surpassed heart disease as the No. 1 cause of death in high-income countries, highlighting the urgent need to change the way this disease is prevented and treated.

  • Reflect On:

    Rather than being a random result of DNA mutations, it's possible that cancer could have much deeper roots that would be better targeted with natural therapies than toxicity.

This article was written by the Greenmedinfo Research Group, originally published by Greenmedinfo.com. Published here with permission. 

Cancer has dethroned heart disease to earn the nefarious title of leading cause of death in high-income and certain middle-income countries.[i] While heart disease remains the No. 1 cause of death globally among adults aged 35 to 70, in high-income countries, which included Saudi Arabia, United Arab Emirates, Canada and Sweden, cancer caused twice as many deaths as heart disease.[ii]

Some middle-income countries, which included the Philippines, Iran, South Africa, Colombia, China, Brazil, Malaysia, Turkey, Poland, Argentina and Chile, also saw cancer become the leading cause of death.

While the U.S. was not included in the new analysis, research published in 2018 suggested, “the United States is in the midst of an epidemiologic transition in the leading cause of death,” moving from heart disease to cancer.[iii]

That study, too, found that cancer was quickly outpacing heart disease as the top killer, with high-income counties transitioning first. In fact, while only 21% of U.S. counties had cancer as the leading cause of death in 2003, this rose to 41% in 2015.

“The shift to cancer as the leading cause of death was greatest in the highest-income counties,” the researchers explained,[iv] echoing the current study, which also cited “a transition in the predominant causes of deaths in middle-age” in high-income countries.[v]

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“The world is witnessing a new epidemiologic transition among the different categories of noncommunicable diseases, with CVD [cardiovascular disease] no longer the leading cause of death in HIC [high-income countries],” lead author Dr. Gilles Dagenais, professor emeritus, Laval University, Quebec, Canada, said in a statement.[vi]

Why is Cancer a Top Killer?

The study suggested cancer is rising to the top because heart disease is better treated in high-income countries, saving more lives from heart disease and paving the way for cancer deaths to flourish. But perhaps a better question is why cancer continues to kill so many.

Even globally, cancer still comes in as the second leading cause of death behind heart disease, responsible for 26% of deaths worldwide.[vii] In the U.S., Americans have a 1 in 3 risk of developing cancer at some point in their lifetimes, along with a 1 in 5 risk of dying from the disease.[viii]

In early 2019, it was announced that cancer death rates in the U.S. declined 27% since 1991,[ix] a statistic that makes it seem as though we’re winning the “war on cancer.” But most of these declines can be attributed to reductions in smoking — and perhaps a limited measure of increased early detection and treatment — and are not a sign that conventional medicine’s model of surgerychemotherapy and/or radiation to treat cancer is, on the whole, working.

While death rates from certain cancer have declined, others have increased. Overall, cancer deaths in the U.S. in 2016 were similar to those in 1930[x] — despite all the “advances” in detection and treatment.

Changing the Way We Think About Cancer

It’s becoming increasingly clear that in order to conquer cancer, it’s necessary to change the way we think about it. Cancer is found in virtually all animals, suggesting it has evolutionary significance.[xi] It’s possible that cancer is an ancient survival program unmasked — even a process the body undergoes in order to survive nutrient deprivation and exposure to toxins.

Rather than being the result of an accumulation of DNA mutations that create rogue cells that multiply out of control, cancer could be cells that have flipped an epigenetic switch into survival mode in the form of a tumor. In the journal Physical Biology, researchers theorized:[xii]

“[C]ancer is an atavistic [primitive] condition that occurs when genetic or epigenetic malfunction unlocks an ancient ‘toolkit’ of pre-existing adaptations, re-establishing the dominance of an earlier layer of genes that controlled loose-knit colonies of only partially differentiated cells, similar to tumors.”

If this is true, it makes sense that conventional cancer treatments aimed to poison or “kill” the cancerous cells may only make the problem worse by creating an even more toxic environment, which could trigger the cancer to reach back into its “ancient toolkit” to find additional means of survival.

This explanation may be overly simplistic, as there are many factors that contribute to cancer, but there is evidence to suggest that natural substances and therapies that support the body’s overall health can be useful in the fight against cancer.

Nearly 1,000 Natural Substances Have Anti-Cancer Potential

GreenMedInfo has a database of 986 substances that have been researched as potential cancer prevention and treatment strategies. There are undoubtedly many more out there that have yet to be discovered. At the top of the list is curcumin, the active ingredient in the curry spice turmeric, which targets cancer stem cells while leaving normal stem cells unharmed.[xiii]

Another top contender is vitamin D, which you can get for free from adequate sun exposure. Higher vitamin D levels are not only known to lower your cancer risk but also to improve outcomes if you’ve already been diagnosed.[xiv] Fiberresveratrolsulforaphane and vitamin E — all substances you can get from your diet — also show anti-cancer promise, as does coffee, perhaps because it improves the body’s ability to efficiently repair DNA damage.[xv]

So if there was one silver lining to the news that cancer is now the leading cause of death in some countries, it would be that it’s a condition that has many promising natural avenues for prevention and treatment. Current conventional cancer treatments are failing, but that doesn’t mean cancer is unstoppable — it means it’s time to broaden our research into and usage of traditional therapies.

Many natural substances, like noni leaf,[xvi] have even been shown to work better than chemotherapy, highlighting why, if we’re going to win the war against cancer, we’re going to need to do it with nature on our side.

For more on how to naturally fight Cancer, visit the GreenMedInfo database on the subject.

Originally published: 2019-09-14

Article Updated: 2019-11-05

References

[i] The Lancet September 3, 2019

[ii] CNN September 3, 2019

[iii] Annals of Internal Medicine December 18, 2018

[iv] Annals of Internal Medicine December 18, 2018

[v] The Lancet September 3, 2019

[vi] Medscape September 3, 2019

[vii] Medscape September 3, 2019

[viii] American Cancer Society, Lifetime Risk of Developing or Dying From Cancer

[ix] CA: A Cancer Journal for Clinicians January 8, 2019

[x] CA: A Cancer Journal for Clinicians January 8, 2019

[xi] Front. Oncol., 10 January 2019

[xii] Physical Biology February 7, 2011

[xiii] Anticancer Res. 2015 Feb ;35(2):599-614.

[xiv] Br J Cancer. 2017 Mar 16. Epub 2017 Mar 16.

[xv] J Nutrigenet Nutrigenomics. 2015 ;8(4-6):174-84.

[xvi] Mol Cell Biochem. 2016 Apr 22. Epub 2016 Apr 22.


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Awareness

Man Fasts For 382 Days Straight & Loses 276 Pounds

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In Brief

  • The Facts:

    Angus Barbieri, a man who, in June of 1965, began a fast under medical supervision for exactly 382 days. He remained completely healthy for the duration of the fast.

  • Reflect On:

    Today, it's firmly established in scientific literature that fasting can have tremendous benefits, if done correctly. It can also be used to treat a variety of diseases. Perhaps it's not emphasized because you can't make money off of not eating?

A study published in the Post Graduate Medical Journal in 1972 brought more attention to a gentleman by the name of Angus Barbieri, a man who, in June of 1965, began a fast under medical supervision for exactly 382 days and, at the time the study was published, had since maintained his ordinary weight. In his case, “prolonged fasting had no ill effects.” Barbieri’s weight decreased from 456 to 180 pounds during the fast.

This isn’t the only example that’s available in the literature, it’s similar to an earlier patient prior to Barbieri who reduced his weight from 432 to 235 pounds during 350 days of intermittent fasting (Stewart, Fleming & Robertson, 1966). Researchers have also fasted patients for 256 days (Collison, 1967, 1971), 249 and 236 days (Thomson et al., 1966) as well as  210 days (Garnett et al., 1969; Runcie & Thomson, 1970), all of which are cited in the 1972 study.

Since the publication of this time, there are many documented examples of prolonged fasting done by highly obese people. Here’s one recent example of a man who fasted for 50 straight days, while being medically supervised and tested the whole time.

When you fast, your body switches from burning glucose, to burning fat. Fasting lowers insulin levels which allows the body to access its fat stores for energy. When you eat, food is converted into glucose and that’s what we usually burn. This is why fasting has become a therapeutic intervention for many people with type two diabetes, and more doctors, like Dr. Jason Fung, a Toronto Based nephrologist, are having great success with utilizing fasting as an appropriate and necessary health intervention. Fung has many great articles regarding the science of fasting, you can access them here if you’re interested in learning more. This article references some of the leading scientists in the field so you can learn more by looking them up as well.

The graph below depicts what happens to your protein while fasting. Interesting isn’t it? People often believe that if you fast, you will experience a tremendous amount of muscle loss during fasting, but that’s simply not true. This graph is from Kevin Hall, from the NIH in the book “Comparative Physiology of Fasting, Starvation, and Food Limitation.”

“It seems that there are always concerns about loss of muscle mass during fasting. I never get away from this question. No matter how many times I answer it, somebody always asks, “Doesn’t fasting burn your muscle?” Let me say straight up, NO.”  – source Dr. Jason Fung

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But what about Angus Barbieri? Obviously we’re not saying long term fasts for this long are healthy, obviously for many people they will probably be unhealthy and unsafe unless medically supervised. In  the 1972 study doctors measured a number of concentrations within the body. For example, plasma potassium concentrations over the first four months decreased systematically. As a result, they provided a very small daily dose that increased his potassium level. After another 10 weeks, no potassium was given, and from there on in until the end of the fast, plasma potassium levels remained normal. Cholesterol concentrations also remained around 230 mg/ 100 ml until 300 days of fasting, but increased to 370 mg/100 ml during refeeding.

Plasma magnesium levels decreased over the first few weeks of the fast but then went up and stabilized. This is interesting to note as there is nothing going into the body, yet levels still stabilized after the initial decrease.

Normal plasma magnesium concentrations, despite magnesium ‘depletion’ in muscle tissue, have been described (Drenick et al., 1969) during short-term fasting (1-3 months). The only other relevant report is a remark (Runcie & Thomson, 1970) that one patient who fasted 71 days had a normal plasma magnesium level of 2-2 mEq/l at the time when she developed latent tetany. The decrease in the plasma magnesium concentration of our patient was systematic and persistent.

Furthermore:

The excretion of sodium, potassium, calcium and inorganic phosphate decreased to low levels throughout the first 100 days, but thereafter the excretion of all four urinary constituents, as well as of magnesium, began to increase. During the subsequent 200 days sodium excretion, previously between 2 and 20 mEq daily, reached over 80 mEq/24 hr, potassium excretion increased to 30-40 mEq daily and calcium excretion increased from 10-30 mg/24 hr to 250- 280 mg/24 hr. Magnesium excretion (which was not measured during the first 100 days) reached 10 mEq/ 24 hr between Days 200-300. Phosphate excretion, which had decreased to under 200 mg/24 hr, also increased to around 800 mg/24 hr, even exceeding 1000 mg/24 hr on occasion. Peak excretions of all these constituents were seen around Day 300, after which there was a marginal decrease, but excretion remained high.

Obviously, this is an extreme fast and such fasts have only been tested on people of tremendous obesity, and it shows that people with a high body fat percentage have the ability to fast longer simply because their body has more stores to pull from.

The study concluded in 1972 that:

We have found, like Munro and colleagues (1970), that prolonged supervised therapeutic starvation of the obese patient can be a safe therapy, which is also effective if the ideal weight is reached. There is, however, likely to be occasionally a risk in some individuals, attributable to failures in different aspects of the adaptative response to fasting. Until the characteristics of these variations in response are identified, and shown to be capable of detection in their prodromal stages, extended starvation therapy must be used cautiously. In our view, unless unusual hypokalaemia is seen, potassium supplements are not mandatory. Xanthine oxidase inhibitors (or uricosuric agents) are not always necessary and could even be potentially harmful (British Medical Journal, 1971) perhaps particularly in the long-term fasting situation.

It’s almost 2020, and the literature, studies and research that’s been published since 1972 is vast. We’ve learned a lot more about it and if done correctly it can be extremely beneficial. Shot term fasting  presents minimal to no health risks, and so does long term fasting that lasts more than 24 hours, that is unless a person already has an underlying condition. That being said, it’s not easy to start. Most people are used to eating three meals plus snacks every single day, therefore they are never adapted to burning their fat stores, something that appears the human body was meant to do.

“Why is it that the normal diet is three meals a day plus snacks? It isn’t that it’s the healthiest eating pattern, now that’s my opinion but I think there is a lot of evidence to support that. There are a lot of pressures to have that eating pattern, there’s a lot of money involved. The food industry — are they going to make money from skipping breakfast like I did today? No, they’re going to lose money. If people fast, the food industry loses money. What about the pharmaceutical industries? What if people do some intermittent fasting, exercise periodically and are very healthy, is the pharmaceutical industry going to make any money on healthy people?” – Mark Mattson (source)

Fasting has also been shown to be effective as a therapeutic intervention for cancer. Fasting protects healthy cells while ‘starving’ cancer cells, it’s now being used as an intervention that’s being combined with chemotherapy. Fasting has also been shown to greatly reduce the risk of age related diseases like Parkinson’s Disease, and Alzheimer’s disease. Mark Mattson, one of the foremost researchers of the cellular and molecular mechanisms underlying multiple neurodegenerative disorders has shown through his work that fasting can have a tremendous effect on the brain, and can even reverse the symptoms of multiple neurodegenerative disorders. You can watch his interesting TED talk here.  Scientists have also discovered strong evidence that fasting is a natural intervention for triggering stem cell-based regeneration of an entire organ or system.

Fasting has actually long been known to have an effect on the brain. Children who suffer from epileptic seizures have fewer of them when placed on caloric restriction or fasts. It is believed that fasting helps kick-start protective measures that help counteract the overexcited signals that epileptic brains often exhibit.  (source)

The list goes on and is quite long. At the end of the day if you do your research, fasting, under proper medical supervision, can have tremendous health benefits that go far beyond what’s mentioned in the paragraph above. Every single study that has looked at fasting as a therapeutic intervention for several diseases has shown nothing but positive benefits. Even studies conducted regarding caloric restriction, something completely different than fasting, have shown promising results in all animal models.

According to a review of fasting literature conducted in 2003, “Calorie restriction (CR) extends life span and retards age-related chronic diseases in a variety of species, including rats, mice, fish, flies, worms, and yeast. The mechanism or mechanisms through which this occurs are unclear.” Since this study was published, a great amount of research has been conducted from many researchers, and the mechanisms are being discovered and have become more clear. If you want to further your research, apart from the names listed above, Dr. Valter Longo and his research is another great place to start.

The body has a tremendous amount of storage, and it hangs on to what it needs during a fast, and uses up ‘bad’ things, repairs damaged cells, and more. When you fast and deplete all your glycogen, your body is going to start using fat for energy, it’s going to use damaged cells for energy, it’s basically going to use all of the bad things first, before it gets to the good thing…Your body will not burn protein, as protein is not a fuel source while fasting.

I bring this up because it’s interesting to see what the body loses and hangs on to during a fast.

The Takeaway

The truth about fasting is that it’s not dangerous at all. Intermittent fasting and short term fasting can be done by just about anybody. From what we’ve seen with regards to prolonged fasting, it’s also not very dangerous when it comes to obese people doing it under medically supervised conditions. Theoretically, based on the science alone, any relatively healthy human being should be able to do a prolonged fast without any harmful consequences.

Obviously, prolonged fasts that are not medically supervised can be very detrimental. We are obviously not recommending this and you must do a lot of research and talk to your doctor if you’re interested in fasting, before trying it. For starters, a little bit of intermittent fasting here and there is a no brainer, and not dangerous at all if you have no underlying health conditions, but everybody’s body is different.

Fasting is making a lot of noise, and has been making a lot of noise within the health community, but it’s still not appropriately taught and used by the mainstream medical industry. Why is this so? The answer is simple, you can’t make money off of fasting.

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America’s Largest Milk Producer Files For Bankruptcy – Cow’s Milk Is Inhumane & Unhealthy

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Image by Erich Westendarp from Pixabay

In Brief

  • The Facts:

    Dean foods, the largest milk producer in the United States has filed for bankruptcy.

  • Reflect On:

    Independent media and activists around the world do have the ability to make change, and this is one of many examples. The world is waking up, even in the face of massive censorship of information. We are more powerful than we know.

Dean Foods, the largest milk company in the United States has recently filed for bankruptcy. The reason? Because Americans, and people all of the world for that matter, are not drinking as much cow’s milk as they used to. Brands that seem to be growing and having success are the ones who are now offering dairy free options.  Oat milk, for example, saw U.S. sales rise 636% to more than $52 million over the past year, according to Nielsen data. Sales of cow’s milk dropped 2.4% in that same time frame.

Chief Executive Officer, Eric Beringause stated: “We continue to be impacted by a challenging operating environment marked by continuing declines in consumer milk consumption.” He’s right, the demand for cow’s milk has dropped nearly 50 percent since 1975.

So, why are people doing this? Well, it’s happening for a number of reasons. First of all, the industry is full of animal cruelty. Cow’s are forcefully impregnated so they can produce milk, and their babies are taken from them for beef so the milk can be drained from the cow so humans can drink it. This causes tremendous heartache. Cows are living in poor conditions where they constantly suffer both emotionally and physically. Furthermore, they can often be abused by workers, but the conditions they live in on factory farms is already seen as abusive to many.

Not only are we starting to become aware that our milk-drinking habit is one of the most cruel industries that exists on Earth,  we are realizing waking up to the fact that 80 percent of the Amazon rainforest destruction is the result of grazing animals for meat and dairy production. It’s one of the main sources of environmental degradation and pollution on our planet. It is destroying our Earth, and the waste is polluting our environment and waterways at an alarming rate. 90 percent of soy used, which is also creating massive amounts of deforestation, is used for animal feed, not humans. So, animal product consumption is clearly the biggest factor when it comes to deforestation and environmental degradation, yet there doesn’t seem to be enough emphasis put on it like there is for C02. Why?

When it comes to the health aspects, I remember being in shock when I came to the realization that we were the only animal on the planet who drank the milk of another animal. Furthermore, we are the only species on the planet that drinks milk after weaning.

There are multiple studies showing that drinking milk from a cow leads to an increased mortality rate and actually makes bones more prone to fracturing, not less. One example would be this giant study from researchers at Uppsala University in Sweden. How ironic is this given the fact that milk has always been marketed to humans as necessary from strong bone health?  Calcium is available in high quantities in a number of planet, how come we weren’t marketed with that?

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One thing milk protein does is trigger metabolic acidosis. This happens when the body produces too much acid and becomes very acidic, which can be caused by multiple things, including the absorption of casein found in animal protein. Casein makes up almost 90 percent of the protein in a cow’s milk. When the body experiences this type of acidosis, it actually forces the body to compensate by leaching calcium from the bones to help neutralize the increased acidity. This became known to me through the work of Dr. Colin Campbell, an American biochemist who specializes in the effect of nutrition on long term health. He is the Jacob Gould Schurman Professor Emeritus of Nutritional Biochemistry at Cornell University. Scholars like Campbell are vital to the world, because they are among the few who actually examine and study nutrition and health, something that our modern day medical industry completely ignores. You can watch a video of him explaining, here.

Dr. Campbell also discovered that animal protein (casein) can accelerate and “turn on” cancer, while plant based protein has the opposite effect. You can read more about that and which him explain in this article.

If we look at all other animals who don’t consume the milk of another animal or after weaning, it is because they do not have the enzymes to break down the sugar found in milk. We are no different, and this explains why in some ethnic populations around the world, lactose intolerance is present in 90 percent of the population. A staggering 70 percent of the world’s population has some degree of lactose intolerance.

Humans actually never had this enzyme, and to digest the sugar in cow’s milk, we had to develop the LTC gene, which was acquired by mutation. This is the lactase gene, which allows us to process lactose as adults. Clearly, we are not doing what is natural and in accordance with our bodies. I first came across this information from Katherine S. Pollard, a PhD at the University of California, San Francisco, in this lecture.

That being said, some people might have evolved and developed on cows milk just fine, which is why this information may not apply to everybody but overall, it definitely appears we are doing something unnatural.

More doctors are waking up, The Physicians Committee for Responsible Medicine (PCRM) recently submitted a citizen petition with the Food and Drug Administration (FDA) to change labeling on cheese to include a cancer warning.

The petition states:

High-fat dairy products, such as cheese, are associated with an increased risk for breast cancer. Components in dairy such as insulin-like growth factor (IGF-1) and other growth hormones may be among the reasons for the increased risk for cancer.

To ensure that Americans understand the potential significant risks, and resulting long-term costs, of consuming dairy cheese products, the FDA should ensure that the notice above is prominently placed on product packaging and labeling for all dairy cheese products.

The list goes on and on, what’s presented in this article is simply a tidbit with regards to why big milk is going out of business. People are waking up.

When it comes to health and cruelty, it’s not just dairy, it’s also meat-eating as well. It’s very in-humane, not all that healthy, and is also destroying our planet.

You can read this article for more information about that: Another Study Suggests That Human Beings Are Not Designed To Eat Meat

The Takeaway

It’s great to see the dairy industry forcing to transition, although there is still a long way to go, it’s quite clear through the efforts of various forms of activism around the world that more people are becoming more empathetic, compassionate, and caring about our treatment of animals and the planet. These are qualities our world certainly needs more of. In conjunction with  the massive amount of animal cruelty that’s being exposed, awareness with regards to the health and environmental consequences of consuming dairy are also skyrocketing.

We are more powerful than we know, and at any time, if we come together, we can change the game big time.

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