Outer surface protein C (OspC) is one of the most abundant surface lipoproteins produced during early infection by the Borrelia spirochete, the causative agent of Lyme disease. The high sequence variability of the ospC gene results in the production of several and strongly divergent OspC types. One of the known roles of OspC is the recruitment of blood components, including complement regulators, to facilitate the bloodstream survival of Borrelia at an essential stage of host infection. Here, we identify and describe a new interaction between OspC and human fibrinogen. To test the ability of OspC to bind fibrinogen, we developed a microscale thermophoresis assay using four fluorescently labeled types of OspC. We show that OspC binds fibrinogen tightly, with nanomolar Kd, and that the binding depends on the OspC type. The binding assays combined with SAXS studies allowed us to map the OspC-binding site on the fibrinogen molecule. Spectrometric measurements of fibrinogen clotting in the presence of OspC indicate that OspC negatively influences the clot formation process. Taken together, our findings are consistent with the hypothesis that OspC interacts with blood protein partners to facilitate Borrelia spreading by the hematogenous route.
Great article on homocysteine and fibrinogen, two biomarkers of inflammation: http://blog.wellnessfx.com/2013/09/16/take-deeper-look-two-biomarkers-inflammation/ There’s even a link between the two biomarkers. High homocysteine levels block the natural breakdown of fibrinogen, leading to a buildup of fibrinogen in the blood which can cause hyper coagulation.
If you struggle with hyper coagulation(thick blood) work with your practitioner as this can hamper the effectiveness of treatment as well as compromise nutrient and oxygen delivery to the body. Also, thicker blood requires the heart to work harder to circulate blood. Some also feel it can deprive the gut of nourishment and may be a factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. https://www.diagnose-me.com/symptoms-of/hypercoagulation-thickened-blood.php. This link also explains testing as well as potential treatments to discuss with your doctor.
Many Lyme/MSIDS struggle with hyper coagulation. My husband does and took heparin for years during treatment. He felt better immediately. He has since weaned from that onto increased fish oil, Berberine, and Systemic Enzymes. Nattokinase is also recommended.
The take home from this study is that Bb uses components of our blood to propagate itself.
Antibiotics can disturb gastrointestinal microbiota which may lead to reduced resistance to pathogens such as Clostridium difficile (C. difficile). Probiotics are live microbial preparations that, when administered in adequate amounts, may confer a health benefit to the host, and are a potential C. difficile prevention strategy. Recent clinical practice guidelines do not recommend probiotic prophylaxis, even though probiotics have the highest quality evidence among cited prophylactic therapies.
Objectives
To assess the efficacy and safety of probiotics for preventing C.difficile‐associated diarrhea (CDAD) in adults and children.
Search methods
We searched PubMed, EMBASE, CENTRAL, and the Cochrane IBD Group Specialized Register from inception to 21 March 2017. Additionally, we conducted an extensive grey literature search.
Selection criteria
Randomized controlled (placebo, alternative prophylaxis, or no treatment control) trials investigating probiotics (any strain, any dose) for prevention of CDAD, or C. difficile infection were considered for inclusion.
Data collection and analysis
Two authors (independently and in duplicate) extracted data and assessed risk of bias. The primary outcome was the incidence of CDAD. Secondary outcomes included detection of C. difficile infection in stool, adverse events, antibiotic‐associated diarrhea (AAD) and length of hospital stay. Dichotomous outcomes (e.g. incidence of CDAD) were pooled using a random‐effects model to calculate the risk ratio (RR) and corresponding 95% confidence interval (95% CI). We calculated the number needed to treat for an additional beneficial outcome (NNTB) where appropriate. Continuous outcomes (e.g. length of hospital stay) were pooled using a random‐effects model to calculate the mean difference and corresponding 95% CI. Sensitivity analyses were conducted to explore the impact of missing data on efficacy and safety outcomes. For the sensitivity analyses, we assumed that the event rate for those participants in the control group who had missing data was the same as the event rate for those participants in the control group who were successfully followed. For the probiotic group, we calculated effects using the following assumed ratios of event rates in those with missing data in comparison to those successfully followed: 1.5:1, 2:1, 3:1, and 5:1. To explore possible explanations for heterogeneity, a priori subgroup analyses were conducted on probiotic species, dose, adult versus pediatric population, and risk of bias as well as a post hoc subgroup analysis on baseline risk of CDAD (low 0% to 2%; moderate 3% to 5%; high > 5%). The overall quality of the evidence supporting each outcome was independently assessed using the GRADE criteria.
Main results
Thirty‐nine studies (9955 participants) met the eligibility requirements for our review. Overall, 27 studies were rated as either high or unclear risk of bias. A complete case analysis (i.e. participants who completed the study) among trials investigating CDAD (31 trials, 8672 participants) suggests that probiotics reduce the risk of CDAD by 60%. The incidence of CDAD was 1.5% (70/4525) in the probiotic group compared to 4.0% (164/4147) in the placebo or no treatment control group (RR 0.40, 95% CI 0.30 to 0.52; GRADE = moderate). Twenty‐two of 31 trials had missing CDAD data ranging from 2% to 45%. Our complete case CDAD results proved robust to sensitivity analyses of plausible and worst‐plausible assumptions regarding missing outcome data and results were similar whether considering subgroups of trials in adults versus children, inpatients versus outpatients, different probiotic species, lower versus higher doses of probiotics, or studies at high versus low risk of bias. However, in a post hoc analysis, we did observe a subgroup effect with respect to baseline risk of developing CDAD. Trials with a baseline CDAD risk of 0% to 2% and 3% to 5% did not show any difference in risk but trials enrolling participants with a baseline risk of > 5% for developing CDAD demonstrated a large 70% risk reduction (interaction P value = 0.01). Among studies with a baseline risk > 5%, the incidence of CDAD in the probiotic group was 3.1% (43/1370) compared to 11.6% (126/1084) in the control group (13 trials, 2454 participants; RR 0.30, 95% CI 0.21 to 0.42; GRADE = moderate). With respect to detection of C. difficile in the stool pooled complete case results from 15 trials (1214 participants) did not show a reduction in infection rates. C. difficile infection was 15.5% (98/633) in the probiotics group compared to 17.0% (99/581) in the placebo or no treatment control group (RR 0.86, 95% CI 0.67 to 1.10; GRADE = moderate). Adverse events were assessed in 32 studies (8305 participants) and our pooled complete case analysis indicates probiotics reduce the risk of adverse events by 17% (RR 0.83, 95% CI 0.71 to 0.97; GRADE = very low). In both treatment and control groups the most common adverse events included abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance.
Authors’ conclusions
Based on this systematic review and meta‐analysis of 31 randomized controlled trials including 8672 patients, moderate certainty evidence suggests that probiotics are effective for preventing CDAD (NNTB = 42 patients, 95% CI 32 to 58). Our post hoc subgroup analyses to explore heterogeneity indicated that probiotics are effective among trials with a CDAD baseline risk >5% (NNTB = 12; moderate certainty evidence), but not among trials with a baseline risk ≤5% (low to moderate certainty evidence). Although adverse effects were reported among 32 included trials, there were more adverse events among patients in the control groups. The short‐term use of probiotics appears to be safe and effective when used along with antibiotics in patients who are not immunocompromised or severely debilitated. Despite the need for further research, hospitalized patients, particularly those at high risk of CDAD, should be informed of the potential benefits and harms of probiotics.
What is Clostridium difficile‐associated diarrhea?
Antibiotics are among the most prescribed medications worldwide. Antibiotic treatment may disturb the balance of organisms that normally populate the gut. This can result in a range of symptoms, most notably, diarrhea. Clostridium difficile (C. difficile) is a particularly dangerous organism that may colonize the gut if the normal healthy balance has been disturbed. Clostridium difficile‐related disease varies from asymptomatic infection, diarrhea, colitis, and pseudo‐membranous colitis to toxic megacolon and death. The cost of treatment is expensive and the financial burden on the medical system is substantial.
What are probiotics?
Probiotics are live organisms (bacteria or yeast) thought to improve the balance of organisms that populate the gut, counteracting potential disturbances to the gut microbial balance that are associated with antibiotic use, and reducing the risk of colonization by pathogenic bacteria. Probiotics can be found in dietary supplements or yogurts and are becoming increasingly available as capsules sold in health food stores and supermarkets. As ‘functional food’ or ‘good bacteria’, probiotics have been suggested as a means of both preventing and treating C. difficile‐associated diarrhea (CDAD).
What did the researchers investigate?
The researchers investigated whether probiotics prevent CDAD in adults and children receiving antibiotic therapy and whether probiotics causes any harms (side effects). The researchers searched the medical literature extensively up to 21 March 2017.
What did the researchers find?
This review includes 39 randomized trials with a total of 9955 participants. Thirty‐one studies (8672 participants) assessed the effectiveness of probiotics for preventing CDAD among participants taking antibiotics. Our results suggest that when probiotics are given with antibiotics the risk of developing CDAD is reduced by 60% on average.Among trials enrolling participants at high risk of developing CDAD (> 5%), the potential benefit of probiotics is more pronounced with a 70% risk reduction on average. Side effects were assessed in 32 studies (8305 participants) and our results suggest that taking probiotics does not increase the risk of developing side effects. The most common side effects reported in these studies include abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance. The short‐term use of probiotics appears to be safe and effective when used along with antibiotics in patients who are not immunocompromised or severely debilitated. Despite the need for further research, hospitalized patients, particularly those at high risk of CDAD, should be informed of the potential benefits and harms of probiotics.
Alzheimer’s disease — the most severe form of dementia for which there is no effective conventional treatment or cure — currently affects an estimated 5.8 million Americans. By 2050, that figure is projected to hit 14 million
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
This data are based on death certificates, which the CDC admits (and a 2014 study demonstrated) underrepresents the true death toll
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, a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease. Early warning signs are discussed
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. Other risk factors and suggestions for how to minimize your risk are discussed
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.
Could Your Memory Problems Be a Symptom of Alzheimer’s?
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 Is Slipping, Switch to a Ketogenic Diet
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.
What Do We Know About the Causes of Alzheimer’s Disease?
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.28Last 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
“Moderate and high intensities have demonstrated a neuroprotective effect through the production of antioxidant enzymes and growth factors such as superoxide dismutase, eNOS, BDNF, nerve growth factors, insulin-like growth factors and vascular endothelial growth factor and by reducing the production of ROS, neuroinflammation, the concentration of Aβ plaques in cognitive regions and tau pathology, leading to the improvement of cerebral blood flow, hyperemia, cerebrovascular reactivity and memory.”
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.
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.
Additional Alzheimer’s Preventive Strategies
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.
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.
There are 17 human-biting ticks known in Australia. The bites of Ixodes holocyclus, Ornithodoros capensis, and Ornithodoros gurneyi can cause paralysis, inflammation, and severe local and systemic reactions in humans, respectively. Six ticks, including Amblyomma triguttatum, Bothriocroton hydrosauri, Haemaphysalis novaeguineae, Ixodes cornuatus, Ixodes holocyclus, and Ixodes tasmani may transmit Coxiella burnetii, Rickettsia australis, Rickettsia honei, or Rickettsia honei subsp. marmionii. These bacterial pathogens cause Q fever, Queensland tick typhus (QTT), Flinders Island spotted fever (FISF), and Australian spotted fever (ASF). It is also believed that babesiosis can be transmitted by ticks to humans in Australia.
In addition, Argas robertsi, Haemaphysalis bancrofti, Haemaphysalis longicornis, Ixodes hirsti, Rhipicephalus australis, and Rhipicephalus sanguineus ticks may play active roles in transmission of other pathogens that already exist or could potentially be introduced into Australia. These pathogens include Anaplasma spp., Bartonella spp., Burkholderia spp., Francisella spp., Dera Ghazi Khan virus (DGKV), tick-borne encephalitis virus (TBEV), Lake Clarendon virus (LCV), Saumarez Reef virus (SREV), Upolu virus (UPOV), or Vinegar Hill virus (VINHV).
It is important to regularly update clinicians’ knowledge about tick-borne infections because these bacteria and arboviruses are pathogens of humans that may cause fatal illness. An increase in the incidence of tick-borne infections of human may be observed in the future due to changes in demography, climate change, and increase in travel and shipments and even migratory patterns of birds or other animals. Moreover, the geographical conditions of Australia are favorable for many exotic ticks, which may become endemic to Australia given an opportunity. There are some human pathogens, such as Rickettsia conorii and Rickettsia rickettsii that are not currently present in Australia, but can be transmitted by some human-biting ticks found in Australia, such as Rhipicephalus sanguineus, if they enter and establish in this country.
Despite these threats, our knowledge of Australian ticks and tick-borne diseases is in its infancy.
**Comment**
I appreciate the way the researchers wrote about the possibility of infection even though there are not recorded cases yet. This open-mindedness is imperative if we are to move forward. Gone are the days where tick-borne illness is presented as if the information were akin to the 10 commandments.
Tick-borne illness has become a true pandemic and is found virtually everywhere.
While Lyme is not mentioned (please note further down that autopsy results showed Lyme all over a man from Sydney) the following infections are on record:
Q fever
Queensland tick typhus (QTT)
Flinders Island spotted fever (FISF)
Australian spotted fever (ASF)
Babesiosis
Anaplasma spp.
Bartonella spp.
Burkholderia spp.
Francisella spp. (Tularemia)
Dera Ghazi Khan virus (DGKV)
tick-borne encephalitis virus (TBEV)
Lake Clarendon virus (LCV)
Saumarez Reef virus (SREV)
Upolu virus (UPOV)
Vinegar Hill virus (VINHV)
I would say that is quite enough to make our Aussie friends quite sick.
The authors of a new study conclude that healthful food prescriptions in Medicare and Medicaid would be more cost-effective after 5 years than preventive drug treatments.
As the cost of healthcare rises, could prescription vegetables save money?
Medicare and Medicaid are the two largest healthcare programs in the United States.
Approximately 57 million people received coverage from Medicare plans in 2016, while Medicaid had about 66 million enrollees in 2018.
Medicare is the federal health insuranceprogram that supports certain groups of people, including those who are 65 years or older, those with permanent kidney failure, and some younger people with disabilities.
Medicaid is a federal and state program that helps people who have limited income and resources.
Medicare accounted for 15 percent of the federal budget in 2017. As the population ages and healthcare costs rise, experts estimate that healthcare spending will continue to grow. According to projections, Medicare spending will reach 18 percent by 2028.
Encouraging people to eat better
A team of researchers from Tufts University and Brigham and Women’s Hospital in Boston, MA analyzed the effects of healthful food prescriptions in Medicare and Medicaid. The study, which the journal PLOS Medicinepublished, found that offsetting the cost of healthful foods by 30 percent through health insurance would improve health and reduce costs.
According to the co-first author Dr. Dariush Mozaffarian, dean of the Friedman School of Nutrition Science and Policy at Tufts:
“Medicare and Medicaid are the two largest healthcare programs in the U.S., together covering one in three Americans and accounting for 1 in every 4 dollars in the entire federal budget.”
The researchers modeled two different scenarios that would play out if Medicare and Medicaidcovered 30 percent of healthful food purchases.
In both scenarios, these programs would cover 30 percent of fruit and vegetable purchases. However, in the second scenario, they would also cover 30 percent of purchases of whole grains, nuts, seafood, and plant oils.
The findings showed that the first scenario would prevent about 1.93 million cases of heart disease, while the second one would prevent close to 3.28 million cases of heart disease as well as 120,000 cases of diabetes.
The positive effect on diabetes is due to the role that whole grains, nuts, and seeds play in diabetes prevention.
“We found that encouraging people to eat healthy foods in Medicare and Medicaid — healthy food prescriptions — could be as or more cost-effective as other common interventions, such as preventative drug treatments for hypertension or high cholesterol,” says Yujin Lee, Ph.D., a postdoctoral fellow at the Friedman School and co-first author of the study.
Reducing the need for healthcare
Both scenario one and scenario two significantly reduced healthcare utilization, leading to savings of about $40 billion and $100 billion respectively. The total costs for subsidizing just fruits and vegetables were $122.6 billion, while it cost $210.4 billion to cover the broader range of healthful foods.
Comparing the net costs with savings and health benefits, both scenarios were highly cost-effective.
To conduct this study, the researchers used a validated micro-simulation model called CVD Predict that generated samples representative of the Medicare, Medicaid, and dual-eligible populations. To achieve this, they used data from recent National Health and Nutrition Examination Surveys (NHANES), published sources, and meta-analyses.
They then applied the two scenarios to each of the different samples and assessed their effect at 5-, 10-, and 20-year horizons and at a simulated lifetime horizon.
This research forms part of the Food Policy Review and Intervention Cost-Effectiveness (Food-PRICE) research initiative, which is a collaboration of international researchers who are working to improve the health of the U.S. population by identifying possible nutrition strategies and evaluating their cost-effectiveness.
“These new findings support the concept of [the public initiative] Food is Medicine: That innovative programs to encourage and reimburse healthy eating can and should be integrated into the healthcare system.”
Dr. Dariush Mozaffarian
The researchers believe that this study provides the best national assessment of the potential effects that these initiatives could have at the federal level, but they caution that these models cannot prove the health and cost effects of the incentives.
My now deceased holistic MD told me that he remembered the original intent of health insurance was only to bridge the gap from when farmers collected money from the sale of their crops to pay their medical bills. Now, insurance is so expensive people have to seriously cut back in other areas – such as budgeting for food.
In this article, you can read about alternatives to traditional health insurance:
You should consider these as typical insurance often won’t cover Lyme/MSIDS anyway. There are also much less expensive programs that actually can cover your treatment. Sometimes the only caveat to that is that you must be a member prior to your diagnosis – i.e. it isn’t a “preexisting condition.”
After going without insurance for a number of years due to cost we finally joined a “medical cost sharing program.” While it didn’t cover Lyme/MSIDS for us because it was a preexisting condition, it does cover many adjunctive therapies regular insurance won’t cover – provided your doctor writes a brief letter explaining why he/she feels it an appropriate treatment. We’ve had colonics, massages, laser therapy, and a whole host of treatment modalities that never in a million years would be covered by regular insurance.
Madison Area Lyme Support Group 