Lyme disease is a notoriously difficult condition to test for, and many doctors aren’t knowledgeable about it, which leads lots of Lyme patients to get misdiagnosed. The misdiagnoses of Lyme range from physical illnesses to psychological ones and often occur because Lyme can affect any organ system in the body in a multitude of ways, leading it to be labeled the “great imitator.”
What further compounds the confusion is that many people don’t notice contracting Lyme. “Infectious nymphal ticks are tiny — poppy seed sized — and tick bites can often go unnoticed. Most people never know they were bitten,” Sunjya K. Schweig, MD, scientific advisor to Bay Area Lyme Foundation, tells Bustle.
“The current ‘gold standard’ diagnostic for Lyme disease misses up to 60 percent of cases of early stage Lyme disease. If caught early, most cases of Lyme disease can be treated, but it is commonly misdiagnosed due to lack of awareness and unreliable diagnostic tests. If not treated promptly, Lyme may progress to a debilitating stage.”
Late-stage Lyme symptoms include paralysis, arthritis, neurological problems, headaches, cognitive impairment, memory problems, hearing and vision problems, inflammation of the brain (meningitis), and inflammation of the heart (carditis or pericarditis), Dr. Schweig says. But when people present with these symptoms, doctors don’t usually think to test for Lyme.
“It is important to recognize that Lyme disease is the most common vector-borne disease in the US, and the diagnosis should always be part of an appropriate differential diagnosis,” Dr. Schweig says. “There are about 329,000 new cases of Lyme disease each year.”
Here are some conditions that Lyme is commonly mistaken for, according to experts.
“The symptoms reported by patients diagnosed with fibromyalgia are almost identical to those associated with chronic Lyme disease,” Bill Rawls, MD, an integrative health expert on Lyme disease and other chronic illnesses, tells Bustle. These include joint pain, stiffness, fatigue, and brain fog. It’s unknown what exactly causes fibromyalgia, but Dr. Rawls believes it’s likely that it is usually caused by Lyme and/or other microbes.
Multiple Sclerosis is a central nervous system disease that affects myelin, the substance surrounding nerve fibers, causing symptoms like numbness, weakness, poor coordination, and vision problems. It has been linked to a variety of microbes including Borrelia burgdorferi, the bacteria known to cause Lyme, as well as chlamydia and the Espstein-Barr virus, Dr. Rawls says.
Lyme can cause pain, swelling, stiffness, and loss of function in the joints — similar symptoms to osteoarthritis and rheumatoid arthritis, Timothy J. Sellati, Ph.D., the Global Lyme Alliance’s chief scientific officer, tells Bustle. You can sometimes distinguish these conditions because Lyme is more likely to affect the large joints of the legs and occasionally the wrists, while other types of arthritis are more often in the hands, wrists, shoulders, knees, and feet. But the distinction isn’t always that clear-cut, so they’re often confused.
One common byproduct of Lyme’s effect on the brain is impaired concentration and memory, which can be confused with disorders like ADHD, Daniel Cameron, MD, MPH, an internist and epidemiologist who specializes in treating Lyme, tells Bustle. The brain fog and sleep disturbances that many people with Lyme experience compounds these issues.
In older people, these symptoms can sometimes be diagnosed as Alzheimer’s disease — and in fact, some research has linked Alzheimer’s to Borrelia burgdorferi. Research has also suggested that lipopeptides, the fatty acids created by Lyme bacteria, could interfere with communication between neurons, which may explain the memory and concentration difficulties.
People with chronic illnesses, especially women, often face the misconception that the root of their symptoms is psychological. This is especially true for Lyme. Lyme can cause a range of mental health symptoms including anxiety, depression, and rage, leading many Lyme patients to be diagnosed with mental illness, Dr. Cameron says.
It’s difficult to tell whether a psychiatric illness is caused by Lyme, but a sudden onset of psychiatric symptoms with no apparent cause, especially in conjunction with a tick bite or other Lyme symptoms, could point toward it.
Dr. Rawls believes anyone diagnosed with the most common Lyme misdiagnoses should look into the possibility that their condition is being caused by Lyme, co-infections, or similar microbes. But treatment doesn’t mean taking a round of antibiotics, which are often ineffective for chronic infections. Most people with Lyme have many different microbes that are very antibiotic-resistant, he explains, so the key is not to go after them in isolation but to strengthen the gut and immune system in order to keep them at bay.
“Restoration of normal immune system functions with natural therapy and suppression of stealth microbes with herbal therapy is often highly effective for restoring a normal state of health in affected individuals,” he says. “This approach is safe, nontoxic, and not dependent on a diagnosis. It should be the foundation for therapy for every one of these chronic illnesses.”
This idea that antibiotics don’t work is a bit premature. The studies have numerous flaws and have only been on a certain subset of patients. All I know is I’d more than likely be dead without them (my husband as well), with many other patients stating the same. Whenever you read someone’s opinion on Lyme treatment, always take into account what they are selling. Dr. Rawls is selling herbs, plain and simple. It’s a business for him. Just keep that in mind. While a patient himself, he has a vested interest in getting you to buy his products.
Recently, an article came out stating there’s an “untreatable” form of Lyme. Read my rebuttal here: https://madisonarealymesupportgroup.com/2019/04/29/is-the-sky-truly-going-to-fall-for-patients-with-the-untreatable-form-of-lyme-disease/
This IS treatable. It very well may not be curable, but then this is nothing new. The chicken pox virus isn’t truly curable in that it lies around in our spine – same with EBV. It’s only when our bodies become weak and out of balance that these things rear their little, ugly heads. So immune regulation IS important, but never, ever buy the line that antibiotics don’t work for this. (Of course there’s always exceptions to each and every rule).
Many advocates believe the Newsweek article is part of an orchestrated ploy to sell an upcoming Lyme vaccine. Authorities refuse to do transmission studies, drug effectiveness studies (on chronic patients), and so many other important issues needing resolution, but they keep coming back to the vaccine issue like buzzards drawn to dead bodies for the simple reason they smell a lot of money and many through the years have patents on the vaccine itself as well as Lyme test kits and other metabolomics: ConflictReport (Patents start on page 80) Conflicts of interest abound in every aspect of this.
As to the Lyme vaccine, please, please, do your reading: https://madisonarealymesupportgroup.com/2018/07/22/why-we-care-so-strongly-about-a-potential-lyme-vaccine/
This podcast features Jari Laukkanen, M.D., Ph.D., a cardiologist and scientist at the Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio. Dr. Laukkanen has been conducting long-term trials looking at the health effects of sauna use in a population of over 2,000 middle-aged men in Finland. The results? Massive reductions in mortality and memory disease in a dose-response fashion at 20-year follow-up. In this almost 25-minute episode, we talk about…
Further, Dr. Mary Shackelton, MPH, ND talks about skin as a pathway for detoxification and how important it is to sweat on a weekly basis. Infrared saunas are one of the most effective ways of releasing toxins from deep within one’s tissues.
https://madisonarealymesupportgroup.com/2018/01/03/the-invisible-universe-of-the-human-microbiome-msm/ Briefly, MSM stands for Methylsulfonylmethane and is 34% sulfur by weight. Sulfur plays a crucial role in detoxification and is an important antioxidant for producing glutathione. If you aren’t getting enough sulfur, glutathione can not work. Even if you have a diet rich in sulfur (think cabbage, onions, garlic, broccoli, etc – essentially the stinky veggies – and many other food items as well) your body still could use supplementation.
https://madisonarealymesupportgroup.com/2019/03/14/melatonin-benefits-uses/ Besides helping sleep, melatonin is known for protecting the brain. Research has shown starting to supplement in middle age protects against Alzheimer’s, reduces the risk of Parkinson’s, shrinks the size of the infarct area in a stroke, minimizes brain swelling & dysfunction after head injury, and increases the “longevity protein” SIRT1.
Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities.
For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame.
Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia.
In addition to plaques and tangles, other potential villains found in the brains of people with a diagnosis of Alzheimer’s include silent strokes and other blood vessel diseases, as well as a poorly understood condition called hippocampal sclerosis.
Potential culprits also include an accumulation of Alpha-synuclein, the abnormal protein that makes up Lewy bodies. And some patients have yet another abnormal protein in their brains, TDP-43.
No one knows how to begin approaching the multitude of other potential problems found in the brains of Alzheimer’s patients. So, until recently, they were mostly ignored.
“I wouldn’t say it’s a dirty little secret,” said Dr. John Hardy, an Alzheimer’s researcher at University College London. “Everybody knows about it. But we don’t know what to do about it.”
In interviews, some experts said they had been reluctant to talk much about mixed pathologies for fear of sounding too negative. But “at a certain point we have to be somewhat more realistic and rethink what we are doing,” said Dr. Albert Hofman, chairman of the epidemiology department at Harvard’s T.H. Chan School of Public Health.
The problem began with the very discovery of Alzheimer’s disease. In 1906, Dr. Alois Alzheimer, a German psychiatrist and neuroanatomist, described a 50-year-old woman with dementia.
On autopsy, he found peculiar plaques and twisted, spaghetti-like proteins known as tangles in her brain. Ever since, they have been considered the defining features of Alzheimer’s disease.
But scientists now believe this woman must have had a very rare genetic mutation that guarantees a person will get a pure form of Alzheimer’s by middle age.
Patients with the mutation appeared to develop only plaques and tangles, and no other pathologies. So for decades, plaques and tangles were the focus of research into dementia.
More plaques usually meant more severe dementia, in both older and younger patients. So researchers tested drugs that could attack amyloid or stop its production in genetically engineered mice. The drugs worked beautifully.
Scientists recognized that mice were an imperfect model — they never develop dementia — but the studies were encouraging. So it was a huge disappointment when, over and over, those drugs failed in clinical trials in patients.
“What motivates us is the depth of the unmet need,” said Dr. Dan Skovronsky, chief scientific officer of the drug company Eli Lilly, which continues to investigate anti-amyloid treatments.
“That’s why we keep going forward. But it is such a tough, tough problem, and made tougher because of the mixed pathology.”
What to do now? Scientists are struggling the reframe the problem. Some think research should be more focused on age.
“We can’t avoid the fact the number one risk factor for Alzheimer’s disease is age, and many of these other pathologies are age-associated,” said Dr. John Morris, a professor of neurology at Washington University in St. Louis. “We don’t see them in younger people.”
Carol Brayne, an epidemiologist at Cambridge University, has been saying as much for decades. There is something significant, she has found, about the obvious fact that the older a person gets, the more likely he or she is to develop dementia. By their 90s, one out of every two people has dementia.
A more optimistic view is that there may be something in the brain that sets off a cascade of multiple pathologies. If true, blocking that factor could stop the process and prevent dementia.
Dr. Hofman is convinced that the precipitating factor is diminished blood flow to the brain.
“Alzheimer’s disease is a vascular disease,” he said.
Supporting this view, he added, are data from nine studies in the United States and Western Europe consistently finding a 15 percent decline in the incidence of new Alzheimer’s cases over the past 25 years.
“Why is that? I think the only reasonable candidate is improved vascular health,” Dr. Hofman said. The most important factor is the decline in smoking, he believes, but people in rich countries also are more likely to better control high blood pressure and cholesterol levels.
Dr. Seth Love, professor of pathology at the University of Bristol in England, noted that a core feature of Alzheimer’s is a reduction in blood flow through the cerebrum of the brain.
That happens even in people with the genetic mutation that leads Alzheimer’s in middle age. Fifteen to 20 years before these people have dementia, blood to their brains slows.
“We don’t know why,” Dr. Love said.
Or perhaps it really is amyloid that begins the avalanche of other problems.
Some researchers still hold out hope that if anti-amyloid drugs are started early enough, they might prevent dementia. Clinical trials are testing the idea now in people genetically disposed to get Alzheimer’s disease.
But even if the drugs work, will they work in the elderly patients who make up the bulk of those with an Alzheimer’s diagnosis — but who don’t have anything resembling a pure form of the disease?
Perhaps those drugs will have only a small effect in patients with mixed pathologies, Dr. Hardy said. It would take gigantic trials going on for years to see such a tiny effect.
“Those aren’t the kind of medicines we are looking for,” said Dr. Skovronsky, of Eli Lilly. “We want something that has a big effect.”
Dr. Skovronsky has been forced to do some soul-searching. Trying anti-amyloid drugs in old people in the early or middle stages of Alzheimer’s just is not working.
But when is it best to intervene, and in whom? And do scientists need to find drugs for all the other pathologies in the brains of dementia patients, as well?
“It’s the right time to focus on these tough questions,” Dr. Skovronsky said.
Researchers are reporting new findings on how bacteria involved in gum disease can travel throughout the body, exuding toxins connected with Alzheimer’s disease, rheumatoid arthritis and aspiration pneumonia. They detected evidence of the bacteria in brain samples from people with Alzheimer’s and used mice to show that the bacterium can find its way from the mouth to the brain.
This article states that 50% of Alzheimer’s is caused by herpes simplex virus 1 (HSV1), the virus responsible for cold sores: https://neurosciencenews.com/herpes-virus-alzheimers-11021/
More than 5 million Americans are living with Alzheimer’s disease. Share the facts and join the fight at alz.org/facts.
By Dr. Mercola
Alzheimer’s disease — the most common form of dementia for which there is no effective conventional treatment or cure — currently affects an estimated 5.8 million Americans,1 up from 5.4 million in 2016. By 2050, that figure is projected to hit 14 million.2
Research3 published in 2014 revealed Alzheimer’s had risen to the point of being the third leading cause of death in the U.S.4 For clarification, while the Centers for Disease Control and Prevention (CDC) continues to list Alzheimer’s as the sixth leading cause of death in the U.S.,5 this ranking is based on death certificates, and the study in question found Alzheimer’s was grossly underreported as a cause of death on death certificates.
Recalculations based on the evaluation of donated organs from the diseased put the actual death toll attributable to dementia at 503,400, making it the third leading cause of death, right behind heart disease and cancer.
According to CDC data, the death rate from Alzheimer’s rose 55 percent between 1999 and 2014.6,7Now, the latest report from the National Center for Health Statistics reveals the rate of death from dementia more than doubled between 2000 and 2017, from 84,000 to 261,914.8,9,10
Forty-six percent of dementia deaths in 2017 were attributed to Alzheimer’s. Other forms of dementia included vascular dementia, unspecified dementia and other degenerative nervous system diseases. But again, this data is based on death certificates, which the CDC admits (and the 2014 study above demonstrated) underrepresents the true death toll.
As noted by CNN, progression of Alzheimer’s disease varies, but often begin with short-term memory lapses that later progress to speech problems and trouble with executive functions.11
If changes in your memory or thinking skills are severe enough to be noticed by your friends and family you could be facing mild cognitive impairment (MCI). MCI is a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease.
If your mental changes are so significant that they interfere with your ability to function or live independently, it could signal the onset of dementia. For instance, it’s normal to have trouble finding the right word on occasion, but if you forget words frequently and repeat phrases and stories during a conversation, there could be a problem.
The video above reviews 10 early warning signs of Alzheimer’s, and compares these signs with examples of typical age-related cognitive changes that are not a major cause for concern. You can also find a similar list compiled by the Alzheimer’s Association.12
Another red flag is getting lost or disoriented in familiar places (as opposed to needing to ask for directions on occasion). If you’re able to later describe a time when you were forgetful, such as misplacing your keys, that’s a good sign; a more serious signal is not being able to recall situations when memory loss caused a problem, even though your loved ones describe it to you. Other warning signs of MCI or dementia include:
|Difficulty performing daily tasks like paying bills or taking care of personal hygiene|
|Asking the same question over and over|
|Difficulty making choices|
|Exhibiting poor judgment or inappropriate social behaviors|
|Changes in personality or loss of interest in favorite activities|
|Memory lapses that put people in danger, like leaving the stove on|
|Inability to recognize faces or familiar objects|
|Denying a memory problem exists and getting angry when others bring it up|
If your memory slips often enough to put even an inkling of concern or doubt in your mind, it’s time to take action. A high-fat, moderate-protein, low-net-carb ketogenic diet is crucial for protecting your brain health and preventing degeneration that can lead to Alzheimer’s.
One of the most striking studies13 showing the effects of a high-fat/low-carb versus high-carb diets on brain health revealed that high-carb diets increase your risk of dementia by a whopping 89 percent, while high-fat diets lower it by 44 percent.
According to the authors, “A dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of mild cognitive impairment or dementia in elderly persons.” A ketogenic diet benefits your brain in a number of different ways. For example, it:
• Triggers ketone production — A cyclical ketogenic diet will help you convert from carb-burning mode to fat-burning mode, which in turn triggers your body to produce ketones, an important source of energy (fuel) for your brain14 that have been shown to help prevent brain atrophy and alleviate symptoms of Alzheimer’s.15 They may even restore and renew neuron and nerve function in your brain after damage has set in.
• Improves your insulin sensitivity — A cyclical ketogenic diet will also improve your insulin sensitivity, which is an important factor in Alzheimer’s.16 The link between insulin sensitivity and Alzheimer’s is so strong, the disease is sometimes referred to as Type 3 diabetes.
Even mild elevation of blood sugar is associated with an elevated risk for dementia.17 Diabetes and heart disease18 are also known to elevate your risk, and both are rooted in insulin resistance.
The connection between high-sugar diets and Alzheimer’s was also highlighted in a longitudinal study published in the journal Diabetologia in January 2018.19 Nearly 5,190 individuals were followed over a decade, and the results showed that the higher an individual’s blood sugar, the faster their rate of cognitive decline.
Studies have also confirmed that the greater an individual’s insulin resistance, the less sugar they have in key parts of their brain, and these areas typically correspond to the areas affected by Alzheimer’s.20,21
• Reduces free radical damage and lowers inflammation in your brain — Ketones not only burn very efficiently and are a superior fuel for your brain, but also generate fewer reactive oxygen species and less free radical damage.
A ketone called beta hydroxybutyrate is also a major epigenetic player, stimulating radical decreases in oxidative stress by decreasing NF-kB, thus reducing inflammation and NADPH levels along with beneficial changes in DNA expression that improve your detoxification and antioxidant production.
I explain the ins and outs of implementing this kind of diet, and its many health benefits, in my new book “KetoFast.” In it, I also explain why cycling through stages of feast and famine, opposed to continuously remaining in nutritional ketosis, is so important.
It’s often said that the underlying causes of Alzheimer’s disease are unknown, but there’s no shortage of theories. Insulin resistance, discussed above, appears to be a really significant factor, but it’s not the only one. Based on the available science, here are several other prominent or likely culprits that can raise your risk of Alzheimer’s disease, and suggestions for how to avoid them:
|High-sugar, processed food diets — Insulin resistance is a direct result of a high-sugar diet. Processed foods also contain a number of other ingredients that are harmful to your brain, including gluten, vegetable oils, genetically engineered ingredients and pesticides.
Solution: Keep your fasting insulin levels below 3; minimize sugar consumption, boost healthy fat intake and focus on real food — If your insulin is high, you’re likely consuming too much sugar and need to cut back. Ideally, keep your added sugar to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you already have insulin/leptin resistance or any related disorders.
To get down to this level, you’ll have to eat real, whole food, as processed foods are chockfull of added sugars. It’s important to realize that your brain actually does not need carbs and sugars; healthy fats such as saturated animal fats and animal-based omega-3 are far more critical for optimal brain function.
Also remember to pay close attention to the kinds of fats you eat — avoid all trans fats or hydrogenated fats. This includes margarine, vegetable oils and various butter-like spreads.
Healthy fats to add to your diet include avocados, butter, organic pastured egg yolks, coconuts and coconut oil, grass fed meats and raw nuts such as pecans and macadamia. MCT oil is also a great source of ketone bodies.
|Alcohol abuse — According to research22 published in 2018, alcohol use is a major risk factor for dementia. The study, the largest of its kind, concluded that alcohol use disorders “are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia,” Science News reports.23
Solution: Limit alcohol use, and get treatment for alcohol use disorder.
|Vitamin D deficiency — The Scotland Dementia Research Centre has noted a very clear link between vitamin D deficiency and dementia.24 Indeed, studies have shown vitamin D plays a critical role in brain health, immune function, gene expression and inflammation — all of which influence Alzheimer’s. A wide variety of brain tissue contains vitamin D receptors, and when they’re activated by vitamin D, it facilitates nerve growth in your brain.
Researchers also believe optimal vitamin D levels boost levels of important brain chemicals and protect brain cells by increasing the effectiveness of glial cells in nursing damaged neurons back to health. In a 2014 study,25 considered to be the most robust study of its kind at the time, those who were severely deficient in vitamin D had a 125 percent higher risk of developing some form of dementia compared to those with normal levels.
The findings also suggest there’s a threshold level of circulating vitamin D, below which your risk for dementia increases. This threshold was found to be right around 20 nanograms per milliliter (ng/ml) or 50 nanomoles per liter (nmol/L) for Europeans. Higher levels are associated with better brain health in general, and based on a broader view of the available science, 20 ng/ml is still far too low.
Solution: Optimize your vitamin D level — The bulk of the research suggests maintaining a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L) year-round. Ideally, get your level checked twice a year, and if you’re unable to maintain a healthy level through sensible sun exposure alone, be sure to take an oral vitamin D3 supplement.
|Low omega-3 level — According to neuroimaging research, low omega-3 may be a factor in Alzheimer’s,26 and omega-3 is certainly a crucial component for optimal brain health in general. People with higher omega-3 levels were found to have increased blood flow in areas of the brain associated with memory and learning.
The Journal of Alzheimer’s Disease also notes animal research showing omega-3 fatty acids have been shown to have anti-amyloid, anti-tau and anti-inflammatory activity in the brain.27
Solution: Optimize your omega-3 index — Ideally, get an omega-3 index test done once a year to make sure you’re in a healthy range. Your omega-3 index should be above 8 percent and your omega 6-to-3 ratio between 0.5 and 3.0.
|Lack of sun exposure — While vitamin D deficiency is directly attributable to lack of sensible sun exposure, vitamin D production is not the only way sun exposure can influence your dementia risk. Evidence suggests sunlight is a beneficial electromagnetic frequency (EMF) that is in fact essential and vital for your health in its own right.
About 40 percent of the rays in sunlight is infrared. The red and near-infrared frequencies interact with cytochrome c oxidase (CCO) — one of the proteins in the inner mitochondrial membrane and a member of the electron transport chain.
CCO is a chromophore, a molecule that attracts and absorbs light. In short, sunlight improves the generation of energy (ATP). The optimal wavelength for stimulating CCO lies in two regions, red at 630 to 660 nanometers (nm) and near-infrared at 810 to 850 nm.
Solution: Get regular sun exposure and/or consider photobiomodulation therapy — I’ve interviewed two different experts on photobiomodulation, a term describing the use of near-infrared light as a treatment for Alzheimer’s. To learn more about this fascinating field, please see my interviews with Michael Hamblin, Ph.D., and Dr. Lew Lim. Both have published papers on using photobiomodulation to improve Alzheimer’s disease.
|Prion infection — In addition to viruses, bacteria and fungi, an infectious protein called TDP-43, which behaves like infectious proteins known as prions — responsible for the brain destruction that occurs in mad cow and chronic wasting diseases — has been linked to Alzheimer’s.
Research presented at the 2014 Alzheimer’s Association International Conference revealed Alzheimer’s patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without.28 Last year, researchers also found they could measure the distribution and levels of prions in the eye,29 thereby improving diagnosis of Creutzfeldt-Jakob disease (CJD), the human version of mad cow disease.
Solution: Avoid eating meat from animals raised in concentrated animal feeding operations (CAFOs) — Due to its similarities with mad cow disease, investigators have raised the possibility that Alzheimer’s disease may be linked to CAFO meat consumption. There are many reasons to avoid CAFO animal products, and this is yet another one, even if this particular risk is small.
|Environmental toxins, including electromagnetic fields (EMF) — Experts at the Edinburgh University’s Alzheimer Scotland Dementia Research Centre have compiled a list of top environmental risk factors thought to be contributing to the epidemic, based on a systematic review of the scientific literature.30,31,32
As much as one-third of your dementia risk is thought to be linked to environmental factors such as air pollution, pesticide exposure and living close to power lines. The risk factor with the most robust body of research behind it is air pollution. In fact, they couldn’t find a single study that didn’t show a link between exposure to air pollution and dementia.
Particulate matter, nitric oxides, ozone and carbon monoxide have all been linked to an increased risk. Living close to power lines also has “limited yet robust” evidence suggesting it may influence your susceptibility to dementia.
Solution: Minimize exposure to environmental toxins and EMFs — In terms of air pollution, it’s worth remembering that your indoor air is often five times more polluted than outdoor air, and indoors, it’s something you can control, using a high-quality air purifier. Pesticides can be avoided by eating certified organic foods.
Non-native EMFs contribute to Alzheimer’s by poisoning your mitochondria, and this is not limited to living in close proximity to power lines. It also includes electromagnetic interference from the electric grid and microwave radiation from your cellphone, cellphone towers, Wi-Fi and more.
Radiation from cellphones and other wireless technologies trigger excessive production of peroxynitrites,33 a highly damaging reactive nitrogen species. Increased peroxynitrites from cellphone exposure will damage your mitochondria,34,35 and your brain is the most mitochondrial-dense organ in your body. To learn more about the mechanisms that place your health in jeopardy, and what you can do about it, see “Top 19 Tips to Reduce Your EMF Exposure.”
|Inactivity / lack of exercise — Exercise has been shown to protect your brain from Alzheimer’s and other dementias,36 and also improves quality of life if you’ve already been diagnosed.
In one study,37,38 patients diagnosed with mild to moderate Alzheimer’s who participated in a four-month-long supervised exercise program had significantly fewer neuropsychiatric symptoms associated with the disease (especially mental speed and attention) than the inactive control group.
Other studies39 have shown aerobic exercise helps reduce tau levels in the brain. (Brain lesions known as tau tangles form when the protein tau collapses into twisted strands that end up killing your brain cells.) Cognitive function and memory40 can also be improved through regular exercise, and this effect is in part related to the effect exercise has on neurogenesis and the regrowth of brain cells.
By targeting a gene pathway called brain-derived neurotrophic factor (BDNF), exercise actually promotes brain cell growth and connectivity. In one yearlong study,41 seniors who exercised grew and expanded their brain’s memory center by as much as 2 percent per year, where typically that center shrinks with age.
Evidence also suggests exercise can trigger a change in the way the amyloid precursor protein is metabolized,42 thus slowing the onset and progression of Alzheimer’s. By increasing levels of the protein PGC-1alpha (which Alzheimer’s patients have less of), brain cells produce less of the toxic amyloid protein associated with Alzheimer’s.43 As noted in one 2016 paper on this topic:44
Solution: Move regularly and consistently throughout the day, and implement a regular exercise routine.
|Hypertension and heart disease — Arterial stiffness (atherosclerosis) is associated with a hallmark process of Alzheimer’s, namely the buildup of beta-amyloid plaque in your brain. The American Heart Association warns there’s a strong association between hypertension and brain diseases such as vascular cognitive impairment (loss of brain function caused by impaired blood flow to your brain) and dementia.45
Solution: Address high blood pressure and risk factors for heart disease — One of the most important all-natural remedies for high blood pressure is to raise your nitric oxide production, which can be done through high-intensity exercise (including the super-simple Nitric Oxide Dump exercise), high-nitrate foods such as beets and arugula.
For more information, see “Top 9 Reasons to Optimize Your Nitric Oxide Production” and “How to Successfully Control High Blood Pressure Without Medications.”
|Genetic predisposition — Several genes that predispose you to Alzheimer’s have been identified.46 The most common gene associated with late onset Alzheimer’s is the apolipoprotein E (APOE) gene. The APOE e2 form is thought to reduce your risk while the APOE e4 form increases it.
That said, some people never develop the disease even though they’ve inherited the APOE e4 gene from both their mother and father (giving them a double set), so while genetics can affect your risk, it is NOT a direct or inevitable cause. Your risk for early onset familial Alzheimer’s can also be ascertained through genetic testing.47 In this case, by looking for mutation in the genes for presenilin 1 and presenilin 2.
Solution: Genetic testing to help ascertain your risk — People with one or more genetic predispositions are at particularly high risk of developing Alzheimer’s at a very young age.
In 2014, Bredesen published a paper that demonstrates the power of lifestyle choices for the prevention and treatment of Alzheimer’s. By leveraging 36 healthy lifestyle parameters, he was able to reverse Alzheimer’s in 9 out of 10 patients. This included the use of exercise, ketogenic diet, optimizing vitamin D and other hormones, increasing sleep, meditation, detoxification and eliminating gluten and processed food.
You can download Bredesen’s full-text case paper online, which details the full program.48 Following are a few lifestyle strategies that, in addition to those already mentioned above, can be helpful for the prevention of dementia and Alzheimer’s.
|Optimize your gut flora — To do this, avoid processed foods, antibiotics and antibacterial products, fluoridated and chlorinated water, and be sure to eat traditionally fermented and cultured foods, along with a high-quality probiotic if needed. Dr. Steven Gundry does an excellent job of expanding on this in his new book “The Plant Paradox.”|
|Intermittently fast — Intermittent fasting is a powerful tool to jump-start your body into remembering how to burn fat and repair the insulin/leptin resistance that is a primary contributing factor for Alzheimer’s.|
|Optimize your magnesium levels — Preliminary research strongly suggests a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Keep in mind that the only magnesium supplement that appears to be able to cross the blood-brain barrier is magnesium threonate.|
|Avoid and eliminate mercury from your body — Dental amalgam fillings are one of the major sources of heavy metal toxicity; however, you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.|
|Avoid and eliminate aluminum from your body — Common sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants. For tips on how to detox aluminum, see “Top Tips to Detox Your Body.”|
|Avoid flu vaccinations — Most flu vaccines contain both mercury and aluminum.|
|Avoid statins and anticholinergic drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers.
Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10, vitamin K2 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.
|Optimize your sleep — Sleep is necessary for maintaining metabolic homeostasis in your brain. Without sufficient sleep, neuron degeneration sets in, and catching up on sleep during weekends will not prevent this damage.49,50,51
Sleep deprivation causes disruption of certain synaptic connections that can impair your brain’s ability for learning, memory formation and other cognitive functions. Poor sleep also accelerates the onset of Alzheimer’s disease.52
Most adults need seven to nine hours of uninterrupted sleep each night. Deep sleep is the most important, as this is when your brain’s glymphatic system performs its cleanout functions, eliminating toxic waste from your brain, including amyloid beta. For a comprehensive sleep guide, see “33 Secret’s to a Good Night’s Sleep.”
|Challenge your mind daily — Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of dementia and Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.|
For more on the link between Lyme/MSIDS & Alzheimer’s/dementia: https://madisonarealymesupportgroup.com/2018/10/03/chronology-of-research-on-lyme-disease-dementia-alzheimers-parkinsons-autism/
https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/ Bacteria are usually ignored despite its historical and current significance in dementia research. Today, the main bacterial threat to acquiring dementia comes from Lyme disease—a bacterium borrelia burgdorferi.
https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/ Kris Kristofferson was wrongly diagnosed with Alzheimer’s but had Lyme Disease. For years doctors told Kristofferson it was either Alzheimer’s or dementia, and may have been the result of blows to his head from boxing, football and rugby. The medication he was given gave him bad side effects and didn’t help. Since starting treatment for Lyme Kristofferson “has made remarkable strides.” His wife Lisa said,
“all of the sudden he was back.” Although he still has some bad days, there are other days when he is “perfectly normal,” she said.
https://madisonarealymesupportgroup.com/2019/03/10/baseballs-tom-seaver-diagnosed-with-dementia/ According to reports by the Associated Press, the New York Times, and other news outlets, baseball Hall of Famer Tom Seaver has been diagnosed with dementia. This comes some 28 years after Seaver was first diagnosed with Lyme disease.
A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.
This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.
Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.
Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.
“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.
Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said:
“The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”
The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.
Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152
Microbes and Alzheimer’s Disease
We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.
AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic.
“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT03282916|
Recruitment Status : Recruiting
First Posted : September 14, 2017
Last Update Posted : January 25, 2019
|Condition or disease||Intervention/treatment||Phase|
|Alzheimer DiseaseHerpes Simplex 1Herpes Simplex 2||Drug: ValacyclovirDrug: Placebo||Phase 2|
Many viruses are latent for decades before being reactivated in the brain by stress, immune compromise, or other factors. After the initial oral infection, herpes simplex virus-1 (HSV1) becomes latent in the trigeminal ganglion and can later enter the brain via retrograde axonal transport, often targeting the temporal lobes.
HSV1 can also enter the brain via olfactory neurons directly. HSV1 (oral herpes) and HSV2 (genital herpes) are known to trigger amyloid aggregation and their DNA is commonly found in amyloid plaques. Anti-HSV drugs reduce Aβ and p-tau accumulation in brains of infected mice. HSV1 reactivation is associated with tau hyperphosphorylation in mice and may play a role in tau propagation across neurons. In humans, recurrent reactivation with newly produced HSV1 particles, ‘drop by drop,’ may produce neuronal damage and eventually lead to neurodegeneration and Alzheimer’s disease (AD) pathology, partly due to effects on amyloid and tau. Clinical studies show cognitive impairment in HSV seropositive patients in different patient groups and in healthy adults, and antiviral treatments show robust efficacy against peripheral HSV infection. The study team will conduct the first-ever clinical trial to directly address the long-standing viral etiology hypothesis of AD which posits that viruses, particularly the very common HSV1 and HSV2, may be etiologic or contribute to the pathology of AD.
In patients with mild AD who test positive for serum antibodies to HSV1 or HSV2, the generic antiviral drug valacyclovir, repurposed as an anti-AD drug, will be compared at oral doses of 2 to 4 grams per day to matching placebo in the treatment of 130 patients (65 valacyclovir, 65 placebo) in a randomized, double-blind, 78-week Phase II proof of concept trial. Patients treated with valacyclovir are hypothesized to show smaller decline in cognition and functioning compared to placebo, and, using 18F-Florbetapir PET imaging, to show less amyloid accumulation than placebo over the 78-week trial. Through the use of tau PET imaging with the tracer 18F-MK-6240 at baseline and 78 weeks, patients treated with valacyclovir are hypothesized to show smaller increases in 18F-MK-6240 binding than patients treated with placebo from baseline to 78 weeks. Apolipoprotein E genotype at baseline, as well as changes in cortical thinning on structural MRI, olfactory identification deficits, and antiviral antibody titers from baseline to 78 weeks, will be evaluated in exploratory analyses. In patients who agree to lumbar puncture, plasma and CSF acyclovir will be assayed to establish the degree of CNS penetration of valacyclovir in mild AD, and the investigators will obtain CSF Aβ42, tau, p-tau for subset exploratory analyses with changes in outcome measures.
If this trial is successful, the investigators will apply for funding to conduct a larger, multicenter, Phase III study using a study design that will be informed by the results of this Phase II trial. This innovative Phase II proof of concept trial clearly has exceptionally high reward potential for the treatment of AD.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||130 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Triple (Participant, Care Provider, Investigator)|
|Official Title:||Anti-viral Therapy in Alzheimer’s Disease|
|Actual Study Start Date :||February 12, 2018|
|Estimated Primary Completion Date :||August 2022|
|Estimated Study Completion Date :||August 2022|