The role of TDP-43 in amyotrophic lateral sclerosis and frontotemporal dementia


Purpose of review

We examine current evidence that the TAR DNA binding protein, TDP-43, plays a pathogenic role in both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

Recent findings

TDP-43 was recently identified as the major pathological protein in sporadic ALS and in the most common pathological subtype of FTD, frontotemporal lobar degeneration with ubiquitinated inclusions (FLTD-U). In these conditions, abnormal C-terminal fragments of TDP-43 are ubiquitinated, hyperphosphorylated and accumulate as cellular inclusions in neurons and glia. Cells with inclusions show absence of the normal nuclear TDP-43 localization. Recently, missense mutations in the gene encoding TDP-43 have been identified in patients with sporadic and familial ALS.

Summary

The recent discovery of pathological TDP-43 in both ALS and FTLD-U confirms that these are closely related conditions within a new biochemical class of neurodegenerative disease, the TDP-43 proteinopathies.

Keywords: TDP-43, amyotrophic lateral sclerosis, frontotemporal dementia, FTLD-U

Introduction

There is growing evidence that amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are closely related conditions with overlapping clinical, genetic and neuropathological features [1]. The recent identification of the transactive response (TAR) DNA binding protein with Mr 43 kDa (TDP-43) as the major pathological protein, in both ALS and the most common pathological subtype of FTD (frontotemporal lobar degeneration with ubiquitinated inclusions, FTLD-U) [2••,3••], provides the strongest evidence to date that these conditions are part of a clinicopathological spectrum of disease. Furthermore, this discovery provides important new insights into the pathogenesis of these conditions and the potential for the development of new diagnostic tests and therapies.

TDP-43 is the pathological protein in ALS and FTLD-U

One of the most characteristic neuropathological features of ALS is the presence of ubiquitin-immunoreactive (ub-ir) neuronal cytoplasmic inclusions (NCI) in the degenerating motor neurons [4]. A significant proportion of ALS patients develop cognitive deficits, often with prominent frontal lobe features [5], and are found to have additional ub-ir NCI and neurites in the frontotemporal neocortex and hippocampus [6,7]. Similar ub-ir, tau- and α-synuclein-negative cortical pathology (FTLD-U) is now recognized to also be the most common pathological substrate for clinical FTD, in the absence of motor features [8,9]. Until recently, it was uncertain whether FTLD-U represented a single disease process, or if it included a number of discrete entities in which the ubiquitinated protein was different. The recognition of several identifiable subtypes of FTLD-U pathology, each with relatively specific clinical and molecular genetic correlations, was initially interpreted as suggesting that FTLD-U was a heterogeneous collection of diseases [10,11]. However, this issue was finally resolved, in late 2006, when two groups independently identified the pathological protein in both FTLD-U and ALS as being TDP-43 [2••,3••].

In those initial studies, immunoblot analysis performed on the high Mr insoluble protein fraction from postmortem FTLD-U brain tissue identified disease specific bands that were excised and analyzed by liquid chromatography-mass spectrometry [2••,3••]. The resulting peptides were found to correspond to amino acid sequences in the C-terminal region of TDP-43. Commercially available antibodies against TDP-43 were found to consistently label the ub-ir inclusions in cases of FTLD-U and also ALS (Figure 1), but not the characteristic inclusions in a variety of other neurodegenerative conditions. An interesting observation, with possible functional implications, was the fact that neurons that contained TDP-43 inclusions showed an absence of the normal diffuse nuclear staining pattern [3••]. In addition to the normal 43 kDa band, TPD-43 immunoblot analysis of FTLD-U and ALS tissue, demonstrated disease specific bands at ~25 and 45 kDa, as well as a high Mr smear (Figure 2). The pathological proteins were shown to represent abnormal C-terminal fragments of TDP-43 that were ubiquitinated and phosphorylated.

Fig. 1

TDP-43 immunohistochemistry in frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS)
Fig. 2

Biochemical analysis of pathologic TDP-43 in frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U)

A number of subsequent studies have confirmed that most clinical and pathological subtypes of FTLD-U and ALS are characterized by TDP-43 immunoreactive inclusions [12••,13• ,14,15••,16,17]. Moreover, by virtue of its greater sensitivity and specificity, TDP-43 immunohistochemistry has proved to be a powerful new tool for investigating the neuropathology of these conditions, demonstrating changes that were not previously recognized. These include TDP-43-immunoreactive cytoplasmic inclusions in glial cells of presumed oligodendroglial lineage [2••,15••,16,18•], granular neuronal cytoplasmic “pre-inclusions” [19], dystrophic neurites in the CA1 region in cases with hippocampal sclerosis [20] and more extensive extramotor pathology in cases of ALS, with and without dementia [19]. Antibodies raised against phosphorylated epitopes of TDP-43 have proven to be even more sensitive and specific, as they only identify the pathological forms of the protein [21•] while the use of C-terminal and N-terminal specific antibodies has suggested that the pathological inclusions in different populations of neurons may be composed of different forms of TDP-43 [22•]. As a result, FTLD-U and ALS are now recognized as representing a clinicopathological spectrum within a new biochemical class of neurodegenerative disease, the TDP-43 proteinopathies.

Normal function of TDP-43 in nervous system

TDP-43 is a 414 amino acid nuclear protein that is encoded by the TARDBP gene on human chromosome 1p36.2. It is highly conserved and ubiquitously expressed in a variety of tissues including brain [23]. TDP-43 contains 2 RNA-recognition motifs (RRM1: ~aa 106–175 and RRM2: ~aa 191–262) and a glycine-rich C-terminal region (~aa 274–413) that allow it to bind single stranded DNA, RNA and proteins [23,24]. It was initially cloned as a human protein capable of binding to the TAR DNA of human HIV-1, where it acts as a transcription repressor [25]. It was subsequently identified as part of a complex involved in splicing the cystic fibrosis transmembrane conductance regulator gene [23] and also the apoA-II gene [26]. The exon skipping and splicing inhibitory activity requires the glycine-rich C-terminal domain that binds to several members of the heterogeneous nuclear ribonucleoprotein (hnRNP) family [24,27]. TDP-43 has also been shown to act as a scaffold for nuclear bodies through an interaction with survival motor neuron protein [28]. It may also be involved in mRNA stability, microRNA biogenesis, apoptosis and cell division [29•]. In the brain, TDP-43 is normally localized to the nucleus of neurons and some glial cells [3••]. Although, its physiological function in the nervous system is not currently known, one recent study has suggested it may act as a neuronal activity-response factor, involved in the regulation of neuronal plasticity [30].

The spectrum TDP-43 proteinopathies

Although the initial reports suggested that pathological TDP-43 is both a specific and sensitive marker of all subtypes of FTLD-U and ALS [2••,3••,13•], subsequent studies have identified some important exceptions. While the vast majority of sporadic FTLD-U cases are found to be TDP-43-positive, most large series have identified a small proportion in which the ub-ir pathology is negative [12••,20]. Two recent papers have provided detailed description of these “atypical” cases (aFTLD-U), which represented 10 – 20 % of all FTLD-U in the respective series [31•,32]. In contrast to TDP-43-positive cases, all aFTLD-U cases were sporadic with very early onset FTD, characterized by severe progressive psychobehavioural abnormalities in the absence of significant aphasia, cognitive-intellectual dysfunction or motor features. The neuropathology consisted of NCI and unique neuronal intranuclear inclusions that were only reactive for ubiquitin. Based on the unusual and highly consistent clinical phenotype and neuropathology, the authors suggested that aFTLD-U represents a newly recognized and specific disease entity.

In familial FTLD-U, different patterns of TDP-43 pathology have been found to correlate with most of the known genetic causes, including mutations in the genes encoding progranulin and valosin-containing protein and in families with FTD and MND linked to chromosome 9p21-13 [12••,14,17]. An exception is FTD linked to chromosome 3, caused by a mutation in the gene encoding the charged multi-vesicular body protein gene (CHMP2B), which is characterized by ub-ir NCI in hippocampal granule cells, that are not reactive for TDP-43 [12••,33•].

In ALS, TDP-43 positive inclusions, in both lower motor neurons and glia, are a consistent feature of all sporadic cases and familial cases without SOD1 mutations [15••,16]. However, the absence of immunohistochemical or biochemical evidence of pathological TDP-43 in human cases and animal models with SOD1 mutations suggests that neurodegeneration in these cases may have a different pathogenesis [15••,16,34•].

A number of recent studies have also raised questions about the disease specificity of TDP-43 pathology by demonstrating some degree of positivity in a variety of conditions, outside the usual spectrum of FTD and ALS. TDP-43 immunoreactivity is reported to be a consistent feature of ALS-parkinsonism-dementia complex of Guam [35•,36•] and present in a significant proportion of cases of hippocampal sclerosis dementia [12••,37••,38], classical Pick’s disease [39], corticobasal degeneration [40], Alzheimer’s disease [37••,40,41], Parkinson’s disease and dementia with Lewy bodies [41,42]. In most of these conditions, the TDP-43 pathology is anatomically restricted to mesial temporal structures, shows only partial co-localization with the other pathological changes and is of uncertain clinical relevance [37••,3842].

It is anticipated that our understanding of the spectrum of TDP-43 proteinopathies will continue to evolve as more cases and additional conditions are examined. Rather than diminish the importance of this protein in the pathogenesis of ALS and FTD, this new information will help to clarify the relationship between different ALS and FTD subtypes and their relationship with other neurodegenerative conditions.

Mutations in TARDBP cause ALS but not dementia

Rare pathogenic missense mutations and multiplications have been identified in genes encoding the major constituents of the pathological deposits in several neurodegenerative diseases [4345]. The gene encoding TDP-43 (TARDBP) therefore represents an excellent candidate for causing or increasing the risk to develop a disease in the spectrum of TDP-43 proteinopathies. Initial sequence analyses of TARDBP in patients with sporadic FTD and ALS, as well as familial FTD, failed to identify mutations [46]. Similarly, no evidence of genetic variation in TARDBP increasing risk for FTD or ALS was observed [4648]. However, subsequent large population-based TARDBP mutation screenings, by us and by others, have identified 16 different missense mutations in 19 genealogically unrelated ALS patients, which were absent in healthy controls [49•,50•,51••,52,53•] (Figure 3). Eight mutations have been found in familial ALS patients [49•,50•,51••,52,53•], while eight others were identified in patients with sporadic ALS [50•,51••]. Mutations c.1077G>A (p.A315T), c.1009A>G (p.M337V) and c.1278G>A (p.A382T) were identified in two families each and haplotype sharing studies supported a common genetic origin for mutations p.M337V and p.A382T. TARDBP mutations were not restricted to Caucasians ALS populations; mutation c.892G>A (p.G298S) was identified in a Chinese family [53•] and c.1028A>G (p.Q343R) in a Japanese family [52].

Fig. 3

Missense mutations in the gene encoding TDP-43 (TARDBP) cause ALS

Depending on the study, the overall TARDBP mutation frequency in ALS has ranged from 3% to 6%, with the exception of the initial report by Sreedharan et al. [51••], in which a much lower TARDBP mutation frequency of 0.6% (3/526) was identified. Both population-based studies in which sporadic mutation carriers were identified, described comparable TARDBP frequencies for sporadic and familial ALS [50•,51••]; however mutation analyses in a large clinical series of sporadic ALS patients of European descent did not identify mutations [54] and other studies have identified TARDBP mutations exclusively in familial ALS [49•,52,53•]. Without supportive functional data, the pathogenic character of each of the TARDBP mutations identified in a single sporadic ALS patient remains uncertain.

The clinical phenotype of TARDBP mutation carriers resembles classical adult onset ALS. Based on the current published literature, the mean onset age for mutation carriers was 56.3 ± 12.1 years (N=30; range 30–83 years) with similar onset ages in familial (N=22; 55.8 ± 12.1 years) and sporadic (N=8; 57.5 ± 12.8 years) cases [49•,50•,51••,52,53•]. The mean duration of disease was 4.3 ± 3.6 years (N=18; range 1–12 years). Even within a single family, the age of onset varied significantly (by as much as 35 years) [53•], suggesting that additional genetic and/or environmental factors determine the disease expression of TARDBP mutations. Thirty-three percent of mutation carriers (11/33) had bulbar onset and 67% (22/33) limb-onset ALS, a distribution comparable to non-TARDBP mutation carriers [55,56]. Interestingly, despite the common co-occurrence of cognitive symptoms in ALS patients [5], none of the TARDBP mutation carriers identified to date, have had a personal or family history of dementia. In agreement with this finding, TARDBP mutations have not been identified in patients with FTD, FTD-ALS or AD, characterized by TDP-43 pathology [50•,53•].

Thus far, pathological examination has only been performed in two families with TARDBP mutations [52,53•]. The neuropathological changes in patients from both families were characteristic of ALS, with motor neuron loss, gliosis and the presence of Bunina bodies. As expected, TDP-43-positive NCIs and glial cytoplasmic inclusions were observed in the anterior horn cells of the spinal cord and in various other regions of the central nervous system. In one family the authors suggested a higher frequency of TDP-43-positive “pre-inclusions” compared to other patients with sporadic ALS [53•]. Biochemical analyses of TDP-43 protein extracted from the spinal cord of the autopsied case carrying the p.Q343R mutation showed elevated levels of the abnormal molecular-weight fragments of ~25 and 45kDa, that were previously observed in sporadic ALS and in SOD-1 negative familial ALS, suggesting TARDBP mutations may accelerate the production of these fragments [52]. Whether these neuropathological findings are characteristic of all TARDBP mutation carriers needs further confirmation.

All but one of the reported mutations cluster in TARDBP exon 6, encoding the highly conserved C-terminal region of TDP-43 (Figure 3). Four mutations involve glycine residues, in close proximity of each other, in the glycine-rich region, while the other mutations affect conserved residues in the remaining portion of the C-terminal domain. No clustering of familial versus sporadic mutations in specific regions of the gene has been observed and no effect of the location of the mutations on the age of onset or disease duration has been demonstrated.

Role of TDP-43 in neurodegeneration

Little is currently known about the pathogenic role of TARDBP mutations or TDP-43 pathology in neurodegeneration. Analogous to other neurodegenerative diseases, characterized by the accumulation of mis-folded protein, the critical step will be to determine whether disease results from a loss-of-function, a toxic gain-of-function or both.

The abnormal localization of TDP-43 to the cytoplasm in affected neurons in FTD and ALS, irrespective of the presence of a genetic mutation, suggests a pathogenic mechanism associated with the loss of the normal nuclear TDP-43 function in regulating transcription, splicing and mRNA stability [29•,57]. In support of this hypothesis, loss of TDP-43 in human cells has been shown to induce morphological nuclear defects and increased apoptosis [58••]. Alternatively, sequestration of TDP-43 in cellular inclusions may induce a toxic gain-of-function, independent of the basic biological role of TDP-43. A study in which TDP-43 was overexpressed in yeast suggested that only aggregating forms of TDP-43 were toxic, although the toxicity depended on an intact RNA recognition motif [59•]. Factors that affect the normal intracellular trafficking of TDP-43, between the cytoplasm and nucleus, may predispose to both the formation of abnormal aggregates (inclusions) and the loss of nuclear localization [60•].

The identification of TARDBP mutations in ALS has provided important clues to the possible pathogenic mechanisms involved in TDP-43 proteinopathies. The clustering of mutations in exon 6, that encodes the highly conserved C-terminal domain, suggests that TARDBP mutations may interfere with the normal protein-protein interactions of TDP-43, affect its transport through the nuclear pore or influence its exon skipping or transcriptional repression activity [50•,51••]. Numerous potential phosphorylation sites have been predicted to occur in the C-terminal region of TDP-43 and some mutations, especially the six substitutions to serine and threonine residues, may increase phosphorylation and aggregation. A single mutation c.640A>T (p.D169G) was identified in TARDBP exon 4 encoding RRM1 [50•]. This mutation may abrogate the RNA binding to this region; however, because it lies outside of exon 6 and lacks evidence of segregation with disease, it may also represent a rare benign sequence variant. Finally, a study of mutant TDP-43 in cell culture and in vivo revealed increased generation of detergent-insoluble TDP-43 fragments that could aggregate and cause a toxic gain-of-function [50•,51••]. Given the multifaceted role of TDP-43, multiple disease mechanism may well be involved.

Conclusions

The identification of pathological TDP-43 in FTLD-U and ALS confirms that these conditions are part of a disease spectrum with a common underlying biochemical mechanism. This insight has helped to clarify the relationship among the various genetic, clinical and pathological subtypes of FTD and ALS and has suggested possible mechanistic links with other neurodegenerative disorders. A better understanding of the role of TDP-43 in neurodegeneration will be crucial to the development of targeted therapeutic strategies for these conditions. Central to this process will be the use of experimental animals and cell systems, expressing pathogenic mutations in TARDBP or FTLD-U causing genes. The recent identification of elevated plasma levels of TDP-43, in some patients with neurodegenerative disease [61•], supports the possible use of TDP-43 as an in vivo biomarker to aid in diagnosis and monitoring the effects of therapy. In summary, the discovery that TDP-43 plays a central role in the pathogenesis of FTD and ALS has been a major advance towards the effective management of these devastating neurodegenerative conditions.

Here are 11 ways to increase serotonin in the brain (naturally) 


What’s the key to improving your mental state and feeling good?

Some of us might say it’s healthy relationships or doing a job you love.

Spiritual gurus might say it’s living in the moment or positive thinking.

But isn’t it more interesting to find out what neuroscientists say? After all, they’re the ones studying our brains.

And despite what you’re led to believe, neuroscience has many things to say about our mental state and what works. According to several research studies, there’s one particular element to mental wellbeing that you might not be aware of.

It’s called serotonin, a neurotransmitter that can influence many things throughout your body like your mood, memory, sleep cycle, and even your sex drive.

 By increasing the serotonin in your body naturally, you can also enhance your mental state and your motivation. Here are 11 natural ways to boost your serotonin.

1. Eat Tryptophan.

Tryptophan is an amino acid that majorly helps in your body’s production of serotonin. Foods that include tryptophan include eggs, dairy, lean meats, nuts, and seeds.

2. Get a massage


Getting a massage can boost your mood no matter what, but did you know that it can reduce your cortisol levels? Cortisol is a stress hormone that is produced when you’re “under attack” or in stressful situations. When you have too much of this hormone in your body, it can block serotonin from being produced.

3. Increase your B Vitamins.

Especially B12 and B6 can help with serotonin production. There is even research suggesting that increasing your intake of these vitamins can help with depression. Most people can enhance their intake of B vitamins with 50-100 mg/day but check with your doctor to be sure.

4. Get some sun.

Unsurprisingly for those of us who live in the north, not getting sun can affect our mood. Sunshine can initiate serotonin production in our brains!

5. Increase your intake of Magnesium.

It’s thought that up to 75% of the American population is deficient in Magnesium. This mineral can help to control blood pressure, regulate nerve cell function enhance serotonin. Magnesium can be found in supplements and foods like dark greens, bananas, and fish.

6. Be positive.


Increasing serotonin isn’t just possible with external things. By changing your attitude, self-talk, and perspective, you can also influence your brain. When you do things that you enjoy, you feel better. These new patterns of positivity can help you create more serotonin.

7. Eat less sugar.

One of the symptoms you may feel when you’re low on serotonin is a craving for sugary foods. But by consuming these foods, you will feel a crash soon after. Be healthy and increase your serotonin in more natural ways.

8. Start a meditation practice.


Meditation raises an acid called 5-HIAA in the brain that is directly related to serotonin. By sitting in meditation every day you can reduce stress, and the production of cortisol and other stress hormones and also enhance the production of serotonin.

9. Exercise.

Any activity that gets your blood going and your heart pumping also contributes to the production of serotonin. Exercise also produces positive chemicals in the body like endorphins, which can enhance your mood right away.

10. Get lots of Vitamin.

Vitamin C is strongly connected to mood and also has antidepressant properties. One study even found people who took in an increase in vitamin C for a week felt happier. Vitamin C may not be directly related to serotonin but it definitely helps the brain to make other neurotransmitters like epinephrine and dopamine, which both make us feel great.

11. Reduce stress by taking care of yourself.


When you you’re stressed, do thing to prevent becoming overwhelmed. The best way to combat stress chemicals like cortisol is to do what you can to stay positive and take care of yourself.

Egyptian study confirms autism is caused by mercury in vaccines


Ever heard of metabolic brain disease? A team of nine scientists from top Egyptian medical schools and universities may have just confirmed that one in every 50 American children has it, and its primary cause could be mercury in vaccines.

How was this determined? Exposure to mercury can be measured by analyzing children’s urinary porphyrins – excreted organic compounds that act as biomarkers for mercury toxicity. Not only does the presence of mercury in urine and blood expose the long-known link between metabolic brain disease (autism) and vaccines, but the severity of autism (and its broad array of symptoms) is directly correlated with the levels of exposure to this known neurotoxin. Yes, you read that correctly.

Image: Egyptian study confirms autism is caused by mercury in vaccines

To put the nails in the coffin for any doubters or skeptics, of the 100 children studied, the 40 with autism spectrum disorder (ASD) had significantly higher mercury levels than their non-autistic siblings and the other healthy children in the study. In addition, the children with the most severe versions of metabolic brain disease revealed the highest levels of mercury exposure. For years and years, natural health enthusiasts have been screaming about the dangers of vaccines and mercury-loaded dental fillings, and now the truth comes out – and scientifically proven at that.

Disordered urinary porphyrin metabolism – the smoking gun of the autism–mercury connection

Six American studies have linked autism to mercury exposure by analyzing disordered porphyrin metabolism in autistic kids, but the mass media has been prohibited from publishing them or even discussing them at all because their sponsors are Big Pharma conglomerates. That is why you never hear anything about them on television, in newspapers or on mainstream media websites.

Another study published this past June was carried out by an international team of scientists who measured pro-inflammatory neuro peptides that indicate the presence of mercury in blood. The results showed a “positive linear relationship between mercury levels and the severity of autism symptoms.”

The previously mentioned study done by the scientists from Egyptian medical schools included analyzing the mothers of autistic children who had multiple dental “silver” amalgams (mercury-loaded fillings), which the scientists said most likely contributed to the children’s body levels of mercury. You could call these the “silver bullets” from the “smoking gun.”

Special note: Ethyl mercury in thimerosal (used for vaccines, especially flu shots) is at least 50 times as toxic to human tissue as the methylmercury in amalgams and fish, and can prove to be twice as persistent in the brain. When mercury is injected into the blood and muscle tissue, it bypasses normal protective human filters, such as the lungs, digestive organs and the skin. This is also how mercury can cross the blood/brain barrier.

It’s not just mercury causing metabolic brain disease, but also lead and aluminum

In 2015, a paper published in Behavioral Neurology by a group of researchers from the National Institute of Standards revealed results of a study of 100 autistic children with significantly high levels of mercury, lead and aluminum that may have resulted from environmental exposure. Aluminum is often also found in vaccines, and lead has been revealed to be in most U.S. tap water, sometimes at alarming levels (think of Flint, Michigan, here).

Detoxification by chelating agents could play a major role in improving the lives and mental and social capacities of children afflicted with metabolic brain disease. Remember, autism is a neurodevelopmental disorder that appears during infancy or childhood (not at birth), with a broad array of communication and learning impairments, from mild to moderate to severe. It is rarely, if ever, inherited, but rather brought on by an overload of neurotoxins either consumed, injected or ingested from environmental factors, or all of the above.

Realize the CDC has formally admitted to covering up the autism-mercury-vaccine link

Mercury is the most toxic non-radioactive element on earth and the second most poisonous element known to mankind, second only to uranium, yet, for some reason, it’s still used in vaccines as a preservative, even when there are several other options that are not toxic that would do the same job. It is scientific fact that human brain neurons permanently disintegrate in the presence of mercury within one hour of exposure. Thimerosal is a mercury containing preservative (about 50 percent mercury), and the World Health Organization warned about its use in vaccines way back in 1990.

Plus, mercury is a cumulative poison, meaning the body has difficulty removing it and it accumulates significantly over time. Some infants receive more mercury in one day than the WHO recommends as a maximum for adults for three months worth of exposure. One scientific fact most Americans do not know is that aluminum (listed as aluminum phosphate) in vaccines greatly increases the toxicity of mercury (listed as thimerosal), therefore caution about minimum mercury tolerance is severely underestimated.

Does the CDC mix vaccines with aluminum and mercury in combination? Absolutely. The Diptheria and Tetanus “toxoid” inoculations have “trace” amounts of mercury combined in the same vaccine with aluminum. What’s in the whooping cough vaccine? Aluminum phosphate and formaldehyde. Mix that aluminum phosphate with a flu shot laced with mercury and measure the level (potency) of mercury and see what that does to the central nervous system and the brain. Remember, aluminum makes the vaccine more “powerful.”

Since 2002, the CDC has been covering up the link between autism and the MMR vaccine. Dr. William W. Thompson, a senior scientist and epidemiologist at the US Centers for Disease Control and Prevention (Immunization Safety Branch) confessed to the vaccine-autism connection in a confession letter (an email Dr. Thompson wrote to officials at CDC via his attorneys). After being silent about the cover-up for over a decade, Dr. Thompson said he could no longer stand to look at parents whose children were suffering from autism and keep silent about the whole conspiracy, so he blew the whistle.

Sources for this article include:

EcoWatch.com

NaturalNews.com

TruthWiki.org

TruthWiki.org

TruthWiki.org

Trying To Quit Smoking? These 8 Natural Ways Kill Nicotine Craving


Share on Facebook Select Language ▼ Smoking is a highly harmful habit, which causes 90% of all lung cancer deaths. More than 1.1 billion people in the world smoke tobacco, and it kills up to 50% of them (ASH). The deadly consequences of tobacco use are due to the inhalation of more than 7,000 ingredients, like arsenic, carbon monoxide (it displaces oxygen on hemoglobin in red blood cell, so cells do not get the needed oxygen), butane (in lighter fluid), and tiny glass particles ( which cut up the lungs to improve nicotine delivery).

The inhalation of these chemicals causes lung-related issues, like lung cancer or chronic obstructive pulmonary disease (COPD), and the plaque deposits might also cause heart diseases, like heart attacks or congestive heart failure, as they damage the heart and blood vessel integrity. Moreover, nicotine also increases cortisol (the stress hormone) and DHEA (the ‘all is good’ hormone) levels, but chronically elevated cortisol levels weaken the immune system. This detrimental habit also contributes to: Insomnia Infertility Hormone imbalance Gastrointestinal issues Blood sugar issues Osteoporosis Nicotine easily becomes addictive, and the withdrawal symptoms which appear quickly after you extinguish the cigarette are edginess and irritability, so you reach for a new one. It actually crosses the blood-brain barrier and leads to pleasant feelings by releasing dopamine.

8 Natural Ways To Kill Nicotine Cravings For Anyone Who Is Trying To Quit Smoking

This addiction is extremely powerful, and some even claim that it is more difficult to quit smoking than to give up the use of cocaine or heroin (ACS, 2015). Many of the negative effects of smoking might be due to the depletion of essential antioxidants, like vitamins C and E, beta-carotene, glutathione, ubiquinol, and alpha-lipoic acid, which collect the additional free radicals and other oxidant species which result from smoking. Additionally, the negative effects of smoking cannot be relieved with the use of supplements, as the best way to supply the body with the needed nutrients is through the consumption of healthy foods.

There are several methods which can help you in the struggle to quit smoking and soothe the withdrawal symptoms. Here are the 8 most effective ones: 1. Magnesium Magnesium reduces the nicotine addiction by antagonizing NMDA receptors, which stimulate the release of the dopamine. This mineral also lowers the effects of nicotine on the NMDA receptors by improving GABA (our relaxing neurotransmitter) synthesis. This means that magnesium will reduce the satisfaction you get from smoking. 2. Hypnotherapy Hypnosis is an altered state of consciousness where one bypasses certain aspects of reality and feels compelled to follow cues from an external source. Therefore, it can help you relate smoking to unpleasant stimuli, and thus accelerate the process of quitting. 3. Acupuncture Acupuncture has been found to help people who try to give up smoking, and the insertion of needles on certain places linked to the mouth, lungs, and airways, lowers the cravings for the taste of tobacco. 4. Exercise Studies have shown that 5-minute moderate-intensity workout causes a short-term reduction in the desire to smoke. 5. Nicotine Patch Numerous people have tried nicotine patches and claim they are really helpful. It has also been found that these patches are even more effective when combined with drugs like varenicline and bupropion. The doses are determined by the number of cigarettes one smokes daily, and how frequently one smokes. 6. Lime Chewing the skin of a lime slice when the cravings hit, will help you reduce them, as they are high in vitamin C and antioxidants. 7. Olfactory Training Researchers exposed smokers to the smell of cigarettes and rotting eggs or fish while they are in Stage 2, non-REM sleep for a week, and they smoked less during this period. 8. Mindfulness Studies have shown that the practice of ‘sitting’ through difficult scenarios, like cravings or withdrawal symptoms, helps smokers give up smoking more easily.

Breast malignancies in children. 


Foto: iStock.com/FatCamera

Pediatric breast malignancies are a thankfully rare occurrence, but this also means that literature is limited on this topic, says the present US-wide study. Here, the authors compared pediatric and adult breast malignancy. They found differences and similarities: Pediatric breast malignancies are more advanced at presentation, but overall survival is similar in adult and pediatric patients with invasive carcinoma.

The retrospective cohort study included close to 2 million cases from the US-American National Cancer Data Base. The authors compared patients ≤ 21 years to those > 21 years at diagnosis and estimated differences in demographic, tumor, and treatment characteristics.

The incidence of invasive breast malignancies in patients ≤ 21 year was 0.02 %. 99 % of adult patients had invasive carcinoma, compared with 64.8 % of pediatric patients; the remaining patients had sarcoma, malignant phyllodes, or malignancy not otherwise specified. Further results:

  • Pediatric patients were twice as likely to have an undifferentiated malignancy (relative risk [RR] 2.19).
  • 50 % of adults versus 22.7 % of pediatric patients presented with Stage I disease (p < 0.001).
  • Pediatric patients were 40 % more likely to have positive axillary nodes (RR 1.42).
  • Among patients with invasive carcinoma, pediatric patients were more than four times as likely to receive a bilateral than a unilateral mastectomy compared with adults (RR 4.56).
  • Overall survival was similar.

Pediatric breast malignancies are more advanced at presentation, but overall survival is similar in adult and pediatric patients.

Source: Richards, M. K. et al.: “Breast Malignancies in Children: Presentation, Management, and Survival”, Ann Surg Oncol. 2017 Jun;24:1482-1491.

There Have Been 296 Earthquakes Near The Yellowstone Supervolcano Within The Last 7 Days


Is it possible that the Yellowstone supervolcano is gearing up for a major eruption? If you follow my work on a regular basis, then you already know that I spend a lot of time documenting how the crust of our planet is becoming increasingly unstable. Most of this shaking is taking place far away from the continental United States, and so most Americans are not too concerned about it. But we should be concerned about it, because a major seismic event could change all of our lives in a single instant. For instance, a full-blown eruption of the Yellowstone supervolcano would have the potential of being an E.L.E. (extinction level event). That is why it is so alarming that there have been 296 earthquakes in the vicinity of the Yellowstone supervolcano within the last 7 days. Scientists are trying to convince us that everything is going to be okay, but there are others that are not so sure.

The biggest earthquake in this swarm occurred last Thursday evening. It was initially measured to be a magnitude 4.5 earthquake, but it was later downgraded to a 4.4. It was the biggest quake in the region since a magnitude 4.8 earthquake struck close to Norris Geyser Basin in March 2014. This magnitude 4.4 earthquake was so powerful that people felt it as far away as Bozeman

The main quake was centered about 5.8 miles underground.

The quake and aftershocks occurred just over 8 miles northeast from West Yellowstone, according to the U.S. Geological Service.

A witness reported that she felt the building she was in move.

Dozens of people reported that they felt it in and around West Yellowstone, Gardiner, Ennis, and Bozeman.

But by itself that one quake would only be of minor concern. What is troubling many of the experts is that this earthquake has been accompanied by 295 smaller ones.

There is normally a rise in seismic activity before a volcano erupts, and according to theoretical physicist Michio Kaku, a long overdue eruption at Yellowstone could “rip the guts out of the USA”

Scientists currently believe that there’s a 10% chance that a “supervolcanic Category 7 eruption” could take place this century, as pointed out by theoretical physicist Michio Kaku who appeared on a segment for Fox News.

The grey haired physicist told Shepard Smith that the “danger” we are now facing with the caldera is that it’s long overdue for an eruption which Kaku said could “rip the guts out of the USA.”

Kaku said that a “pocket of lava” located under the park has turned out to be twice as big as scientists originally thought.

I would like to try to describe for you what a full-blown eruption of the Yellowstone supervolcano would mean for this country.

Hundreds of cubic miles of ash, rock and lava would be blasted into the atmosphere, and this would likely plunge much of the northern hemisphere into several days of complete darkness. Virtually everything within 100 miles of Yellowstone would be immediately killed, but a much more cruel fate would befall those that live in major cities outside of the immediate blast zone such as Salt Lake City and Denver.

Hot volcanic ash, rock and dust would rain down on those cities literally for weeks. In the end, it would be extremely difficult for anyone living in those communities to survive. In fact, it has been estimated that 90 percent of all people living within 600 miles of Yellowstone would be killed.

Experts project that such an eruption would dump a layer of volcanic ash that is at least 10 feet deep up to 1,000 miles away, and approximately two-thirds of the United States would suddenly become uninhabitable. The volcanic ash would severely contaminate most of our water supplies, and growing food in the middle of the country would become next to impossible.

In other words, it would be the end of our country as we know it today.

The rest of the planet, and this would especially be true for the northern hemisphere, would experience what is known as a “nuclear winter”. An extreme period of “global cooling” would take place, and temperatures around the world would fall by up to 20 degrees. Crops would fail all over the planet, and severe famine would sweep the globe.

In the end, billions could die.

So yes, this is a threat that we should take very seriously.

But today, most Americans think of Yellowstone as little more than a fun tourist attraction. But the truth is that many tourists have discovered just how dangerous Yellowstone can be. Some have been scalded by boiling water from geysers that can get as hot as 250 degrees Fahrenheit, and one man from North Carolina recently had to be flown to a burn center after he mistakenly fell into a hot spring

A North Carolina man was flown to the University of Utah Burn Center after falling into a hot spring at Yellowstone National Park late Tuesday night.

Gervais Dylan Gatete, 21, was with seven other people in the Lower Geyser Basin north of Old Faithful when he fell, according to a park news release.

The group attempted to transport Gatete, an employee with Xanterra Parks and Resorts, by car for medical treatment. Just before midnight, they flagged down a park ranger near Seven Mile Bridge on the West Entrance Road.

Since Yellowstone is still very active, scientists assure us that it will erupt again one day.

And when that happens, all of our lives will be completely turned upside down in a single moment.

5 Reasons You Should Have Sex Every Day


We know you don’t need a justification to have more sex. But knowledge is power and hence we believe in enriching you fully. Having sex regularly can better your health, improve your performance at work and keep you looking younger for longer, among many other things.

MensXP brings you a list of five such things to begin with:

Seduce Her To Prevent Heartache

Reasons To Have Sex Every Day - Seduce Her To Prevent Heartache

 

Well, no pun intended here! As much as having sex produces enormous amounts of the feel-good hormones, it also makes you heart-healthy. Researchers across the globe have agreed upon the fact that having sex two to three times a week can halve your likelihood of a heart attack or stroke.

Orgasm More To Say Goodbye To Cancer

Reasons To Have Sex Every Day - Orgasm More To Say Goodbye To Cancer

 

Release to breathe free of the deadly C-word! Carcinogens build up if you do not get to periodically clean up your pipes. A study in the journal of the American Medical Association state that those who enjoy 21 or more ejaculations per month have a lower risk of prostate cancer than those who did four to seven times.

Have Sex, Sleep Better!

Reasons To Have Sex Every Day - Have Sex, Sleep Better!

 

Yes, you read it right. Move over sleeping pills! Not just the exertion will act like a tranquiliser, but the hormones such as oxytocin and prolactin released during orgasm also helps to promote sleep. No wonder most couples agree that the next best thing after a session between the sheets is sound sleep!

Delay Ageing With Sex

Reasons To Have Sex Every Day - Delay Ageing With Sex

You can easily look younger and reduce your risk of death within a 10-year period by almost 50 per cent if you have sex at least twice a week, compared to those who were lucky once a month. Higher levels of anti-ageing growth hormone, oxygen and testosterone are the tools to fight ageing.

Make Love To Make More Money

Reasons To Have Sex Every Day - Make Love To Make More Money

 

Your next hike depends on how you lucky you have been in bed lately! So, in order to excel in the boardroom, you need to perform in the bedroom. Research shows that the blood pressure of those who had sex in the previous fortnight raised less during public speaking and returned to normal more quickly. Sex reduces stress, hence preparing you to face that important presentation with full confidence.

Two Exciting Alzheimer’s Advances: A Novel Early Detection Test Using Peanut Butter, and a Study Evaluating Coconut Oil


Story at-a-glance

  • At present, an estimated 5.4 million Americans have Alzheimer’s disease. By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans
  • The ability to smell is associated with the first cranial nerve and is often one of the first senses to be adversely affected by cognitive decline.
  • In patients with Alzheimer’s, the ability to smell peanut butter through the left nostril was found to be significantly impaired
  • Patients diagnosed with mild to moderate Alzheimer’s have been enrolled in a clinical study—the first of its kind—to evaluate the effects of coconut oil versus placebo. Results are expected in about a year
  • Previous investigation suggests that ketone bodies, an alternative fuel for your brain that your body makes when digesting coconut oil, might offer profound healing benefits in the fight against Alzheimer’s disease

By Dr. Mercola

At present, some 5.4 million Americans have Alzheimer’s disease, according to the Alzheimer’s Association’s 2011 Alzheimer’s Disease Facts and Figures.1

By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans, rivaling the current prevalence of obesity and diabetes.

Since treatments are few and rarely effective, early diagnosis and prevention become all the more important.

Interestingly, simple tools like a tablespoon of peanut butter and a ruler could potentially be used to confirm a diagnosis of the disease in its early stages. As reported by Medical News Today:2

“Jennifer Stamps, a graduate student in the University of Florida (UF) McKnight Brain Institute Center for Smell and Taste, and her colleagues reported the findings of a small pilot study in the Journal of the Neurological Sciences.3

Stamps came up with the idea of using peanut butter to test for smell sensitivity while she was working with Dr. Kenneth Heilman, one of the world’s best known behavioral neurologists, from the UF College of Medicine’s department of neurology.

…The ability to smell is associated with the first cranial nerve and is often one of the first things to be affected in cognitive decline… She thought of peanut butter because, she said, it is a ‘pure odorant’ that is only detected by the olfactory nerve and is easy to access.”

The pilot study tested the ability to smell of 24 patients diagnosed with mild cognitive impairment. To perform the test, the patient was asked to close their eyes and mouth, and hold one nostril closed while breathing normally through the other.

Using a ruler, the clinician measured the distance between the open nostril and the peanut butter, marking the distance at which the patient was able to detect the distinct odor. After a 90 second delay, the procedure was repeated with the other nostril.

They discovered that those diagnosed with early stage Alzheimer’s (which was done through other clinical testing) experienced a significant difference in their ability to detect the odor between the two nostrils. According to the featured report:

“[T]he left nostril was impaired and did not detect the smell until it was an average of 10 cm closer to the nose than the right nostril had made the detection in patients with Alzheimer’s disease.

This was not the case in patients with other kinds of dementia; instead, these patients had either no differences in odor detection between nostrils or the right nostril was worse at detecting odor than the left one.”

Of course, it’s too early to tell whether this test might be reliable enough to become widely used. More research needs to be done. But according to Stamps, the test can be used to confirm a diagnosis. The team is planning to study patients with mild cognitive impairment next, to assess whether it might help predict a future diagnosis of Alzheimer’s.

Benefits of Coconut Oil Make Headlines Again

In related news, Florida researchers are also looking into whether coconut oil might be of benefit against Alzheimer’s. Three years ago, I published Dr. Mary Newport’s theory that ketone bodies, an alternative fuel for your brain that your body makes when digesting coconut oil, might offer profound benefits in the fight against Alzheimer’s disease.

At the time I said that, should her theory turn out to be accurate, it could be one of the greatest natural health discoveries in a long time. Now, Dr. Newport’s research is being used to launch one of the first clinical trials of its kind to test her theory. The research is being done at the USF Health Byrd Alzheimer’s Institute.

Sixty-five patients diagnosed with mild to moderate Alzheimer’s have been enrolled to evaluate the effects of coconut oil on the disease, compared to a placebo. Dr. Newport hopes to have the results within a year.

This issue strikes close to home for Dr. Newport, whose husband has been battling the disease for years. As reported by CTV News:4

“While there is currently no clinical data showing the benefits of coconut oil on the prevention and treatment of dementia, Newport — whose husband Steve was diagnosed with Alzheimer’s at age 51 — said she began to see improvements after starting him on four teaspoons of coconut oil per day.

‘Before the coconut oil, he could not tie his shoes. His weird slow gait… That improved. He walked normally and he was able to start running again.

He was able to start reading again, his conversation improved dramatically and then over several months we saw improvements in his memory,’ Newport said. Prior to starting him on coconut oil, Newport said none of the existing medications were working.”

Coconut Oil Appears to Be an Ideal Brain Food

There are only two types of fuel your body can convert into energy: carbs/sugar, or fat. Again, ketones are what your body produces when it converts fat (as opposed to glucose) into energy. And a primary source of ketone bodies are the medium-chain triglycerides (MCT) found in coconut oil. In fact, coconut oil contains about 66 percent MCTs.

Medium-chain triglycerides (MCT) are fats that are not processed by your body in the same manner as long-chain triglycerides. Normally, a fat taken into your body must be mixed with bile released from your gallbladder before it can be broken down in your digestive system.

But medium-chain triglycerides go directly to your liver, which naturally converts the oil into ketones, bypassing the bile entirely. Your liver then immediately releases the ketones into your bloodstream where they are transported to your brain to be readily used as fuel.

While your brain is quite happy running on glucose, there’s evidence suggesting that ketone bodies may actually help restore and renew neurons and nerve function in your brain, even after damage has set in. Interestingly, the mechanism of this MCT-ketone metabolism appears to be that your body treats MCTs as a carbohydrate and not a fat.  This allows the ketone energy to hit your bloodstream without the normal insulin spike associated with carbohydrates entering your bloodstream. So in effect, coconut oil is a fat that acts like a carbohydrate when it comes to brain fuel.

How Much Coconut Oil Might You Need?

Therapeutic levels of MCTs have been studied at 20 grams per day. According to Dr. Newport’s calculations,5 just over two tablespoons of coconut oil (about 35 ml or seven level teaspoons) would supply you with the equivalent of 20 grams of MCT, which is indicated as either a preventative measure against degenerative neurological diseases, or as a treatment for an already established case.

While more research certainly needs to be done in this area as well, I see no reason not to incorporate coconut oil in your diet, or the diet of a loved one who is exhibiting symptoms of brain degeneration. Coconut oil has so many profound health benefits; it’s not going to do any harm.

It’s worth noting that people tolerate coconut oil differently, and you may have to start slowly and build up to these therapeutic levels. My recommendation is to start with one teaspoon, taken with food in the mornings. Gradually add more coconut oil every few days until you are able to tolerate about four tablespoons. It’s best to take it with food, to avoid upsetting your stomach.

Low-Fat Craze Has Likely Contributed to Dramatic Rise in Alzheimer’s

A number of seriously flawed nutritional guidelines have contributed to more than a few health problems in the US, and the low-fat craze (aimed at preventing heart disease) is toward the top of that list. Not only does avoiding healthful fat promote heart disease, it also promotes brain diseases like Alzheimer’s.

According to neurologist Dr. David Perlmutter, fat avoidance and carbohydrate overconsumption are at the heart of the Alzheimer’s epidemic—which is an entirely preventable disease, driven by lifestyle factors such as diet. Dr. Perlmutter’s book, Grain Brain, provides a powerful argument for eliminating grains from your diet to protect your brain health. Another major factor is the development and increased consumption of genetically engineered (GE) grains, which are now pervasive in most processed foods sold in the US. Unfortunately, despite dire need, there’s little money available for research into treatments using regular food items. As Amanda Smith, Medical Director at University of South Florida (USF) Health Byrd Alzheimer’s Institute told CTV News:

“The pharmaceutical industry is in this — of course to make money for their companies, and of course they want to help people theoretically — but at the end of the day it is about dollars and cents, and so money gets invested in things that are new or patentable rather than things that are sitting on the shelf already.”

Intermittent Fasting Can Also Increase Ketone Production

There are two additional ways to increase ketone production: restricting carbohydrates, and intermittent fasting. Personally, I believe all three of these strategies are best applied together, as you need to replace the lost carbs with high quality fat (and coconut oil certainly fits that bill), and intermittent fasting will help your body shift to burning fat as its primary fuel. It takes about six to eight hours for your body to metabolize your glycogen stores, after which you start to shift to burning stored fat, and hence producing ketone bodies.

Contrary to more stringent and challenging fasts, intermittent fasting simply involves timing your meals to allow your body to enter the fat-burning “window.” To be effective, the length of your fast must be at least 16 hours. For example, this would mean eating only between the hours of 11am until 7pm, or noon until 8pm. You can restrict it even further — down to six, four, or even two hours if you want, but you can still reap many of the health benefits associated with intermittent fasting by limiting your eating to an eight-hour window each day.

I recommend easing yourself into this type of eating schedule. Start by not eating anything for three hours prior to bed, and then gradually extend the time before you eat breakfast each day to the point that you have skipped breakfast and have your first meal at lunch. This typically takes a few weeks to a few months. Also, this is not something that needs to be done continuously once your body has shifted to fat burning mode. However, your desire to eat will be dramatically reduced so you won’t feel the need to eat like you did before shifting your body’s primary fuel burning preference.

Tips for Maintaining Healthy Brain Function and Avoiding Alzheimer’s Disease

Knowing that Alzheimer’s is a preventable disease, predicated on your lifestyle choices, puts the power into your hands.  Diet is paramount, and the beauty of following my optimized nutrition plan is that it helps prevent and treat virtually ALL chronic degenerative diseases, including Alzheimer’s disease.

People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’s entirely possible to prevent the damage from occurring in the first place… and one of the best ways to do this is by leading a healthy lifestyle. The following guidelines will help you protect your brain health well into old age:

Avoid sugar and refined fructoseIdeally, you’ll want to keep your sugar levels to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you have insulin resistance or any related disorders.

Avoid gluten (primarily wheat). Research shows that your blood-brain barrier, the barrier that keeps things out of your brain where they don’t belong, is negatively affected by gluten. Gluten also makes your gut more permeable, which allows proteins to get into your bloodstream, where they don’t belong. That then sensitizes your immune system and promotes inflammation and autoimmunity, both of which play a role in the development of Alzheimer’s.

Optimize your gut flora by regularly eating fermented foods or taking a high-potency and high quality probiotic supplement.

Increase consumption of all healthful fats, including animal-based omega-3. Beneficial health-promoting fats that your brain needs for optimal function include organic butter from raw milk, clarified butter called organic grass-fed raw butter, olives, organic virgin olive oil and coconut oil, nuts like pecans and macadamia, free-range eggs, wild Alaskan salmon, and avocado.

Contrary to popular belief, the ideal fuel for your brain is not glucose but ketones. Ketones are what your body produces when it converts fat (as opposed to glucose) into energy. The medium-chain triglycerides (MCT) found in coconut oil are GREAT source of ketone bodies, because coconut oil is about 66 percent MCTs. In fact, ketones appear to be the preferred source of brain food in patients affected by diabetes or Alzheimer’s.

Also make sure you’re getting enough animal-based omega-3 fats, such as krill oil. (I recommend avoiding most fish because, although fish is naturally high in omega-3, most fish are now severely contaminated with mercury.) High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder.

Reduce your overall calorie consumption, and/or intermittently fast. As mentioned above, ketones are mobilized when you replace carbs with coconut oil and other sources of healthy fats. A one-day fast can help your body to “reset” itself, and start to burn fat instead of sugar.

As part of a healthy lifestyle, I prefer an intermittent fasting schedule that simply calls for limiting your eating to a narrower window of time each day. By restricting your eating to a 6-8 hour window, you effectively fast 16-18 hours each day. To learn more, please see this previous article.

Improve your magnesium levels. There is some exciting preliminary research strongly suggesting a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately, most magnesium supplements do not pass the blood brain levels, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition and may be superior to other forms.

Optimize your vitamin D levels with safe sun exposure. Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health.

Vitamin D may also exert some of its beneficial effects on Alzheimer’s through its anti-inflammatory and immune-boosting properties. Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation that is also associated with Alzheimer’s.

Keep your fasting insulin levels below 3. This is indirectly related to fructose, as it will clearly lead to insulin resistance. However, other sugars (sucrose is 50 percent fructose by weight), grains and lack of exercise are also important factors. Lowering insulin will also help lower leptin levels which is another factor for Alzheimer’s.

Eat a nutritious diet, rich in folate, such as the one described in my nutrition plan. Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day.

Avoid and eliminate mercury from your body. Dental amalgam fillings, which are 50 percent mercury by weight, 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 aluminum, such as antiperspirants, non-stick cookware, vaccine adjuvants, etc.

Exercise regularly. It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,6 thus, slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has also shown that people with Alzheimer’s have less PGC-1alpha in their brains7 and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s. I would strongly recommend reviewing the Peak Fitness Technique for my specific recommendations.

Avoid flu vaccinations as most contain mercury, a well-known neurotoxic and immunotoxic agent.

Eat blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases. Like any fruit though, avoid excesses here.

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 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.

Avoid anticholinergics and statin 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 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.

Other Natural Treatments for Your Anti-Alzheimer’s Arsenal

Finally, there are a few other nutritional recommendations worth noting for their specific benefits in preventing and treating dementia. So, although your fundamental strategy for preventing dementia should involve a comprehensive lifestyle approach, you may want to consider adding a few of these natural dietary agents to your anti-Alzheimer’s arsenal. These four natural foods/supplements have good science behind them, in terms of preventing age-related cognitive changes:

1.Astaxanthin is a natural pigment with unique properties and many clinical benefits, including some of the most potent antioxidant activity currently known. As a fat-soluble nutrient, astaxanthin readily crosses your blood-brain barrier. One study8found it may help prevent neurodegeneration associated with oxidative stress, as well as make a potent natural “brain food.”

The molecules of astaxanthin neutralize free radicals and other oxidants without being destroyed or becoming pro-oxidants themselves in the process. It’s is a unique molecule whose shape allows it to precisely fit into a cell membrane and span its entire width. In this position, astaxanthin can intercept potentially damaging molecules before they can damage your cells.

You can get some astaxanthin by taking krill oil, which is a fantastic omega-3 fat supplement. But you can boost your astaxanthin even MORE by adding a pure astaxanthin supplement to your nutritional regimen. For optimal absorption, make sure to take krill oil and/or astaxanthin with a fat-containing meal, since both are fat-soluble.

2.Ginkgo bilobaMany scientific studies have found that Ginkgo biloba has positive effects for dementia. Ginkgo, which is derived from a tree native to Asia, has long been used medicinally in China and other countries. A 1997 study from JAMAshowed clear evidence that Ginkgo improves cognitive performance and social functioning for those suffering from dementia. Research since then has been equally promising. One study in 2006 found Ginkgo as effective as the dementia drug Aricept (donepezil) for treating mild to moderate Alzheimer’s type dementia. A 2010 meta-analysis found Ginkgo biloba to be effective for a variety of types of dementia.

3.Alpha lipoic acid (ALA): ALA can stabilize cognitive functions among Alzheimer’s patients and may slow the progression of the disease.

4.Vitamin B12: A small Finnish study published in the journal Neurology9 found that people who consume foods rich in B12 may reduce their risk of Alzheimer’s in their later years. For each unit increase in the marker of vitamin B12, the risk of developing Alzheimer’s was reduced by two percent. Remember, sublingual methylcobalamin may be your best bet here.

PHARMA COMPANY THREATENS SHORTAGES TO HIKE UP CANCER DRUG PRICES BY 4000%


There is not lack of controversy in the pharmaceutical industry, particularly when it comes to drug prices. Unethical, profit-generating tactics used by Big Pharma have never been clearer than the recent actions taken by South African Aspen Pharmacare. This company tried to drive up the price of five different cancer drugs as much as 4,000 percent. Moreover, it threatened to stop supplying the much-needed medication if health authorities didn’t agree to the higher prices.

Foul Tactics Used to Increase Cancer Drug Prices

Aspen Pharmacare purchased the rights to five different cancer drugs from British firm GlaxoSmithKline (GSK) in 2009. As part of the deal, GSK became one of Aspen’s main investors. It received 16 percent stake in the company, which it sold off in 2013 and 2016.

In 2012, Aspen started to raise cancer drug prices in major European markets such as Britain, Spain and Italy. The Times reports:

The price rises meant that the cost of busulfan, used by leukaemia patients, rose from £5.20 to £65.22 a pack in England and Wales during 2013, an increase of more than 1,100 per cent. The price of chlorambucil, also used to treat blood cancer, rose from £8.36 to £40.51 a pack in the same year.

When Aspen purchased the rights from GSK, it dropped the brand names. In Britain, the drug maker was able to exploit a loophole that allows companies to raise drug prices for unbranded generics.

 

In mainland Europe, Aspen targeted health authorities with its price hikes. The Timesclaims that it has documents and internal emails that show how Aspen “took an ‘aggressive’ approach to negotiations, sometimes creating shortages of the medicines or threatening to stop supplying the drugs altogether to force health authorities to accept its demands.”

For example, Aspen pressured Italian authorities to pay price increases of up to 2,100 percent. The increase took effect over only three months. Moreover, Spanish authorities faced price hikes of up to 4,000 percent. The Spanish Ministry did not agree to pay the higher prices. As a result, Aspen stopped supplying the Spanish market with its five cancer drugs.

In addition to busulfan, Aspen purchased rights to mercaptopurine, a treatment for acute lymphoblastic leukaemia, which occurs in children. Some of Aspen’s medicines treat several types of cancer particularly prevalent among the elderly.

Big Pharma’s Price Gouging in the U.S.

Price gouging by drug makers is not exclusive to Aspen Pharmacare or the European region. Currently, the United States is one of the most lucrative markets for Big Pharma. This isn’t just because of the sheer amount of people in the U.S. population who take prescription medications. More importantly, in the U.S. drug companies are charging up to 10 times as much for pharmaceuticals when compared to other developed countries.

Breastfeeding lowers risk of heart disease and stroke for mothers, study suggests


Breastfeeding may reset metabolism after birth, scientists believe
Breastfeeding may reset metabolism after birth, scientists believe  

Breastfeedingis not only beneficial for babies but it could prevent women suffering a stroke or developing heart disease in later life, scientists have concluded.

Previous studies have suggested that mothers get short-term health benefits from breastfeeding, such as weight loss and lower cholesterol, blood pressure and glucose levels after pregnancy, but there have been no research into the long-term impact.

When researchers at Oxford University and the Chinese Academy for Medical Sciences studied nearly 300,000 middle-aged women for eight years, they discovered that those who had breast fed were nine per cent less likely to develop heart disease and eight per cent less less likely to suffer a stroke.

And the health benefits increased the longer they had breast fed their children. Women who put off the bottle until two  years old lowered their risk of heart disease by 18 per cent, and stroke 17 per cent. For every additional six months after that the risk lowered by an extra four per cent and three per cent respectively.

Women's body change to store large amounts of fat, which without breastfeeding may accumulate
Women’s body change to store large amounts of fat, which without breastfeeding may accumulate  

Researchers say that breastfeeding may help restore a woman’s fat clearing systems after the birth.

“Although we cannot establish the causal effects, the health benefits to the mother from breastfeeding may be explained by a faster “reset” of the mother’s metabolism after pregnancy,” said Dr Sanne Peters,  research fellow at Oxford University.

“Pregnancy changes a woman’s metabolism dramatically as she stores fat to provide the energy necessary for her baby’s growth and for breastfeeding once the baby is born. Breastfeeding could eliminate the stored fat faster and more completely.”

British women have the some of the lowest breastfeeding rates in the world with just one in 200 women (0.5 per cent) still breastfeeding a year after becoming mothers. The figure is 23 per cent in Germany and 27 per cent in the United States.

The World Health Organisation recommends that all babies are breastfed for up to two years or longer

Only around two per cent of women is unable to lactate, and experts believe social reasons, such as the desire for life to return to normal after the birth, is behind the disparity. More than half of British babies have had some formula by the end of their first week, according to the University of Swansea. It is estimated that increasing breast feeding rates could save the NHS around £40 million a year.

Just one in 200 women in Britain continuing breastfeeding after the first year 
Just one in 200 women in Britain continuing breastfeeding after the first year  CREDIT:BLEND I

Although the authors cautioned that women who breastfeed may be more likely to engage in other beneficial health behaviors that lower their risk of cardiovascular disease compared to women who do not breastfeed, they said the findings provide more evidence of the long-term benefits for both mother and child.

“The findings should encourage more widespread breastfeeding for the benefit of the mother as well as the child,” said Dr Zhengming Chen, Professor of Epidemiology, at Oxford University.

“The study provides support for the World Health Organization’s recommendation that mothers should breastfeed their babies exclusively for their first six months of life.”

The research was published in the Journal of the American Heart Association.