A study of around 500,000 medical records has suggested that severe viral infections like encephalitis and pneumonia increase the risk of neurodegenerative diseases like Parkinson’s and Alzheimer’s.
Amyloid plaques in Alzheimer’s disease (Kateryna Kon/Science Photo Library/Getty Images)
A study of around 500,000 medical records has suggested that severe viral infections like encephalitis and pneumonia increase the risk of neurodegenerative diseases like Parkinson’s and Alzheimer’s.
Researchers found 22 connections between viral infections and neurodegenerative conditions in the study of around 450,000 people.
People treated for a type of inflammation of the brain called viral encephalitis were 31 times more likely to develop Alzheimer’s disease. (For every 406 viral encephalitis cases, 24 went on to develop Alzheimer’s disease – around 6 percent.)
Those who were hospitalized with pneumonia after catching the flu seemed to be more susceptible to Alzheimer’s disease, dementia, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).
Intestinal infections and meningitis (both often caused by a virus), as well as the varicella-zoster virus, which causes shingles, were also implicated in the development of several neurodegenerative diseases.
The impact of viral infections on the brain persisted for up to 15 years in some cases. And there were no instances where exposure to viruses was protective.
Around 80 percent of the viruses implicated in brain diseases were considered ‘neurotrophic’, which means they could cross the blood-brain barrier.
“Strikingly, vaccines are currently available for some of these viruses, including influenza, shingles (varicella-zoster), and pneumonia,” the researchers write.
“Although vaccines do not prevent all cases of illness, they are known to dramatically reduce hospitalization rates. This evidence suggests that vaccination may mitigate some risk of developing neurodegenerative disease.”
“After reading [this] study, we realized that for years scientists had been searching – one-by-one – for links between an individual neurodegenerative disorder and a specific virus,” said senior author Michael Nalls, a neurogeneticist at the National Institute on Aging in the US.
“That’s when we decided to try a different, more data science-based approach,” he said. “By using medical records, we were able to systematically search for all possible links in one shot.”
First, the researchers analyzed the medical records of around 35,000 Finns with six different types of neurodegenerative diseases and compared this against a group of 310,000 controls who did not have a brain disease.
This analysis yielded 45 links between viral exposure and neurodegenerative diseases, and this was narrowed down to 22 links in a subsequent analysis of 100,000 medical records from the UK Biobank.
While this retrospective observational study cannot demonstrate a causal link, it adds to the pile of research hinting at the role of viruses in Parkinson’s and Alzheimer’s disease.
“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” said co-author Andrew Singleton, a neurogeneticist and Alzheimer’s researcher and the director of the Center for Alzheimer’s and Related Dementias.
“Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”
This is the THIRD time in one week that Biden has finished short remarks on a stage he walked onto just minutes before and then appeared completely lost.
Joe Biden got lost again after finishing a speech at the 45th annual Congressional Hispanic Caucus Institute gala in Washington DC.
This is the THIRD time in one week that Biden has finished short remarks on a stage he walked onto just minutes before and then appeared completely lost.
Antidepressants and antihistamines are among the most common types of medications people take, and they belong to a class of drugs known as anticholinergics. These drugs can treat a variety of health problems, including COPD, asthma, depression, dizziness, gastrointestinal problems, overactive bladder, and the symptoms of Parkinson’s. Although they can be effective, a large new study has shown that if you take them, you might just be trading one problem for another, possibly bigger one: dementia.
Although people who suffer from depression may be desperate to get relief from this illness that can have such a negative impact on daily life, tricyclic antidepressants fall into this category, so it’s important to pay attention the concerning new findings if you take medications like Elavil, Deptran, Sinequan, or Silenor. The same can be said for antihistamines like Benadryl, among other drugs.
The study, which was published in BMJ, involved more than 40,000 dementia patients and more than 283,000 people who don’t have dementia and followed them from 2006 to 2015. They found that people who had dementia had a greater likelihood of having taken class 3 anticholinergic drugs prior to developing the illness.
These medications block the actions of acetylcholine in the brain, which can prevent it from causing involuntary movements in the muscles in the lungs, urinary tract, gastrointestinal tract, and other parts of the body.
Although the higher risk varied depending on the drugs, some of them raised the risk by 30 percent. Not every anticholinergic drug had the effect, but using some of them even as far back as 20 years raised a person’s risk of dementia later on. Generally speaking, they believe that a person aged 65 to 70 sees their risk of dementia increase by 19 percent if they’ve used anticholinergic antidepressants. The association with dementia goes up with greater levels of exposure to the meds.
The study was praised by experts for its strength and using U.K. healthcare databases rather than relying on patient recall, which isn’t always dependable.
The drugs are believed to have this effect because anticholinergic medications lower the levels of a chemical called acetylcholine in the brain, which is a crucial messenger in memory pathways. This is a known effect that already stops some doctors from prescribing such drugs to older and more frail patients.
Other studies have reached a similar conclusion about anticholinergic drugs
In a different study involving nearly 3,500 people, researchers reached a similar conclusion, finding that those who used anticholinergic drugs had a greater likelihood of developing dementia, and their risk increased according to their cumulative dose. For example, taking such meds for three years or longer was linked to a 54 percent rise in dementia risk compared to taking the same dose for less than three months.
Experts say such findings are a good reminder that people should evaluate all the medications they’re taking from time to time to see if they are really working for you. For example, if you’re taking antidepressants and are still depressed, the medications may not be helping. Many of these drugs have safer alternatives, including non-medication approaches that could make a difference safely and effectively.
With the number of people suffering from Alzheimer’s expected to triple by 2050, it’s important to do all you can to minimize your risk – and that includes staying away from anticholinergic drugs if possible.
(Natural News) Americans walk, run, and march “for the cure” for all kinds of different diseases, helping to raise awareness and funds for research, but what if you found out right now there’s a cure for Alzheimer’s Disease, would you “take care of business” starting now or keep wishing someone else might come along to possibly save you later?
Sure, right about now you’re hoping the cure will come in some magical pill or prolific injection, and do the job “overnight,” so you won’t have to do any work or garner long-term diligence – well, there’s good news and bad news – and they’re both the same. Scientists have figured out what causes Alzheimer’s Disease and what cures it, but it’s not some chemical pill or experimental vaccine, so let’s get to work.
Understanding the neuroscience of Alzheimer’s and Parkinson’s shows us the cause and the cure at the same time
The point of connection of neurons is called a synapse, and that’s where neurotransmitters are released and communication happens in the brain. This is where we experiences all of our senses and engage in thought processes, including critical thinking and memory. This is also exactly where dementia happens.
The synapse is where neurons release hormones, glutamates, and small peptides called amyloid beta. The amyloid beta are the brain’s “trash” and a prime factor involved in Alzheimer’s disease, functioning as the main component of plaques that cling to each other and clog up the neural pathway. These are the plaques found in the brains of Alzheimer’s patients.
Normally, these amyloid plaques are swept out of the neural pathway (like trash) by the “custodians of the brain” called microglea. These amazing microglea are the brain’s own immune cells and are the answer to beating brain diseases. Scientists recently discovered through sophisticated experiments that these cells constantly search for brain damage, like a perpetually-running computer virus scan, running surveillance for different levels of damage. The microglea are literally capable of eating infected and damaged cells before infection spreads, while clearing out “debris” from dying cells.
Diseases of dementia therefore begin when amyloid beta begins to accumulate, because too much is released, overwhelming the microglea, and leaving waste in the neural pathways, blocking communication. The synapse piles up with plaques (trash and waste) that become sticky and bind to themselves (think of animal fat clogging your sink drain).
At a certain tipping point, when the body and brain have created too much “trash” for too long, creating massive inflammation and tangles, the microglea become overwhelmed and enter a hyper-mode, where they actually begin attacking healthy cells. Scientists believe the microglea may even, at the tipping point, begin clearing away the synapses themselves. Get it? The cure lives in keeping amyloid plaques from reaching the “tipping point.” Here’s how you do that.
Stop consuming foods that create plaques in the brain – so your brain’s “custodians” can clear out the sticky trash that blocks your synapses
Amyloid plaque accumulation may never be “cured” with a chemical drug or vaccine, but that doesn’t matter, because you can cure the problem yourself. Are you ready to start taking your preventative medicine? It’s not very difficult you know. Let’s break it down to its simplest form, then you decide if you can “pull it off.”
You wouldn’t pick up a poisonous snake just to see if it bites you, and then start searching the internet for the anecdote, would you? You wouldn’t pick some poison ivy and rub it on your skin on purpose, would you? If you were severely allergic to peanuts, you certainly wouldn’t eat a handful just to see what happens. That’s just common sense.
So what if you knew what caused dementia, would you stop eating it? Guess what. Now is the time to stop marching for the cure and start living it, because knowledge is power. Now get this.
White foods are known to cause excess plaque build-up in the brain, leading to dementia. These white foods include white bread, white flour, white rice (except basmati, which is naturally white), white pasta, and white sugar. Stop eating bleached food.
Processed foods and meats cause excess plaque in the synapses, fueling dementia. Avoid processed cheeses (think American cheese especially here), and processed meats, like sausages, bacon, hot dogs, and cold cuts (especially smoked deli meats), and even beer. Nitrosamines in smoked meats cause the liver to produce fats that are toxic to the brain.
Stop eating foods that contain diacetyl, a chemical commonly found in microwave popcorn. Diacetyl increases amyloid plaques in the brain.
Animal fat and canola oil coagulate in your blood and create tangles of plaque in the brain
You’ll hear it time and time again, that a plant-based diet cures almost every preventable disease and disorder known to humans. It’s true. If you’re a heavy meat eater, your body is struggling to process all that animal fat, creating heart and brain “trash” that your body’s “janitors” just can’t sweep away fast enough.
If you think organic or “expeller pressed” canola oil means that the oil doesn’t coagulate in your body, you’d be dead wrong. After about six weeks, any canola oil that your body hasn’t cleared out looks like a sticky glue you could use to bond cement. Think of all that “trash” blocking your synapses and causing dementia, because that’s exactly what happens.
Did you know that in the U.S. alone, Alzheimer’s care already costs $2 billion a year (one out of every five Medicare dollars)? Dementia kills more people than cancer. Did you know that? Sure, Big Pharma will tell you Alzheimer’s and Parkinson’s are not preventable, but both are, and the cure lives in prevention. You may begin now.
Daily consumption of tea may help keep dementia at bay, new research says. Researcher at the National University of Singapore examined the tea intake of 957 adults older than 55 years old for more than 12 years. Study data show that regular tea consumption is associated with a 50 percent reduced risk of developing dementia. Data also reveals that people carrying the dementia gene may decrease the risk of beta-amyloid plaque formation by 86 percent. Beta-amyloid plaques is shown to trigger the onset of cognitive disorders in patients. Researchers note similar effects regardless of whether the tea was green or black.
“The data from our study suggests that a simple and inexpensive lifestyle measure such as daily tea drinking can reduce a person’s risk of developing neurocognitive disorders in late life. Our findings have important implications for dementia prevention. Despite high quality drug trials, effective pharmacological therapy for neurocognitive disorders such as dementia remains elusive and current prevention strategies are far from satisfactory,” said researcher Dr Feng Lei of the National University of Singapore.
The results were published in The Journal of Nutrition, Health & Aging.
Tea break proves beneficial in many previous studies
The recent study is only one of many that demonstrates the benefits of regular tea intake. A 2014 study published in the journal Psychopharmacology showedthat regular green tea intake results in improved cognitive function, which may prove beneficial for patients with Alzheimer’s disease or dementia. MRI data show that patients who were given a drink with green tea extracts exhibit increased brain activity in areas associated with memory function.
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An analysis of 2,500 participants also reveals that those who drank two to three cups of tea a day had a 55 percent reduced risk of dementia, while those who consumed six to 10 cups daily had a 63 percent decreased likelihood of developing dementia. In contrast, people who drank coffee do not demonstrate the same effect, but show an increased risk of dementia. “Because tea is cheap, non-toxic and widely consumed, it has huge potential in promoting cognitive health and perhaps delaying the onset of dementia,” the researchers note.
Another study shows that regular green tea intake helps stave off dementia in people aged 60 years and older. Researchers examined more than 700 participants and found that those who did not drink green tea fared worse on a cognitive test called the Mini-Mental State Examination. The findings demonstrate that green tea consumption may help protect the brain from the debilitating effects of dementia.
Additional research also reveal that taking digested polyphenol compounds from green tea is even more effective in preventing the onset of dementia in patients compared with freshly-brewed tea.
What’s in a leaf: The source behind tea’s power against dementia
Tea leaves are packed with a number of antioxidants that keep cognitive disorders at bay. Green tea contains a flavonoid called epigallocatechin-3-gallate (EGCG) that can bind with beta-amyloid proteins, which in turn prevents the formation of dangerous plaques associated with cognitive decline. Polyphenols found in tea leaves are also shown to inhibit the oxidation of brain cells and prevent the build-up of plaque. Compounds such as catechins and theaflavins found in tea leaves have anti-inflammatory and antioxidant properties, which may help protect the brain from from neurodegeneration and vascular damage, a researcher said. In addition, various research show that compounds found in tea leaves can help lower cholesterol levels, reduce blood clots, and reduce the risk cancer onset.
(Natural News) The reason there are no prescription medications available today where the side effects aren’t worse than the ailment being treated is because Big Pharma will not treat or heal anything without creating several new issues that keep their “customers for life” coming back for more. Most Americans do not want to stop eating junk food, fast food, corporate franchise restaurant food, microwaveable food, prepared food bar “stuff,” and “diet” food that’s mostly chock full of synthetic sweeteners, GMOs and MSG.
Due almost entirely to these nasty eating habits, about 200 million Americans seek medical doctors to prescribe them chemical-filled pills to kill the pain, quell the hypertension, reduce the inflammation, unclog the clots, numb the anxiety, and nullify the depression.
The FDA and CDC do not allow anything that cures disease or disorders to be labeled “medicine”
Most Americans think the FDA was created to protect us from dangerous chemicals that might wind up in food and medicine, but just the opposite is true. Over the past century, the FDA has tried to destroy all forms of holistic care in America that compete with “slash-and-burn” drug and vaccine treatments that are readily dished out by the allopathic Ponzi sick-care scheme that masquerades as ‘health’ care in this country.
The CDC is a actually a for-profit corporation listed on Dun and Bradstreet. As a health protection agency, the CDC is supposed to save lives and conduct critical science for responding to threats when they arise, but pharma corporations have lobbyists and their vice presidents now in positions of control in the bureaucracy, writing legislation that favors new, untested drug approvals, as they have for decades.
Both the FDA and the CDC promote toxic chemicals as medicine, including prescription medications, chemotherapy, and vaccines. Meanwhile, any food, herb, tincture, plant, seed, or essential oil that treats, prevents or cures disease is banned as “medicine” while being manipulated in labs, weakened or deadened, patented, and then declared a failure.
Prescription drug deaths skyrocket while the Big Pharma world pretends to search for cures for cancer, dementia, and diabetes
Twenty years ago, only four in every 100,000 people died from taking prescription drugs “as recommended” by their medical doctors. Now, one in every ten Americans struggle with addiction to prescription drugs (think opioids and SSRIs). Right now, over three million Americans are abusing painkillers, two million are misusing tranquilizers, 1.7 million are abusing stimulants, and half a million are misusing sedatives.
More Americans use and abuse “controlled” prescription drugs than heroin, cocaine and methamphetamines combined. How many of them will die this year? About 50 people will die today from overdosing on opioids. And now heroin is the death drug of choice for most people who become addicted to opioid pain relievers. Most teenagers think it’s safer to take a friend’s prescription drugs than to dose some illegal street drugs, just because they were prescribed by a doctor, but that’s not true at all.
The side effects of most prescription drugs that treat depression and anxiety include worsened depression and thoughts of suicide. How ridiculous is that? Every prescription drug advertised on television for all American children and teens to see comes slathered with side effects you wouldn’t wish on your worst enemies. Then they all feature the same tag line, “Ask your doctor if (fill in complex chemical name here) is right for you.”
It would only make sense that natural cures would be banned if they caused side effects like all the prescription medications do, but they don’t. If organic foods caused the health problems conventional foods do, they too would be banned, recalled or stuck with warning labels.
It’s as if we are all living in total idiocy like the movie “Idiocracy.” More than 200 million Americans think it’s okay if their medical doctor prescribes them “medicine” that can cause internal bleeding, loss of vision, coma, feelings of suicide, and thoughts of committing homicide. Wake up America. You’re living inside a real-life nightmare, where the food is toxic, the medicine is more toxic, and the medical doctors have no nutrition education, yet go to school for eight years to learn how to juggle chemical medicines like some Bozo science clowns. Maybe all M.D.s should wear big red wigs with big red noses and big red shoes while scribbling out those toxic prescriptions.
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).
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).
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.
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13. Kaplan, M.S., & Hinds, J.W. (1977). Neurogenesis in the adult rat: electron microscopic analysis of light radioautographs. Science, 197, 1092-1094.
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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.
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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.
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Ali Le Vere holds dual Bachelor of Science degrees in Human Biology and Psychology, minors in Health Promotion and in Bioethics, Humanities, and Society, and is a Master of Science in Human Nutrition and Functional Medicine candidate. Having contended with chronic illness, her mission is to educate the public about the transformative potential of therapeutic nutrition and to disseminate information on evidence-based, empirically rooted holistic healing modalities. Read more at @empoweredautoimmune on Instagram and atwww.EmpoweredAutoimmune.com: Science-based natural remedies for autoimmune disease, dysautonomia, Lyme disease, and other chronic, inflammatory illnesses.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
More than five million Americans have Alzheimer’s disease, the most common type of dementia. Meanwhile, 740,000 people die annually in the U.S. because of heart disease and stroke. To resolve this health concern, scientists are studying the link between high levels of the amino acid homocysteine and these life-threatening conditions.
Research on homocysteine and health conditions
According to a study by researchers from the Lewis Katz School of Medicineat Temple University, B-complex vitamins play a crucial role when it comes to controlling homocysteine. Findings from the study, which was published in Molecular Psychiatry, determined that elevated levels of the amino acid can result in Alzheimer’s, along with other forms of dementia.
Alarmingly enough, there are many reports of vitamin B deficiencies in the U.S. More patients are also being diagnosed with Alzheimer’s disease. These concerns highlight the need to maintain healthy levels of these B-complex vitamins for disease prevention.
For the study, the researchers gave mice a diet lacking in vitamin B6, vitamin B9 (folate), and vitamin B12. Eight months after the mice were fed the B-complex deficient diet, the research team used a water maze test to gauge their memory and learning. Unlike the control mice that were fed a normal diet, the vitamin B-deficient mice had trouble learning a new task. The vitamin deficiency also affected their ability to remember it.
The study revealed that the mice brains had both elevated levels of homocysteine and “tau,” a protein that damages or destroys brain nerve cells/neurons. Tau can also disrupt synapses, which are the junctions that allow neuronal communication.
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Rodents deprived of B vitamins also had a 50 percent increase in neurofibrillary tau tangles in the hippocampus and cortex, two areas necessary for learning and memory. A hallmark of Alzheimer’s disease, tau tangles are also the main factors of “cell death, dementia, and neurodegenerative conditions.”
During the study, the research team discovered data linked to the formation of tau tangles. The authors shared that one of the key changes caused by high levels of homocysteine was elevated levels of 5-lipoxygenase (5LO), the pro-inflammatory chemical that causes tau tangles.
Further studies can help determine if thwarting the production of 5LO can prevent or reverse the brain damage linked to elevated homocysteine levels.
Domenico Pratico, study leader and a professor in the Departments of Pharmacology and Microbiology at Lewis Katz, commented that high homocysteine levels were previously associated with amyloid beta plaques that are also linked to Alzheimer’s disease.
However, until the study findings from the Lewis Katz study, the connection with tau tangles remained unknown.
How can you prevent hyperhomocysteinemia?
Homocysteine is a non-protein amino acid that can naturally be found in the human body. The amino acid is a byproduct of the metabolism of another amino acid called methionine.
Hyperhomocysteinemia, the medical term for high homocysteine levels, may have a genetic component. The disease can also occur due to deficiencies of B vitamins and folic acid, improper diet, or stress.
Data from the study showed that elevated homocysteine damages fragile arterial linings, causes inflammation and oxidative stress, and minimizes blood flow to the heart and brain. These destructive processes can eventually cause atherosclerosis and coronary artery disease. In fact, blood levels of homocysteine can be used to correctly predict the risk of heart disease.
Research has also revealed that hyperhomocysteinemia is linked to a whopping 42 percent increase in the risk of the narrowing of the carotid arteries. Individuals with elevated homocysteine who have already had a heart attack are at a 30 percent higher risk of suffering another adverse event such as another heart attack, stroke, or even death.
High homocysteine levels can also double your chance of developing dementia. Consult a healthcare professional if you want to check your homocysteine levels with a simple blood test. Levels below 10 micromoles per liter (umol/L) are healthy while seven umol/L to eigh umol/L is optimal.
The following tips can help prevent a vitamin B-complex deficiency and hyperhomocysteinemia:
Eat foods rich in B12 like grass-fed beef, organic dairy, and wild-caught salmon.
Take B complex vitamin supplements, especially if you already have hyperhomocysteinemia. Talk to a healthcare professional before you take any supplements.
To lower high homocysteine levels, take 25 to 100 milligrams (mg) of vitamin B2, 100 to 200 mg of vitamin B6, 1,000 to 10,000 micrograms (mcg) of vitamin B9, and 300 to 1,000 mcg of vitamin B1 (methylcobalamin) daily. These B complex vitamins, which can all help detoxify homocysteine, must be taken together with the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in fish oil.
To prevent hyperhomocysteinemia and lower the risk of developing life-threatening health conditions, follow a healthy diet and increase your intake of B complex vitamins.
You can read more articles about how to manage or prevent Alzheimer’s and lower your homocysteine levels at Alzheimers.news.
(Natural News) Being physically active does not only make you physically fit, but also makes you mentally healthy. In a Swedish study of women and fitness, it was revealed that people who have a high level of cardiovascular fitness are 90 percent less likely to develop dementia later in life.
The study, published in the medical journal American Academy of Neurology, evaluated the cardiovascular fitness of women based on an exercise test. The test required 191 women, with an average age of 50, to ride a stationary bike to exhaustion to measure their peak cardiovascular capacity. The workload for a high fitness level was at least 103 watts, while the workload for a low fitness level was 80 watts or less. In total, 40 women met the criteria for a high fitness level, 92 women were in the medium fitness category, and 59 women were in the low fitness category or stopped the exercise test because of chest pain, high blood pressure, or other cardiovascular problems.
Throughout the next 44 years, the participants came back for dementia testing six times. During that time, a total of 44 women developed dementia. Only five percent of highly fit women developed dementia, in comparison to 32 percent of women with low fitness level and 25 percent of moderately fit women. In addition, 45 percent of those who stopped the exercise test developed dementia. Moreover, highly fit women who did develop dementia had the disease an average of 11 years later compared to moderately fit women, or at 90 years old instead of 79.
Simple ways to increase your cardiovascular fitness
It is important to make According to research, high-intensity exercise performed in intervals or for short bursts of time can improve cardiovascular fitness. There are five everyday exercises that can help you enhance your heart rate and your fitness level:
Walking – Instead of a slow-paced walking, walk briskly. The average person weighing 155 pounds (lbs) who walks at a brisk pace of 3.5 miles per hour for 30 minutes can burn about 150 calories. This can also improve your heart rate. If that is too fast for you, try to increase your speed at intervals. Increase your pace for a minute and then go back to a more leisurely walk for the next minute.
Running – When running, try to change your speed and intensity at slightly random intervals. This will allow your heart rate to increase without breaking your energy bank. Try to run hard for 30 seconds with a minute of walking in between.
Strength-training – To keep your heart rate elevated, perform circuits that involve different muscle groups. Alternating exercises that involve various muscles lets you rest the ones you recently worked on, at the same time, continuing to move.
Yoga – To improve your cardiovascular fitness with yoga, try a Vinsaya, power, or flow class. In this type of yoga, you will continuously move with your breath, keeping your heart rate elevated.
Cycling – Whether cycling indoors or outdoors, pedal for 40 seconds with a cadence of 80 and as much resistance as you can endure. Then, pedal for 20 seconds with a 100-stroke cadence but without resistance. Do this 10 times. The spike in resistance when pedaling will make you work harder.
Read more news stories and studies on preventing dementia through exercise by going to Alzheimers.news.
Diagnosed with Alzheimer’s in 2015, 75-year-old Brenda Whittle still enjoys jigsaws, sewing and dancing. New activities are less appealing, but participating in Alzheimer’s research and drug trials is an exception. She’s so at ease with loud brain scans, she even falls asleep during them.
“This can’t be sustained by any medical health system – it is too much in terms of numbers, says Antonella Santuccione-Chadha, a physician and Alzheimer’s specialist based in Switzerland. “And as women are more confronted by the disease, we need to investigate the differences between the male and female specifics of it.”
Much of the gender gap comes down to one of dementia’s biggest risk factors: age. The older you are, the more likely you are to develop late-onset Alzheimer’s. Women typically live longer than men, so more have dementia.
The older you are, the more likely to develop dementia (Credit: Getty Images)
But recent research hints that we would be wrong to assume that ageing means Alzheimer’s is inevitable. Results from two major Cognitive Function and Ageing Studies (CFAS) suggest that over the last 20 years, new dementia cases in the UK have dropped by 20% – driven mostly by a fall in incidence among men over 65 years old.
Over the past 20 years, new dementia cases in the UK have dropped by 20% – driven mostly by a fall in incidence among men over 65
Experts say this may be because of public health campaigns targeting heart disease and smoking. Both are risk factors for Alzheimer’s. But because men tend to get heart disease younger and smoke more than women, these campaigns also may have helped stave off these risk factors more for men than women.
“Sex-specific prevention might start from having more of this information about female-specific risk factors,” says Maria Teresa Ferretti, a biomedical researcher in the field of Alzheimer’s disease at the University of Zurich.
The “quick facts” provided by the Alzheimer’s Association are pretty concerning: More than five million people in America are living with Alzheimer’s, and that number is projected to reach 16 million by the year 2050. As the sixth leading cause of death in our nation, it kills more Americans than prostate cancer and breast cancer combined. Someone in the U.S. develops Alzheimer’s every 66 seconds; will you be one of them?
With statistics like these, it’s no wonder that people want to do everything they can to reduce their odds. However, it’s also important to note that Alzheimer’s is only one of the potential causes of dementia. While many people use the terms interchangeably, Alzheimer’s is really only responsible for around 50 to 70 percent of dementia cases. The misleading terminology is obscuring one very dark fact about dementia: Many times, it’s being caused not by something scientists are still struggling to understand like Alzheimer’s but rather by things that are masquerading as tools for good health; vaccines and prescription drugs.
In fact, the Alzheimer’s Association that publicizes these statistics is subsidized by Big Pharma. It’s simply good business sense that they want people to believe that every memory-loss patient falls under the Alzheimer’s umbrella because then they can sell you drugs that purportedly address it. Their research has led them to an approach that pays dividends: promoting and destigmatizing what many think of as “mental illnesses,” making them seem unpreventable but manageable with drugs. Many people who work for the Alzheimer’s Association and similar organizations are well-meaning people who want to help and are often unaware of the connection to Big Pharma.
You have more control over “dementia” than you’re being led to believe
It’s no coincidence that dementia cases have been spiking during the same time that children and adults alike are being over-vaccinated (flu shot, anyone?) and the over-prescription of brain-altering drugs like antidepressants is prevalent.
A help guide based on a Harvard University report admits as much. According to the report, “medications are common culprits in mental decline.” As the body ages, the liver’s efficiency when it comes to metabolizing drugs declines, and the kidneys do not eliminate them as quickly as they once did. This causes the drugs to accumulate in the body, which means those who take multiple medications are particularly susceptible to this effect.
Included in the list of drugs published in the guide that cause dementia-like symptoms are antidepressants, anti-anxiety medications, sedatives, corticosteroids, narcotics, antihistamines, cardiovascular drugs, and anticonvulsants. It’s a very broad range of drugs, and many elderly people take medications from one or more of those categories. In fact, you might want to go check your medicine cabinet right now.
A study published in JAMA Internal Medicine correlated the use of popular medications like Benadryl and other anticholinergic drugs with dementia onset. According to the researchers, patients who took these medications for three years or more had a 54 percent higher chance of going on to develop the disorder.
Vaccines are also responsible for causing symptoms mistaken for dementia. People in their 40s are increasingly being diagnosed with “dementia,” and experts believe that environmental factors must be responsible in these cases. Mercury-containing thimerosalwas used widely in childhood vaccines until 2001 and remains in some vaccines, including flu shots, to this day. A study published in the Journal of Alzheimer’s Disease found that exposure to mercury could produce many of the changes that are seen in Alzheimer’s patients, including impaired cognitive function and memory as well as confusion.
Researcher Richard Deth stated: “Mercury is clearly contributing to neurological problems, whose rate is increasing in parallel with rising levels of mercury. It seems that the two are tied together.”
Another common ingredient found in vaccines, aluminum, has been linked to dementia as well.
It’s a pretty smart way to keep the profit machine turning for Big Pharma: Convince people they need vaccines or drugs, and when those vaccines or drugs cause further side effects and illnesses, sell them even more drugs to counteract them. And the best part for them is that because mental decline is involved, it reduces the chances that people will wake up to what is really going on here.
By Crawford KilianToday | TheTyee.ca Crawford Kilian is a contributing editor of The Tyee and at 77 considers himself “cognitively OK.”
Edith and Pat McGeer have investigated Alzheimer’s and other neurological problems for decades. Photo from McGeer and Associates.
According to the Alzheimer Society of Canada, 1,125,000 Canadians will have dementia in 20 years. The cumulative economic burden will be $872 billion, and the demand for long-term care will increase tenfold.
In 2008, just over 100,000 new dementia cases were diagnosed each year in Canada. By 2038, the ASC predicts more than 250,000 new cases each year. About half of those diagnosed with dementia will have Alzheimer’s disease.
Like death itself, such numbers don’t bear thinking about. Nor do we want to think about our own partners and children dedicating their old age to caring for us.
But a lot of experts are thinking hard about this problem, and one of them is 90-year-old neuroscientist Dr. Patrick McGeer. Now CEO of Aurin Biotech, McGeer had a long career at the University of British Columbia as well as a tumultuous one as a Liberal and Socred MLA and cabinet minister from 1962 to 1986. He may have dropped out of the public eye after leaving politics, but McGeer has kept very busy.
Since 1990, McGeer has been studying the causes of Alzheimer’s. Now, almost 30 years later, he says a simple test can identify those at risk, and an over-the-counter pain reliever can prevent it.
When we hear a strong claim, we expect strong evidence. And if the evidence holds up, we need to explore the implications.
A ‘crazy hypothesis’
McGeer’s evidence is indeed generally strong. In a recent review article in the Journal of Alzheimer’s Disease, McGeer and his colleagues summarize how their view of Alzheimer’s went from a “crazy hypothesis” in the 1980s to today’s widely accepted view that neuroinflammation causes damage to brain cells. That in turn results in Alzheimer’s.
In 1990, McGeer reported in the British journal The Lancet that patients using nonsteroidal anti-inflammatory drugs (NSAIDS) for rheumatoid arthritis seemed to develop fewer cases of Alzheimer’s than statistics said they should. Further research indicated that a major cause of neuroinflammation was a buildup of “amyloid-β” protein in the brain. Eventually, over years, this Aβ buildup destroys nearby nerve cells and results in Alzheimer’s.
Further research by McGeer and others established that NSAIDS — like aspirin and ibuprofen — could reduce the number of Alzheimer’s cases below the rate to be expected in a given group. But there was no effect unless the NSAIDS were administered well before the members of the group were statistically likely to be diagnosed with Alzheimer’s. Once diagnosed, Alzheimer’s wasn’t affected by NSAIDS.
McGeer and his team found a solution: Aβ may accumulate in brain cells, but it’s produced in all body tissues. A simple saliva test seems able to detect Aβ levels — and these can predict the likelihood that a given individual will develop Alzheimer’s. Some people produce low levels of Aβ all their lives, and don’t develop Alzheimer’s; other produce high levels, and are virtually certain to develop it.
Six phases of Alzheimer’s
In their review article, McGeer and his colleagues wrote: “A theoretical construct suggests the development of AD [Alzheimer’s] goes through six phases, each with decreasing opportunity for therapeutic intervention. Since the prevalence of clinical AD commences at age 65, the prevalence for actual AD disease onset can be hypothesized to occur at least 10 years earlier, or at age 55. Without intervention, the prevalence will then double every five years…. Any strategy which limits Aβ production, enhances its clearance, or prevents its aggregation, should be disease modifying. Effectiveness of treatment should be measurable by CSF Aβ levels returning toward normal.”
A major Canadian observational study identified alcohol use disorders as the biggest risk factor for the onset of dementia. It’s also the most preventable factor, so people wary of early-onset dementia can avoid it by controlling their alcohol intake, reported a ScienceDaily article.
Implemented by the Center for Addiction and Mental Health (CAMH) and published in The Lancet Public Health journal, the study took a very close look at the effect of alcohol use disorders. To this end, it canvassed the health records of more than a million French citizens.
The study included patients with mental and behavioral disorders or chronic diseases caused by chronic heavy drinking.
According to the World Health Organization (WHO), “chronic heavy drinking” is defined as the daily consumption of more than 60 grams of pure alcohol for men and 40 grams for women. WHO identifies alcohol consumption as the root cause of more than 200 diseases and injuries, including mental and behavioral disorders.
For their study, CAMH researchers viewed 57,000 cases of early-onset dementia, where the patient developed dementia before turning 65. They found that 57 percent of these cases were linked to chronic heavy drinking.
The significant association between chronic heavy drinking and dementia led the authors to suggest several actions that would reduce the burden of dementia attributed to alcohol. They believed screening, brief interventions for heavy drinking, and treatment for alcohol use disorders would be highly effective in curbing the onset of dementia.
“The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths,” remarked Dr. Jürgen Rehm, the co-author of the massive study and Director of the CAMH Institute for Mental Health Policy Research.
He warned that alcohol use disorders have been proven to reduce life expectancy by more than 20 years. He identified dementia as a major cause of death for people who suffered from alcohol-related disorders.
More women suffer from dementia, but more men get early-onset dementia
Dr. Rehm and his team identified a major gender split for early-onset dementia patients. Women comprised the majority of dementia patients, but two out of every three early-onset dementia patients turned out to be men.
Other independent risk factors for the onset of dementia included smoking, high blood pressure, diabetes, depression, and hearing loss. These factors are also linked to alcohol use disorders.
The data from the study imply that alcohol use disorders can increase the risk of dementia in more ways than one.
“As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition,” said Dr. Bruce Pollock, co-author and Vice-President of Research for CAMH.
Much like his colleague, Dr. Pollock advised treating the alcohol use disorder ahead of time before dementia takes over.
“Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care,” he said.
One limitation of the study was that it only covered the most severe cases of alcohol use disorder. The authors explained that they focused on cases that required hospitalization.
Patients are often reluctant to report alcohol-related problems due to social stigma regarding alcoholics. The correlation between alcoholism and dementia could be even higher than the study has shown.
More health-related news can be found in Health.news.
Summary: According to researchers, alcohol use disorder poses an increased risk for the early development of dementia.
Source: CAMH.
Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study, published in The Lancet Public Health journal, of over one million adults diagnosed with dementia in France.
This study looked specifically at the effect of alcohol use disorders, and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol.
Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.
The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women.
As a result of the strong association found in this study, the authors suggest that screening, brief interventions for heavy drinking, and treatment for alcohol use disorders should be implemented to reduce the alcohol-attributable burden of dementia.
“The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths,” says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm. “Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths.”
The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women. NeuroscienceNews.com image is adapted from the CAMH news release.
Dr. Rehm points out that on average, alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death for these people.
For early-onset dementia, there was a significant gender split. While the overall majority of dementia patients were women, almost two-thirds of all early-onset dementia patients (64.9%) were men.
Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.
“As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition,” says CAMH Vice-President of Research Dr. Bruce Pollock. “Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care.” The authors also noted that only the most severe cases of alcohol use disorder – ones involving hospitalization – were included in the study. This could mean that, because of ongoing stigma regarding the reporting of alcohol-use disorders, the association between chronic heavy drinking and dementia may be even stronger.
Scientists are continuously discovering new ways that cannabis can benefit human health. Typically, researchers publish these discoveries in peer-reviewed journals. Yet, most cannabis research never makes its way into mainstream news. In the public eye, these studies go unnoticed.
Here are five examples of cannabis research that warrant our attention.
Opioids have recently received a fair share of scrutiny, and for a good reason. Thomas Gilson, the medical examiner for Cuyahoga County, Ohio, stated:
“If you look at how many people die in the country from opiate overdose, we’re looking at the same number of casualties as the entire Vietnam conflict.”
Could cannabis be a safer treatment for pain, without the high risk of overdose?
New cannabis research from Israel examined the safety of cannabis use among the elderly. The researchers administered cannabis treatment to 2,736 patients, with a median age of 74.5.
Research participants answered an initial questionnaire. During the study, two-thirds of the participants took cannabis for pain, and another 60.8% for cancer. After six months of cannabis treatment, the researchers administered another questionnaire.
After six months of treatment, 93.7% of the respondents reported improvement in their condition and the reported pain level was reduced from a median of 8 on a scale of 0-10 to a median of 4. After six months, 18.1% stopped using opioid analgesics or reduced their does.
Our study finds that the therapeutic use of cannabis is safe and efficacious in the elderly population. Cannabis use may decrease the use of other prescription medicines, including opioids.
This research shows that cannabis has promise when it comes to offering an alternative to opioids.
2. Cannabis May Protect Alcohol Users from Liver Disease
We’ve all heard that drinking too much alcohol compromises liver health. Do the observed anti-inflammatory effects of cannabis also affect the development of liver disease?
A group of researchers from the University of Massachusetts Medical School set out to “determine the effects of cannabis use on the incidence of liver disease in individuals who abuse alcohol.” In their study, they analyzed discharge records from the 2014 Healthcare Cost and Utilization Project – Nationwide Inpatient Sample (NIS)
They studied four phases of liver disease in 319,000 patients, who had a past or current history of abusive alcohol use. The stages include: alcoholic steatosis (AS) or alcoholic fatty liver; steatohepatitis (AH) or non-alcoholic fatty liver; cirrhosis (AC); and hepatocellular carcinoma (HCC) or essentially liver cancer.
Our study revealed that among alcohol users, individuals who additionally use cannabis (dependent and non-dependent cannabis use) showed significantly lower odds of developing AS, AH, AC and HCC. Further, dependent users had significantly lower odds than non-dependent users for developing liver disease.
One of the biggest anti-cannabis arguments is that it impairs our cognitive abilities. Yet, is cannabis really all that bad for the brain?
According to recent animal research published in May 2017, tetrahydrocannabinol (THC) has a beneficial influence on the aging brain. Researchers tested the learning, memory, orientation and recognition skills in laboratory animals. They found that 18-month-old mice given THC demonstrated cognitive skills equal to 2-month-old controls. On the other hand, the placebo group showed cognitive deterioration normal in their age group.
Neurobiologist Andreas Zimmer of the University of Bonn stated:
The treatment completely reversed the loss of performance in the old animals. We repeated these experiments many times. It’s a very robust and profound effect.” Even more remarkable, gene activity and the molecular profile in the brain tissue was that of much younger animals. Specifically, neurons in the hippocampus grew more synaptic spines — points of contact necessary for communication between neurons.
Rather than dulling or impairing cognition, THC appears to reverse the aging process and improve mental processes. This raises the possibility it might be useful for the treatment of dementia.
4. Cannabinoids Have Anti-Tumor Potential
There is a plethora of anecdotal evidence that cannabinoids have helped patients slow down, control or even reverse cancer disease. Thus, many researchers have set out to understand the exact effect that cannabinoids have on cancer cells.
Specifically, much research surrounds the effects of THC and cannabidiol (CBD) cannabinoids, with many studies concluding that cannabis kills cancer cells.
For example, Dr. Christina Sanchez from the Complutense University of Madrid was involved in several studies that indicated THC is a cancer killer. One of her studies entailed the application of THC compounds to brain cancer cell cultures.
Sanchez and her team discovered that after being treated with THC, cancer cells were committing suicide. Sanchez explains why cannabis treatment is preferred over conventional treatments:
One of the advantages of cannabinoids, or cannabinoid based medicines, would be that they target a specifically, tumor cells. They don’t have any toxic effect on normal, non-tumoral cells. This is an advantage with respect to standard chemotherapy that target basically everything.
In another study, a synthetic form of THC called Dronabinol was just as effective. Researchers from University Hospital Tübingen in Germany evaluated the anti-leukemic efficacy of THC. They administered this cannabinoid to several types of leukemia cells ex vivo.
Our study provides rigorous data to support clinical evaluation of THC as a low-toxic therapy option in a well-defined subset of acute leukemia patients.
Mounting cannabis research indicates that cannabinoids may become the most promising cancer treatments yet available. Dr. Allen Herman, Chief Medical Officer at Cannabis Science, states:
Cannabis Science believes that cannabis extracts are critical instruments in cancer treatment and that we have an obligation to produce and make available the most effective and efficient cannabis products to our anti-cancer modalities.
5. Cannabis’ Impact on Cardiovascular Health is Still Unclear
There is some speculation that cannabis use may increase your risk of hypertension. But how much do we really know about the link between cardiovascular health and cannabis?
A group of researchers in California, Pennsylvania and New York evaluated 24 studies to see if they could identify a clear correlation. All the studies enrolled adults using some form of cannabis.
Some of the evaluated studies examined associations between cannabis use and vascular risk factors. These risk factors include hyperglycemia, diabetes, dyslipidemia, and obesity. The remainder of the studies examined the link between cannabis use and outcomes such as stroke, myocardial infarction, cardiovascular mortality, and all-cause mortality.
In the end, the researchers concluded that all of the evaluated studies were insufficient in offering sound evidence.
Evidence examining the effect of marijuana on diabetes, dyslipidemia, acute myocardial infarction, stroke, or cardiovascular and all-cause mortality was insufficient. Although the current literature includes several long-term prospective studies, they are limited by recall bias, inadequate exposure assessment, minimal marijuana exposure, and a predominance of low-risk cohorts.
Final Thoughts
The lack of mainstream reporting on cannabis research results from persistent opposition to the medical cannabis movement. Federal drug laws have stigmatized cannabis use, equating it to heroine and crack cocaine. As well, the mainstream medical industry aligns with the belief that cannabis is a dangerous drug. Therefore, it will take some time for the mainstream to recognize and publicize discoveries of the many health benefits of cannabis.
Regardless, it is important to remember that potential downsides to cannabis use do exist. As with all substances that affect the body, adverse effects may surface. With cannabis, for example, these effects include dizziness and increased anxiety. All the researchers involved in the studies mentioned herein have concluded that more cannabis research is imperative to fully understand the benefits and potential dangers of this plant.
Anna Hunt is writer, yoga instructor, mother of three, and lover of healthy food. She’s the founder of Awareness Junkie, an online community paving the way for better health and personal transformation. She’s also the co-editor at Waking Times, where she writes about optimal health and wellness. Anna spent 6 years in Costa Rica as a teacher of Hatha and therapeutic yoga. She now teaches at Asheville Yoga Center and is pursuing her Yoga Therapy certification. During her free time, you’ll find her on the mat or in the kitchen, creating new kid-friendly superfood recipes.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of Waking Times or its staff.
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