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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

22 Out Of 25 Popular Burger Chains Just Failed Their Antibiotic Use Report

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In Brief

  • The Facts:

    A recent study was done examining how well top fast food chains actually implemented their antibiotic use policies in their beef. 22 of 25 failed including McDonald's, Sonic, Burger King and In-N-Out.

  • Reflect On:

    Do you still eat fast food? If so, why do you find yourself doing so? What healthier choices can be made instead? If we want to see a healthier world, population and animal kingdom, we have to choose what we support more wisely.

The modern-day food industry seems to pay no attention to health. Thankfully, global consciousness is shifting in several ways including how we live as humans, view our health, our economy, education, politics, and the environment. You could say that humanity is going through one MASSIVE change.

Today, billions of animals in the United States alone are raised, tortured, and slaughtered for human consumption. This reckless production and consumption, in turn, has created enormous environmental and health problems that continue to accelerate. That being said, awareness on this issue (food) in particular, has come along way. We are seeing changes in the food guide, a shift towards plant-based diets, and more corporations catering to new choices people are making around food and health. This is a good thing!

One common trend helping to create change is the continues ‘bad press’ unhealthy players in the food industry are getting.

The latest news to come out regarding food quality within fast food comes from a report recently released by six major consumer and environmental groups. They graded America’s 25 largest burger chains and their use of antibiotics in their beef supply.

22 popular fast food restaurants completely failed, including giants like McDonald’s, Burger King, Sonic and In-N-Out.  The evaluation looked at each chain’s antibiotic use policies and whether these policies were truly implemented in their product. They also examined how transparent the chains were with their antibiotic use.

The Problem With Antibiotic Use

Antibiotics given to farm animals can lead to antibiotic-resistant bacteria, among other things. This is actually one of the top threats to global public health, which is exemplified by the fact that each year, more than 2 million Americans alone suffer from these infections.

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In September 1999, Albrecht and Schutte published “Homeopathy Versus Antibiotics in Metaphylaxis of Infectious Diseases: A Clinical Study in Pig Fattening and Its Significance to Consumers” in Alternative Therapies. The study compared outcomes for four randomly assigned groups of pigs that were given placebo, homeopathic treatment, a standard blend of antibiotics and other conventional drugs in a routine low prophylactic dose, or conventional drugs in a high therapeutic dose.

There were 1440 pigs involved in the study, which took place at an intensive livestock farm in Germany. The primary outcome measured was the incidence of respiratory disease, a common problem for pigs on such farms.

The results were astounding.

Homeopathic treatment was far superior to prophylactic doses of antibiotics in preventing respiratory disease. The prophylactic antibiotic treatment made it only 11 percent less likely (than placebo) that the pigs would become sick. But homeopathic remedies made it 40 percent less likely. When the antibiotics were raised to therapeutic levels, meaning a level that is only given when people or an animal was sick, it became 70 percent less likely that the pigs would become diseased.

The significance of this is that homeopathic treatment on animals would already be better than routine antibiotic treatment. When an animal is actually sick, the farmer would then have the choice to increase homeopathic or use a legitimately high-level dose of antibiotics. This, significantly less cost and significantly fewer antibiotics in meat.

The List

The Takeaway

Simple, avoid fast food. There are many out there who seem to believe that people will always consume this food, but we fail to recognize that it’s not just our choice. The “food” these corporations offer is highly addictive to people, and that’s done on purpose.

If we can connect with caring about our health, quality of life and well-being of animals and the planet, these are places you must steer away from. In general, eating meat does not support the health and wellbeing of us nor animals, but this is a choice we each make.

Recommended Articles

A Native American Perspective On Veganism

Plant-Based Protein VS. Protein From Meat: Which One Is Better For You? 

Doctor Explains How Humans Have A “Strict” Vegan Physiology

Vegan Activist James Aspey Beautifully Shows How To Consciously Inform People

9 Things That Happen When You Stop Eating Meat

Internal Medicine Physician Shares What Happens To Your Body When You Stop Eating Meat

Animals – Why Do We Love One But Eat The Other? 

The Heart Disease Rates of Meat-Eaters Versus Vegetarians & Vegans

Were Those Who Roamed The Earth Before US Nearly All Vegetarian?

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Alternative News

Consider This Before Indulging In Legal Cannabis In Canada

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In Brief

  • The Facts:

    Cannabis is now legal in Canada for recreational and medicinal use.

  • Reflect On:

    Will the legalization of cannabis change our relationship and habits with cannabis? Should it?

For some Canadians, October 17th is a day they have been anticipating for a long time. For others, it may pass by without much notice. Yet, one thing is for sure. Eventually, virtually all Canadians will be impacted in one way or another by Canada’s decision to legalize cannabis. Parents. Children. Regular Users. Non-users. Teenagers. The Elderly. Those of all ages suffering from illnesses of all kinds.

And not only will this impact the everyday lives of people in Canada, most Canadian institutions will be going through a learning curve and devoting attention to this new phenomenon. The government. Law Enforcement Agencies. Growers and farms. Wholesalers and retailers. Advertisers and marketers. Who in Canada will be able to say they have not been touched by this one way or another, once the intoxicating and healing powers of cannabis become more accessible even than alcohol?

What Will Change

Some changes will happen immediately, some changes will evolve over time. Some people argue that Canada is not yet ready for all the implications of legalizing cannabis at this point, but the prevailing attitude is that things will sort themselves out in an orderly fashion over the next 1-3 years.

Law enforcement: The change in the criminal code means that limited possession of cannabis is no longer a crime, though people who are currently in jail for possession of cannabis are not being automatically let out of jail. Much of law enforcement rhetoric focuses on preventing youth from indulging in cannabis, in a fashion similar to the restrictions on alcohol. More likely, the majority of funds and manpower will be diverted to combating black market enterprises, given that the government now stands to gain $675 million per year in tax revenues from the sale of legal cannabis. Regulations for impaired driving as a result of cannabis consumption look to evolve over time as technologies for measuring impairment like alcohol ‘breathalizers’ improve.

Home Growing: Individuals will be permitted to grow up to four plants for their own use. While the sale of edibles (baked goods, drinks, etc) will not be allowed initially, individuals can make edibles at home for their own use.

Marketing and Retail: The way in which legal cannabis is promoted and sold to the public will likely go through a push-pull transition between advertising regulations and the way wholesalers and retailers will try to get around those regulations to sell their products. The same can probably be said for the business chain as a whole from growth to consumption.

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Usage in General: Usage in Canada is bound to increase, simply due to an increase in the availability for those who have not actively sought it out in the past, and the removal of the stigma of its illegality, as well as the social acceptance of the consumption of cannabis which is bound to grow over the next couple of years.

What Will Not Change

There are two things that will not change when cannabis is made legal in Canada on October 17th: cannabis and you.

Cannabis itself is not suddenly safer or better for you than it was before just because it has become legalized. The same decisions you were making on whether or not to indulge in the past still pretty much apply, so ubiquitous was its use despite being illegal. Will regulation make the quality of cannabis you receive better? Not necessarily. It may become more consistent, if less potent, if the quality controls in place are reliable. But remember, black market dealers and sellers had an intrinsic investment in the quality of their product if they were to hope to have regular customers.

By ‘you,’ I am referring to your deepest, truest sense of self, the person you are and who you want to be in the highest vision of yourself. This does not change with any change of regulation in the outer world, and certainly you have to be wary if this change of regulation arbitrarily changes the choices you make and impacts your habits, goals, and dreams.

What To Watch Out For

You may be one who will be inclined to be more open to the personal recreational use of cannabis once it becomes legal. With this comes the possibility of gradually developing a dependence, facilitated by a greater legal and social acceptability. It is important to take notice if recreational use begins to devolve into a catch-all means of escaping from the stress and discomfort of real-life problems, in ways that you get out of the habit of confronting problems and discomfort at their source.

The same can be said about the use of cannabis for medicinal purposes. No doubt, cannabis and CBD oil will be marketed as the healthy sedative for physical ailments and will also be touted as a curative agent for certain types of diseases. While this may be true in some particular cases, you have to be cautious about the claims made by sellers and marketers of the product, whose job is to sell rather than research and diagnose exactly what conditions will benefit from cannabis treatment, and even more particularly what strains of cannabis will work for given conditions.

There is a body of research about the curative effects of cannabis made from an Eastern holistic perspective, which treats each individual case not based on outward symptoms, as Western medicine does, but in terms the particular physiological, emotional and spiritual conditions an individual is in which seen to be at the root of the individual’s ailment. Hence, being wary of marketing practices does not mean avoid cannabis or CBD oil as medicinal treatment for a particular condition, but try to do so in consultation with an unbiased and trusted practitioner/researcher whose motives are healing your particular condition rather than making profits selling cannabis.

The Takeaway

The consumption of cannabis has the potential to be both consciousness-expanding and consciousness-numbing. It does have healing properties but you really have to do your due diligence and use it in a very disciplined way in order to truly gain healing benefits from it rather than getting into the habit of simply escaping from pains and difficulties that are part of a normal life. It is an exciting time for Canadians in that we are now more free to choose something that never should have been illegal to begin with. Let’s make sure this newfound freedom serves us in the best ways as individuals and as a community.

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Epigenetic Memories Are Passed Down 14 Successive Generations, Game-Changing Research Reveals

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In Brief

  • The Facts:

    It's amazing how much information can be passed on to our offspring. Scientist have discovered that our DNA has memories, and these can also be passed down. We are talking about thoughts, feelings, emotions and perceptions.

  • Reflect On:

    Biological changes are shaped by our environment, as well as our thoughts, feelings, emotions and reaction to that environment. Our DNA can be changed with belief, the placebo is a great example. Thoughts feelings and emotions are huge in biology.

This article was written by the Greenmedinfo research group, from Greenmedinfo.com. Posted here with permission.

Until recently, it was believed that our genes dictate our destiny. That we are slated for the diseases that will ultimately beset us based upon the pre-wired indecipherable code written in stone in our genetic material. The burgeoning field of epigenetics, however, is overturning these tenets, and ushering in a school of thought where nurture, not nature, is seen to be the predominant influence when it comes to genetic expression and our freedom from or affliction by chronic disease.

Epigenetics: The Demise of Biological Determinism

Epigenetics, or the study of the physiological mechanisms that silence or activate genes, encompasses processes which alter gene function without changing the sequence of nucleotide base pairs in our DNA. Translated literally to mean “in addition to changes in genetic sequence,” epigenetics includes processes such as methylation, acetylation, phosphorylation, sumolyation, and ubiquitylation which can be transmitted to daughter cells upon cell division (1). Methylation, for example, is the attachment of simple methyl group tags to DNA molecules, which can repress transcription of a gene when it occurs in the region of a gene promoter. This simple methyl group, or a carbon bound to three hydrogen molecules, effectively turns the gene off.

Post-translational modifications of histone proteins is another epigenetic process. Histones help to package and condense the DNA double helix into the cell nucleus in a complex called chromatin, which can be modified by enzymes, acetyl groups, and forms of RNA called small interfering RNAs and microRNAs (1). These chemical modifications of chromatin influence its three-dimensional structure, which in turn governs its accessibility for DNA transcription and dictates whether genes are expressed or not.

We inherit one allele, or variant, of each gene from our mother and the other from our father. If the result of epigenetic processes is imprinting, a phenomenon where one of the two alleles of a gene pair is turned off, this can generate a deleterious health outcome if the expressed allele is defective or increases our susceptibility to infections or toxicants (1). Studies link cancers of nearly all types, neurobehavioral and cognitive dysfunction, respiratory illnessesautoimmune disorders, reproductive anomalies, and cardiovascular disease to epigenetic mechanisms (1). For example, the cardiac antiarrhythmic drug procainamide and the antihypertensive agent hydralazine can cause lupus in some people by causing aberrant patterns of DNA methylation and disrupting signalling pathways (1).

Genes Load the Gun, Environment Pulls the Trigger

Pharmaceuticals, however, are not the only agents that can induce epigenetic disturbances. Whether you were born via vaginal birth or Cesarean section, breastfed or bottle-fed, raised with a pet in the house, or infected with certain childhood illnesses all influence your epigenetic expression. Whether you are sedentary, pray, smoke, mediate, do yoga, have an extensive network of social support or are alienated from your community—all of your lifestyle choices play into your risk for disease operating through mechanisms of epigenetics.

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In fact, the Centers for Disease Control (CDC) states that genetics account for only 10% of disease, with the remaining 90% owing to environmental variables (2). An article published in the Public Library of Science One (PLoS One) entitled “Genetic factors are not the major causes of chronic diseases” echoes these claims, citing that chronic disease is only 16.4% genetic, and 84.6% environmental (3). These concepts make sense in light of research on the exposome, the cumulative measure of all the environmental insults an individual incurs during their life course that determines susceptibility to disease (4)

In delineating the totality of exposures to which an individual is subjected over their lifetime, the exposome can be subdivided into three overlapping and intertwined domains. One segment of the exposome called the internal environment is comprised of processes innate to the body which impinge on the cellular milieu. This encompasses hormones and other cellular messengers, oxidative stress, inflammation, lipid peroxidation, bodily morphology, the gut microbiotaaging and biochemical stress (5).

Another portion of the exposome, the specific external environment, consists of exposures including pathogens, radiation, chemical contaminants and pollutants, and medical interventions, as well as dietary, lifestyle, and occupational elements (5). At an even broader sociocultural and ecological level is the segment of the exposome called the general external environment, which may circumscribe factors such as psychological stress, socioeconomic status, geopolitical variables, educational attainment, urban or rural residence, and climate (5).

Transgenerational Inheritance of Epigenetic Change: Endocrine Disruptors Trigger Infertility in Future Generations

Scientists formerly speculated that epigenetic changes disappear with each new generation during gametogenesis, the formation of sperm and ovum, and after fertilization. However, this theory was first challenged by research published in the journal Science which demonstrated that transient exposure of pregnant rats to the insecticide methoxychlor, an estrogenic compound, or the fungicide vinclozolin, an antiandrogenic compound, resulted in increased incidence of male infertility and decreased sperm production and viability in 90% of the males of four subsequent generations that were tracked (1).

Most notably, these reproductive effects were associated with derangements in DNA methylation patterns in the germ line, suggesting that epigenetic changes are passed on to future generations. The authors concluded, “The ability of an environmental factor (for example, endocrine disruptor) to reprogram the germ line and to promote a transgenerational disease state has significant implications for evolutionary biology and disease etiology” (6, p. 1466). This may suggest that the endocrine-disrupting, fragrance-laden personal care products and commercial cleaning supplies to which we are all exposed may trigger fertility problems in multiple future generations.

Transgenerational Inheritance of Traumatic Episodes: Parental Experience Shapes Traits of Offspring

In addition, traumatic experiences may be transmitted to future generations via epigenetics as a way to inform progeny about salient information needed for their survival (7). In one study, researchers wafted the cherry-like chemical acetophenone into the chambers of mice while administering electric shocks, conditioning the mice to fear the scent (7). This reaction was passed onto two successive generations, which shuddered significantly more in the presence of acetophenone despite never having encountered it compared to descendants of mice that had not received this conditioning (7).

The study suggests that certain characteristics of the parental sensory environment experienced before conception can remodel the sensory nervous system and neuroanatomy in subsequently conceived generations (7). Alterations in brain structures that process olfactory stimuli were observed, as well as enhanced representation of the receptor that perceives the odor compared to control mice and their progeny (7). These changes were conveyed by epigenetic mechanisms, as illustrated by evidence that the acetophenone-sensing genes in fearful mice were hypomethylated, which may have enhanced expression of odorant-receptor genes during development leading to acetophenone sensitivity (7).

The Human Experience of Famine and Tragedy Spans Generations

The mouse study, which illustrates how germ cells (egg and sperm) exhibit dynamic plasticity and adaptability in response to environmental signals, is mirrored by human studies. For instance, exposures to certain stressors such as starvation during the gestational period are associated with poor health outcomes for offspring. Women who undergo famine before conception of her offspring have been demonstrated to give birth to children with lower self-reported mental health and quality of life, for example (8).

Studies similarly highlight that, “Maternal famine exposure around the time of conception has been related to prevalence of major affective disorders, antisocial personality disorders, schizophrenia, decreased intracranial volume, and congenital abnormalities of the central nervous system” (8). Gestational exposure to the Dutch Famine of the mid-twentieth century is also associated with lower perceived health (9), as well as enhanced incidence of cardiovascular disease, hypertension, and obesity in offspring (8). Maternal undernourishment during pregnancy leads to neonatal adiposity, which is a predictor of future obesity (10), in the grandchildren (11).

The impact of epigenetics is also exemplified by research on the intergenerational effects of trauma, which illuminates that descendants of people who survived the Holocaust exhibit abnormal stresshormone profiles, and low cortisol production in particular (12). Because of their impaired cortisol response and altered stress reactivity, children of Holocaust survivors are often at enhanced risk for post-traumatic stress disorder (PTSD), anxiety, and depression (13).

Intrauterine exposure to maternal stress in the form of intimate partner violence during pregnancy can also lead to changes in the methylation status of the glucocorticoid receptor (GR) of their adolescent offspring (14). These studies suggest that an individual’s experience of trauma can predispose their descendants to mental illness, behavioral problems, and psychological abnormalities due to “transgenerational epigenetic programming of genes operating in the hypothalamic-pituitary-adrenal axis,” a complex set of interactions among endocrine glands which determine stress response and resilience (14).

Body Cells Pass Genetic Information Directly Into Sperm Cells

Not only that, but studies are illuminating that genetic information can be transferred through the germ line cells of a species in real time. These paradigm-shifting findings overturn conventional logic which postulates that genetic change occurs over the protracted time scale of hundreds of thousands or even millions of years. In a relatively recent study, exosomes were found to be the medium through which information was transferred from somatic cells to gametes.

This experiment entailed xenotransplantation, a process where living cells from one species are grafted into a recipient of another species. Specifically, human melanoma tumor cells genetically engineered to express genes for a fluorescent tracer enzyme called EGFP-encoding plasmid were transplanted into mice. The experimenters found that information-containing molecules containing the EGFP tracer were released into the animals’ blood (15). Exosomes, or “specialized membranous nano-sized vesicles derived from endocytic compartments that are released by many cell types” were found among the EGFP trackable molecules (16, p. 447).

Exosomes, which are synthesized by all plant and animal cells, contain distinct protein repertoires and are created when inward budding occurs from the membrane of multivesicular bodies (MVBs), a type of organelle that serves as a membrane-bound sorting compartment within eukaryotic cells (16). Exosomes contain microRNA (miRNA) and small RNA, types of non-coding RNA involved in regulating gene expression (16). In this study, exosomes delivered RNAs to mature sperm cells (spermatozoa) and remained stored there (15).

The researchers highlight that this kind of RNA can behave as a “transgenerational determinant of inheritable epigenetic variations and that spermatozoal RNA can carry and deliver information that cause phenotypic variations in the progeny” (15). In other words, the RNA carried to sperm cells by exosomes can preside over gene expression in a way that changes the observable traits and disease risk of the offspring as well as its morphology, development, and physiology.

This study was the first to elucidate RNA-mediated transfer of information from somatic to germ cells, which fundamentally overturns what is known as the Weisman barrier, a principle which states that the movement of hereditary information from genes to body cells is unidirectional, and that the information transmitted by egg and sperm to future generations remains independent of somatic cells and parental experience (15).

Further, this may bear implications for cancer risk, as exosomes contain vast amounts of genetic information which can be source of lateral gene transfer (17) and are abundantly liberated from tumor cells (18). This can be reconciled with the fact that exosome-resembling vesicles have been observed in various mammals (15), including humans, in close proximity to sperm in anatomical structures such as the epididymis as well as in seminal fluid (19). These exosomes may thereafter be propagated to future generations with fertilization and augment cancer risk in the offspring (20).

The researchers concluded that sperm cells can act as the final repositories of somatic cell-derived information, which suggests that epigenetic insults to our body cells can be relayed to future generations. This notion is confirmatory of the evolutionary theory of “soft inheritance” proposed by French naturalist Jean-Baptiste Lamarck, whereby characteristics acquired over the life of an organism are transmitted to offspring, a concept which modern genetics previously rejected before the epigenetics arrived on the scene. In this way, the sperm are able to spontaneously assimilate exogenous DNA and RNA molecules, behaving both as vector of their native genome and of extrachromosomal foreign genetic material which is “then delivered to oocytes at fertilization with the ensuing generation of phenotypically modified animals” (15).

Epigenetic Changes Endure Longer Than Ever Predicted

In a recent study, nematode worms were manipulated to harbor a transgene for a fluorescent protein, which made the worms glow under ultraviolet light when the gene was activated (21). When the worms were incubated under the ambient temperature of 20° Celsius (68° Fahrenheit), negligible glowing was observed, indicating low activity of the transgene (21). However, transferring the worms to a warmer climate of 25°C (77° F) stimulated expression of the gene, as the worms glowed brightly (21).

In addition, this temperature-induced alteration in gene expression was found to persist for at least 14 generations, representing the preservation of epigenetic memories of environmental change across an unprecedented number of generations (21). In other words, the worms transmitted memories of past environmental conditions to their descendants, through the vehicle of epigenetic change, as a way to prepare their offspring for prevailing environmental conditions and ensure their survivability.

Future Directions: Where Do We Go From Here?

Taken cumulatively, the aforementioned research challenges traditional Mendelian laws of genetics, which postulate that genetic inheritance occurs exclusively through sexual reproduction and that traits are passed to offspring through the chromosomes contained in germ line cells, and never through somatic (bodily) cells. Effectively, this proves the existence of non-Mendelian transgenerational inheritance, where traits separate from chromosomal genes are transmitted to progeny, resulting in persistent phenotypes that endure across generations (22).

This research imparts new meaning to the principle of seven generation stewardship taught by Native Americans, which mandates that we consider the welfare of seven generations to come in each of our decisions. Not only should we embody this approach in practices of environmental sustainability, but we would be wise to consider how the conditions to which we subject our bodies—the pollution and toxicants which permeate the landscape and pervade our bodies, the nutrient-devoid soil that engenders micronutrient-poor food, the disruptions to our circadian rhythm due to the ubiquity of electronic devices, our divorce from nature and the demise of our tribal affiliations—may translate into ill health effects and diminished quality of life for a previously unfathomed number of subsequent generations.

Hazards of modern agriculture, the industrial revolution, and contemporary living are the “known or suspected drivers behind epigenetic processes…including heavy metals, pesticides, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria, and basic nutrients” (1, p. A160). Serendipitously, however, many inputs such as exercise, mindfulness, and bioactive components in fruits and vegetables such as sulforaphane in cruciferous vegetables, resveratrol from red grapes, genistein from soy, diallyl sulphide from garlic, curcumin from turmeric, betaine from beets, and green tea catechin can favorably modify epigenetic phenomena “either by directly inhibiting enzymes that catalyze DNA methylation or histone modifications, or by altering the availability of substrates necessary for those enzymatic reactions” (23, p. 8).

This quintessentially underscores that the air we breathe, the food we eat, the thoughts we allow, the toxins to which we are exposed, and the experiences we undergo may persevere in our descendants and remain in our progeny long after we are gone. We must be cognizant of the effects of our actions, as they elicit a ripple effect through the proverbial sands of time.

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References

1. Weinhold, B. (2006). Epigenetics: The Science of Change. Environmental Health Perspectives, 114(3), A160-A167.

2. Centers for Disease Control and Prevention. (2014). Exposome and Exposomics. Retrieved from https://www.cdc.gov/niosh/topics/exposome/

3. Rappaport, S.M. (2016). Genetic factors are not the major causes of chronic diseases. PLoS One, 11(4), e0154387.

4. Vrijheid, M. (2014). The exposome: a new paradigm to study the impact of environment on health. Thorax, 69(9), 876-878. doi: 10.1136/thoraxjnl-2013-204949.

5. Wild, C.P. (2012). The exposome: from concept to utility. International Journal of Epidemiology, 41, 24–32. doi:10.1093/ije/dyr236

6. Anway, M.D. et al. (2005). Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science, 308(5727), 1466-1469.

7. Dias, B.G., & Ressler, K.J. (2014). Parental olfactory experience influences behavior and neural structure in subsequent generations. Nature Neuroscience, 17(1), 89-98.

8. Stein, A.D. et al. (2009). Maternal exposure to the Dutch Famine before conception and during pregnancy: quality of life and depressive symptoms in adult offspring. Epidemiology, 20(6), doi:  10.1097/EDE.0b013e3181b5f227.

9. Roseboom, T.J. et al. (2003). Perceived health of adults after prenatal exposure to the Dutch famine. Paediatrics Perinatal Epidemiology, 17, 391–397.

10. Badon, S.E. et al. (2014). Gestational Weight Gain and Neonatal Adiposity in the Hyperglycemia and Adverse Pregnancy Outcome Study-North American Region. Obesity (Silver Spring), 22(7), 1731–1738.

11. Veenendaal, M.V. et al. (2013). Transgenerational effects of prenatal exposure to the 1944-45 Dutch famine. BJOG, 120(5), 548-53. doi: 10.1111/1471-0528.

12. Yehuda, R., & Bierer, L.M. (2008). Transgenerational transmission of cortisol and PTSD risk. Progress in Brain Research, 167, 121-135.

13. Aviad-Wilcheck, Y. et al. (2013). The effects of the survival characteristics of parent Holocaust survivors on offsprings’ anxiety and depression symptoms. The Israel Journal of Psychiatry and Related Sciences, 50(3), 210-216.

14. Radke, K.M. et al. (2011). Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Translational Psychiatry, 1, e21. doi: 10.1038/tp.2011.21.

15. Cossetti, C. et al. (2014). Soma-to-Germline Transmission of RNA in Mice Xenografted with Human Tumour Cells: Possible Transport by Exosomes. PLoS One, https://doi.org/10.1371/journal.pone.0101629.

16. Zomer, A. et al. (2010). Exosomes: Fit to deliver small RNA. Communicative and Integrative Biology, 3(5), 447–450.

17. Balaj, L. et al. (2011) Tumour microvesicles contain retrotransposon elements and amplified oncogene sequences. Natural Communications, 2, 180.

18. Azmi, A.S., Bao, B., & Sarkar, F.H. (2013). Exosomes in cancer development, metastasis, and drug resistance: a comprehensive review. Cancer Metastasis Review, 32, 623-643

19. Poliakov, A. et al. (2009). Structural heterogeneity and protein composition of exosomes-like vesicles (prostasomes) in human semen. Prostate, 69, 159-167.

20. Cheng, R.Y. et al. (2004) Epigenetic and gene expression changes related to transgenerational carcinogenesis. Molecular Carcinogenesis, 40, 1–11.

21. Klosin, A. et al. (2017). Transgenerational transmission of environmental information in C. elegans. Science, 356(6335).

22. Lim, J.P., & Brunet, A. (2013). Bridging the transgenerational gap with epigenetic memory. Trends in Genetics, 29(3), 176-186. doi: 10.1016/j.tig.2012.12.008

23. Choi, S.-W., & Friso, S. (2010). Epigenetics: A New Bridge between Nutrition and Health Advances in Nutrition: An International Review Journal, 1(1), 8-16. doi:10.3945/an.110.1004.

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