TCM niu bang zi Traditional Chinese Medicine herb proven to be a powerful anti-cancer agent

(Natural News) The greater burdock (Arctium lappa) is a popular medicinal plant used in traditional Chinese medicine. Its fruit, known as niu bang zi, is especially well-known: It is used to treat multiple ailments, such as boils, acute tonsillitis, abscesses, and constipation. According to researchers at Wonkwang University in South Korea, the fruit can potentially be used as an anticancer agent. In their study published in The…

Misc Conversation and an Afternoon Dream of First Contact

—–Patterson, Denice on 6/4/2019 4:36 AM wrote:
> Fully awake. Eyes closed. Screens on. Saw the inside of an institutional bldg. Beige cinderblock walls. Flat white tile floors, what little furniture was stacked in the hallway. I was facing a locked metal exterior door, fire exit, then turned right. Entered a large room. Same decor. A few more chairs and a table or two all pushed to the walls for floor waxing? Felt like a family visiting room. A few windows, but high up. The vibe was, it is being emptied and cleaned. Your hotel?

Love you!!


Heather wrote back:

yes…exactly…very accurate details, denice…all the way to the stacked furniture for buffing in the lobbies/visiting room!

well done 🙂

love you!

Martha to Denice: Impressive!

Martha: I spent most of my day funeraling. Service, graveside, to the old country church for a meal. Cousins by dozens. Came home and fell asleep. A detailed dream about the church I grew up in (different one) and it had been made a daycare/school. Since my car was locked in their parking unaccountably, I told them the church building history.

Martha: Today there was much talk of Jean being so very down to earth and just rolling with whatever happened. And her family did just this. No tears. Lots of hugs. A big family. It was beautiful.

Denice: oh beautiful! That is a tribute!

Martha: On the way to the cemetery, we drove through the hardest hit tornado area. Heartbreaking. Houses leveled to fields of rubble. They had drug trees and junk to a pile and were burning it. But Jean would have loved seeing it because it’s part of life.

Denice: ??

Martha: ? 

Denice: Yes, there is something to be said about LIVING and being. and doing. I am feeling now how very unique this human experience must seem to those on the ‘outside’

Martha: Yes indeed. I was aware the ceremony today was watched and under examination.
Denice: perfect!
Martha: Just the fact we view death as final and mourn is astounding to them. Visible evidence of how blind we are to All.  And evidence of how deeply programmed we are.
Denice: yes! but reverse the roles? Interesting prospect for a new perspective from the ‘galactic viewpoint’ 🙂
Martha: What do you mean?
Denice: I mean, them really, really experiencing pain and grief at perceived ‘loss’. . .the true human experience. Live. love. grieve. maybe they would jump in sooner, if they truly knew and felt how difficult it is?
Martha: Yes. I got you. And yes, a huge learning experience for them.  Our role – to experience what couldn’t be fathomed on the other side of the fence and to bring that Home.
Denice: oh, yes!  ‘what couldn’t be fathomed’ precisely!

Martha: Only understood by living it.

Denice: and ‘dying it’ 
Martha: Yes.
Denice: (bow) thanks! another new feeling flowing ? A big warm hug for you, Martha! ??
Martha: Yes indeed. Me too. I’ll be thinking on this.  Right back at you!
Denice: try your screens! they are ‘on’ when you are ready!
Martha: We are perhaps brave warriors after all.
Denice: and “you know who” is in his big chair ?? [Denice is referring to Jai]

Martha: I will start watching. Oh that chair. Lol. You know he said I picked it. Lol. The pipe smoking chair. For reading, music and pondering.

Denice: beautiful!!!
Martha: Thanks! I will look toward the screens as often as possible.  Have a wonderful evening. ??
Denice: ? 
Terran to Denice: Congrats Denice! [on the screens activating. Denice’s abilities had shut down for a bit with this new influx of energies] 
Terran: I am feeling really tired, getting called to lay down. Haven’t heard from H in days. But I feel her at moments.  (I laid down around 3:30 PM didn’t wake till about 1 AM body was really out of sorts… I went next door and borrowed Bev’s red and near infrared LED light to balance my body before drifting off to sleep)

Terran: Weird stuff going on in this house. Bedroom door half closed this AM.

Terran: Just heard some sounds that sounded vaguely like an old transistor radio with an AM radio station on it… Couldn’t locate the source.

5:03 PM

Martha: I’m seeing many posts in fb about people seeing people around them in their true form. Elves, aliens (not specific), etc. and glitches like cars changing or disappearing. All in recent days.

5:04 PM

Denice: Today, I am seeing people in their original form. . . (whew)

Martha: You mean human?

Denice: yes, facades were dropped today. . .

5/5/19 1:03 AM CST

Skye: I quite definitely felt a tap on the shoulder yesterday..: looked around, no one there ?

Skye: And talking of people ‘dying’… in the last few months 4 climbers I know have died! 1 on Mount Everest two weeks ago – he was found dead in his tent at 7000 metres cause of death unknown; one this last week in the Indian himalaya in a big avalanche; one in a climbing accident in Scotland a few months ago and 1 of illness 3 weeks ago!

Martha: I just this moment jolted awake realizing the car I was driving in Dreamtime had suddenly lost headlights and engine stopped, and the sky was turning orange.

Skye: sounds interesting!

Martha: Oh my. That’s a lot of loss.

Skye: Yes. I had known 3 of them for 30 years

Martha: ??loss or change of form.

Skye: Hard for their families who don’t know it’s not the end… but even so it’s hard when they leave the physical- for all of us

Martha: Yes indeed. We miss them.

5/5/19 1:52 AM

Terran: Cars often lose their power in the presence of ET ships

Terran: Hi Skye!

Skye: ?

Martha: “Cars often lose their power in the presence of ET ships”

Yes, it was yet another arrival dream, I think. I was a bit frustrated at the car stopping in the road instead of being able to pull over, but then realized no one else would be moving. I’d decided to just get on with it, as it was clear something was about to happen. I’d opened the car door to get out, and then woke up. And then heard Skype bloop. Lol.

5/5/19  3:30PM

Terran: Laid down for a nap after my weird night of sleep last night… my feet felt heavy…

Terran: I had a dream the first official contact was with the Fun-kins I turned to Denice and said “who are the Fun-kins?” Apparently in the dream they are a Nordic race… that we knew nothing about…

Which prompted a childhood memory of Denice’s:

Denice: Funkins! I know them! Don’t know how I do. I feel it. . . .the name is familiar. . .and it is from my preschool years. .. 1970 – 1972. I started kindergarten in ’72.

Denice: here is what I have for you: the name is from this side. . .earth kids named them that. . .
kind, curious, soft, smell like baby powder or baby oil, gentle. . .perhaps even squeaky?
blue eyes. . .pale white ‘skin’/’form’

Denice: they are from “TAURIUS 6”. ??

Terran Note: there appears to have been a toy called “Funkins” a few years back. Art imitating life in the Universe?  We’ll see where this goes…Its odd that Me, Denice and Martha got a hit on the Funkins in our internal codexes. 

Sriracha: Here’s Why This Spice Can Be Good for Your Body

Although sriracha’s rise to popularity occurred in the last 30 or 40 years, its origins are humble. Sriracha sauce (pronounced sir-rotch-ah1) is named after the seaside city of Si Racha in eastern Thailand,2 where it was created by a villager, Thanom Chakkapak, over 80 years ago.

Chakkapak first shared the sauce with her family and friends, but its rising popularity prompted her to begin manufacturing it commercially under the name Sriraja Panich. Sriracha’s popularity quickly spread, and it was eventually hailed the best-selling chile-based sauce in Thailand.3

In the U.S., production of this sauce began in 1980, when Vietnamese immigrant David Tran founded Huy Fong Foods in Los Angeles, and marketed his own version of sriracha, along with other types of hot sauces.4

Tran’s sriracha packaging is actually the design most of us are familiar with — a clear, green-capped, squirt bottle with a rooster in the middle. It became the most popular version of sriracha not just in the U.S., but across the globe.5

Since then, other brands have taken their own spin to this spicy sauce. Organic sriracha brands are even available today.

Unfortunately, while sriracha is made of simple ingredients like red chilies, garlic, vinegar and salt, most brands contain high amounts of sugar, which can upset your metabolism and add to your daily carb and sodium intake in a way you may not realize. According to Refinery29:6

“A one-teaspoon serving size contains 80 milligrams of sodium, and 1 gram of sugar. ‘To put that into perspective, ketchup contains about the same amount of sugar and a little more than half the sodium of sriracha,’ says Tracy Lockwood, MS, RD, CDN, a registered dietitian in New York City.”

As such, making homemade sriracha sauce is better, so you can control what goes into your blend. Read on to see how you can use hot sriracha sauce for many of your recipes, and how to make it at home using healthy ingredients — a great alternative to processed, sugar-loaded commercial varieties.

Is Sriracha a Healthy Sauce?

Most of sriracha’s benefits come from the red chili peppers that form the base of the sauce. Spicy foods like peppers contain a compound called capsaicin, which can assist in boosting metabolism and weight loss7 by increasing satiety8 and helping limit fat accumulation in your tissues.9

Capsaicin also has antioxidant and anti-inflammatory properties.10 One study notes that its anti-inflammatory effect may even be comparable to the drug diclofenac.11 Capsaicin may also help lower the risk for cancer and tumors. According to a 2016 study in the Anticancer Research journal, it targets “multiple signaling pathways and cancer-associated genes in different tumor stages including initiation, promotion, progression and metastasis.”12

This compound may also reduce platelet aggregation,13 provide pain relief (particularly when applied topically)14 and address nasal congestion by helping clear mucus from the nose.15 Capsaicin’s antibacterial properties may help thwart chronic sinus infections, as well.16

Vitamins A and C are found in chili peppers,17 both of which have antioxidant effects to help combat pathogens.18,19 Chili peppers can also assist in managing your blood sugar levels and even lower your risk of hyperinsulinemia (high insulin levels in your blood).20

Common Uses of Sriracha Sauce

Sriracha is a multipurpose sauce, and can be incorporated in various recipes. Here are ideas from The Spruce Eats on how to use sriracha sauce for your meals:21

  • Use sriracha as a dipping sauce by itself or combine it with cream, sour cream or mayonnaise.
  • Add sriracha to soups or stews. While it’s often used to flavor pho, a Vietnamese soup dish, you can also mix sriracha into ramen, tomato soup or gazpacho.
  • Flavor your meats (chicken wings, meatballs or meat loaf) or take your marinades (teriyaki sauce or barbecue sauce) up a notch with some sriracha.
  • Incorporate sriracha into your tomato or vegetable juice for a spicy kick.

How to Make Your Own Sriracha at Home

If you want that sriracha kick in your meals, I recommend making your own homemade version instead of relying on processed sauces sold in supermarkets. Here’s a simple recipe adapted from Nourishing Meals:22

Homemade Sriracha Sauce


1 pound fresh hot red chili peppers (padron, cayenne, serrano, jalapeno, cherry bomb or Thai)

1 pound sweet red peppers, seeded

4 to 6 garlic cloves

1 1/2 cups raw apple cider vinegar or coconut vinegar

1/2 cup water

2 to 3 teaspoons of sea salt


  1. Cut the stem off each of the hot peppers and place into a high-powered blender. (There is no need to wear gloves because you are not opening the pepper to remove the seeds.)
  2. Add the remaining ingredients to the blender and blend on high until very smooth.
  3. Pour the sauce into a 3- to 6-quart saucepan and bring to a simmer. Reduce heat to low and simmer for about 30 minutes until thickened. Add more water for a thinner sauce and simmer for a few more minutes.
  4. Pour into clean glass jars and store in your refrigerator for up to six months. You can also preserve it by canning it: Pour the sauce into small sterilized canning jars (4- or 8-ounce) and boil a batch for 10 minutes. Then store jars in your pantry for up to a year.

This recipe makes about 4 cups of sauce.

Healthy and Tasty Sriracha Sauce Recipes

Greatist has compiled 50 recipes that use sriracha seasoning, either for breakfast, lunch, dinner or snacks.23 Here are some examples of the healthy recipes that use this spicy sauce:

  • Breakfast — Bake Your Day’s sriracha and veggie frittata24
  • Lunch — Leaf + Grain’s sriracha quinoa bites25
  • Dinner — Alysa Bajenaru’s chicken coconut curry soup26
  • Snack — Authentic Suburban Gourmet’s roasted Brussels sprouts with Sriracha Aioli27

The HuffPost also suggests trying these sriracha substitutes, which are just as spicy and flavorful:28

  • Sambal oelek — An Indonesian sauce created using freshly ground chili peppers29
  • Gochujang — A traditional Korean spicy paste made from fermented soybeans
  • Piri piri sauce — A Portuguese hot sauce made using bird’s eye chilies
  • Harissa — A chili paste that traces its origins to North Africa

How Temperature Affects Your Sleep

If you’ve ever woken up because you’re too hot or cold, you know that temperature extremes can significantly affect your sleep quality. But even subtle differences in temperature can influence your sleep, for better or worse. Your body temperature cycles along with your sleep-wake rhythm, decreasing at night while you’re asleep and increasing during the day.1

You’re most likely to sleep when your core body temperature decreases and unlikely to sleep while it’s on the rise. Further, after you fall asleep, your core body temperature will decrease even more, but your peripheral skin temperature, which plays a role in maintaining your body’s core temperature by adjusting blood flow to your skin, remains high.2

Both your core body temperature and your peripheral skin temperature are further influenced by external factors in your sleep environment, such as whether you sleep nude or in pajamas, and whether you use a comforter while you sleep.

Taken together, if you’re having trouble sleeping, paying attention to your thermal environment and making changes where necessary could help you get a good night’s rest.

How Heat Exposure Affects Your Sleep

In people who slept nude except for shorts, without any covers and, for research purposes, on a bed made from nylon webbing, the ambient temperature of 21 degrees C (69.8 degrees F), which was the coolest temperature tested, was most disruptive to sleep.3

Cold ambient temperatures were generally more disruptive to the participants’ sleep than warm temperatures, although sensitivity to heat or cold varied according to the person. Further, this doesn’t take into account the way many people sleep, which is wearing pajamas and under the covers.

“In real-life situations where bed covers and clothing are used, sleep is actually disturbed during heat exposure rather than cold exposure in the young, as well as in the elderly,” researchers wrote in the Journal of Physiological Anthropology.4

Heat combined with high levels of humidity may be worst of all, as humid heat exposure suppresses the decrease in core body temperature that normally occurs with sleep, leading to increases in wakefulness and decreases in rapid eye movement (REM) and slow wave sleep (SWS) stages. The researchers continued:5

“Humid heat exposure most probably increases heat stress because of the difference in the sweat response caused by the humidity.

Decreased ambient humidity allows sweat to evaporate, thereby dissipating the heat, whereas increased humidity does not allow the sweat to evaporate, causing the skin to remain wet. The dripping sweat and increased skin wetness decrease the sweat response due to hidromeiosis preventing dehydration.”

Also important, exposure to humid heat appears to have a more significant effect on your sleep when it occurs in the initial segment of sleep as opposed to later. If you’re only going to use air conditioning for a few hours a night, then it makes sense to turn it on when you’re first going to sleep.6

Exposure to higher temperatures at night may be particularly disruptive for elderly men, a population easily awakened by even mild heat exposures and who have an already reduced heat tolerance.7

What Does Cold Exposure Do to Your Sleep?

Whereas heat exposure has a greater effect on the first segment of sleep, cold exposure primarily affects the later segment, when REM sleep occurs. In people sleeping semi-nude, the disruption occurs due to the suppression of your body’s thermoregulatory response. However, cold is unlikely to have as great an effect in real-life situations, when most people use sleepwear or bedding to offset cold temperatures at night.

According to the Journal of Physiological Anthropology study, in real-life settings using clothing and/or bedding, no significant differences were observed in sleep at temperatures ranging from 13 degrees C (55.4 degrees F) to 23 degrees C (73.4 degrees F).

That being said, although cold exposure doesn’t appear to affect sleep stages, it did lead to changes in autonomic heart activity, enough so that researchers suggested it could be one reason why cardiac events peak during cold winter temperatures.8 In fact, research suggests that mortality from ischaemic heart disease is associated with cooler homes and limited bedroom heating.9

If you take this into account, the Journal of Physiological Anthropology researchers noted, ” … the impact of cold exposure may be greater than that of heat exposure in real-life situations; thus, further studies are warranted that consider the effect of cold exposure on sleep and other physiological parameters.”10

Increases in Nighttime Temperatures Linked to Worse Sleep

When measured subjectively, data from 765,000 Americans showed that increases in nighttime temperatures increased self-reported nights of insufficient sleep.11 Other research also found that high temperatures affected multiple aspects of sleep, leading to:12

  • Worse sleep duration
  • Shallow sleep
  • Less sleep calmness
  • Difficulty falling asleep
  • Lower sleep satisfaction

Sleeping in a cooler room may therefore lead to fewer disruptions in your sleep, with the National Sleep Foundation (NSF) suggesting the ideal bedroom temperature is somewhere between 15.5 degrees C (60 degrees F) and 19.4 degrees C (67 degrees F).13

You want to avoid extreme temperatures (either too hot or too cold), as these could activate thermoregulatory defense mechanisms that cause you to wake up.14 NSF noted:15

“If your room is cool, rather than warm, it will be much easier to shut your eyes for the night. Thermostat settings far lower or higher than what’s recommended could lead to restlessness and can also affect the quality of [REM], the stage in which you dream. It can also help to think of your bedroom as a cave — it should be quiet, cool, and dark for the best chance at getting enough rest.”

Showering Before Bed and Wearing Socks to Bed May Improve Your Sleep

Raising your skin temperature promotes the onset of sleep,16 as it increases neuronal activity in brain areas involved in sleep regulation.

An increase in skin temperature of just 0.4 degrees C has been found to suppress nighttime wakefulness and shift sleep to deeper stages in the young, the elderly and people with insomnia — even though it didn’t alter core body temperature. The effect was especially pronounced in the elderly, with researchers writing in the journal Brain:17

“Elderly subjects showed such a pronounced sensitivity, that the induced 0.4 degrees C increase in skin temperature was sufficient to almost double the proportion of nocturnal slow wave sleep and to decrease the probability of early morning awakening from 0.58 to 0.04.

Therefore, skin warming strongly improved the two most typical age-related sleep problems; a decreased slow wave sleep and an increased risk of early morning awakening.”

There are a number of ways to take advantage of this science in your bedroom. One simple method is to take a shower before bed. A 10-minute shower at a temperature of about 40 degrees C (104 degrees F) increased skin temperature and helped participants fall asleep faster and maintain greater sleep efficiency.18

Soaking your feet in hot water before bed may also help and has been shown to help people fall asleep faster.19 Wearing socks to bed is another option. When participants in one small study wore socks to sleep, they fell asleep faster, slept longer and had fewer nighttime awakenings.20

An interesting aside — people with insomnia who wore special caps filled with cool circulating water were able to sleep better, in this case likely because the cap helped to cool their brain. Many insomniacs report that they can’t fall asleep because they “can’t turn their brains off” at night. The extra brain activity was keeping their brains too hot for sleep, and the cap helped resolve this.21

Sleeping in a Cool Room Increases Beneficial Brown Fat

Another reason to sleep in a cool room is its beneficial effect on brown fat, which generates heat by burning calories in order to help maintain your core temperature. Sleeping in a cool room (19 degrees C or 66.2 degrees F) for four weeks doubled the volume of brown fat in study volunteers, improving insulin sensitivity at the same time.22,23

Shivering may be the mechanism that triggers brown fat to produce heat and burn calories,24 but if you’re shivering it’s not conducive to sleep. Finding the sleep temperature Goldilocks zone is what you’re after — cool enough to help you sleep and increase brown fat but not so cool that it makes you uncomfortable.

The exact best temperature will vary by individual, but sleeping in a cool room with a thin sheet and blanket is generally enough to keep your skin temperature warm, so you feel comfortable, while still benefiting from the cool sleep temperatures.25

Proper Sleep Is Essential for Good Health

Adults need an average of seven to nine hours of sleep a night, with most doing well with about eight. If you have trouble achieving this duration, or you wake frequently during the night, it’s time to take steps to improve your sleep hygiene, starting with your bedroom — but temperature is only one factor.

Be sure you’re sleeping in complete darkness, as light (even that from a night light or alarm clock) can disrupt your internal clock and your production of melatonin and serotonin, thereby interfering with your sleep.

In the morning, bright, blue light-rich sunlight signals to your body that it’s time to wake up. At night, as the sun sets, darkness should signal to your body that it’s time to sleep. Ideally, eliminate electromagnetic fields (EMFs) and shut down the electricity to your bedroom by pulling your circuit breaker before bed and turning off your Wi-Fi at night.

This is just a starting point. Other ways to improve your sleep including adopting a neutral sleeping position, going to bed earlier and considering a separate bedroom if your partner is interfering with your sleep. If you’ve already addressed these issues and are still struggling with sleep, see my 33 healthy sleep secrets for a more comprehensive list of strategies for a better night’s rest — and improved overall health.

Study Claims Alzheimer’s Disease Is a Double-Prion Disorder

Prions are abnormal and infectious forms of proteins that collect in brain tissue, causing cells to die. The sponge-like holes left in the brain are a hallmark of transmissible spongiform encephalopathies such as bovine spongiform encephalopathy (BSE, also known as mad cow disease in cows and Chronic Wasting Disease1 in deer and elk) and Creutzfeldt-Jakob disease2 (CJD), the human version of BSE.

Both BSE and CJD are the result of a prion infection; both are untreatable and always fatal. Sporadic CJD (sCJD), a form that appears without known risk factors, accounts for nearly 85% of diagnosed CJD cases:3,4

CJD is difficult to diagnose, as taking a brain biopsy to rule out a disease is impractical. However, in 2018, the National Institutes of Health published work from colleagues at the University of California San Diego and San Francisco, showing you can measure the distribution and level of prions in the human eye.5

According to Dr. Christina J. Sigurdson, professor of pathology at UC San Diego and Davis, who was on the team,6 “Our findings have implications for both estimating the risk of sCJD transmission and for development of diagnostic tests for prion diseases before symptoms become apparent.”

Alzheimer’s Disease Linked to Prions

For a number of years now, researchers have theorized and found evidence suggesting Alzheimer’s disease may in fact be a type of prion-based disease,7,8,9 capable of being contracted via meat10 and transmitted via certain invasive medical procedures.11

Researchers have noted that Alzheimer’s behaves like a slow moving version of CJD,12,13,14 and according to one paper,15 “Prions are considered a subclass of amyloids in which protein aggregation becomes self-perpetuating and infectious.” As reported by Scientific American:16

“Between 1958 and 1985, a number of individuals with short stature received shots of human growth hormone extracted from the pituitary glands of cadavers… Some of these samples were contaminated with prions that caused certain patients to develop Creutzfeldt-Jakob disease (CJD), a rare and fatal brain disorder.

Treatments ceased once these reports came to light, but by that time an estimated 30,000 people had already received the injections. As of 2012, researchers have identified 450 cases of CJD worldwide that are the result of these growth hormone injections and other medical procedures, including neurosurgery and transplants.”

Previous animal research17 has also found that when tiny amounts of amyloid-beta proteins — which are a hallmark of Alzheimer’s — are injected into mice or monkeys, they act as self-propagating “seeds,” unleashing a chain reaction of protein misfolding that results in pathology that is very reminiscent of that seen in Alzheimer’s patients.

As Many as Half of Alzheimer’s Patients Have Prion-Like Proteins

Mounting research reveals a compelling link between a protein known as TDP-43 and neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Lou Gehrig’s disease. TDP-43 behaves like the prions responsible for the brain destruction seen in Mad Cow and Chronic Wasting Disease.18

According to research19 published in 2011, TDP-43 pathology is detected in 25% to 50% of Alzheimer’s patients, particularly in those with hippocampal sclerosis, characterized by selective loss of neurons in the hippocampus, which is associated with memory loss.

Research presented at the 2014 Alzheimer’s Association International Conference also revealed Alzheimer’s patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without it.20,21

Alzheimer’s Disease — A Double-Prion Disorder

More recent research by scientists at the University of California San Francisco (UCSF) adds further weight to the hypothesis that Alzheimer’s disease is a prion-related disease. The study,22,23 published in the May, 2019, issue of Science Translational Medicine, found that the two hallmark proteins associated with Alzheimer’s — amyloid beta and tau — indeed act as prions, effectively making it a double-prion disease.

Prions, while being misfolded proteins and not viruses or bacteria, have the curious capacity to spread in a self-propagating manner by forcing normal proteins to misfold. The first prion, called PrP, was discovered in the 1980s, when it was identified as the cause of CJD and SBE.24

As noted by UCSF,25 it was “long suspected that PrP was not the only protein capable of acting as a self-propagating prion, and that distinct types of prion could be responsible for other neurodegenerative diseases caused by the progressive toxic buildup of misfolded proteins.”

Indeed, by applying recently developed laboratory tests, the UCSF research team was able to measure “self-propagating prion forms of the proteins amyloid beta and tau in postmortem brain tissue of 75 Alzheimer’s patients,”26 confirming previous findings that amyloid plaques and tau tangles spread in much the same way as PrP, causing similar damage but at a slower rate.27

Tau Prion Levels Strongly Correlate to Longevity

Importantly, higher levels of prion-like amyloid beta and tau were found in those with early onset of Alzheimer’s who died at an earlier age, with tau buildup showing the strongest correlation. Compared to a patient who died of Alzheimer’s at the age of 90, a patient who died at 40 had on average 32 times higher amounts of tau prions in their brain. As noted by UCSF:28

“Alzheimer’s disease is currently defined based on the presence of toxic protein aggregations in the brain known as amyloid plaques and tau tangles, accompanied by cognitive decline and dementia.

But attempts to treat the disease by clearing out these inert proteins have been unsuccessful. The new evidence that active Aß and tau prions could be driving the disease … could lead researchers to explore new therapies that focus on prions directly.”

Senior author Dr. Stanley Prusiner, director of the UCSF Institute for Neurodegenerative Diseases, commented on the results:29

“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain.

The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease.”

One of the study’s lead authors, Carlo Condello, Ph.D., assistant professor of neurology in the Institute for Neurodegenerative Diseases, added:30

“We have recently seen many seemingly promising Alzheimer’s therapies fail in clinical trials, leading some to speculate that we have been targeting the wrong proteins. But what if we just haven’t been designing drugs against the distinctive prion forms of these proteins that actually cause disease?

Now that we can effectively measure the prion forms of Aß and tau, there’s hope that we can develop drugs that either prevent them from forming or spreading, or help the brain clear them before they cause damage.”

What Makes Amyloid Infectious?

A study31 published in the journal Prion in 2014 sought to determine why certain proteins prone to form amyloids have the capacity to infect their neighbors. Here, too, the author referred to Alzheimer’s as a prion disease, specifically with reference to the amyloid plaques formed:

“The conformational diseases, linked to protein aggregation into amyloid conformations, range from non-infectious neurodegenerative disorders, such as Alzheimer’s disease (AD), to highly infectious ones, such as human transmissible spongiform encephalopathies (TSEs). They are commonly known as prion diseases.

However, since all amyloids could be considered prions … it is necessary to find an underlying cause of the different capacity to infect that each of the proteins prone to form amyloids has.

As proposed here, both the intrinsic cytotoxicity and the number of nuclei of aggregation per cell could be key factors in this transmission capacity of each amyloid.”32

The author goes on to state that while amyloids are universal and share certain internal structural characteristics, “prions represent only a tiny drop in the amyloid ocean.” In order for an amyloid to become a prion, something has to occur causing the aggregation process to become self-perpetuating and infectious.

He points out that the Alzheimer’s disease process, while similar to that of CJD, is much slower, and doesn’t follow the same pathway of transfer (from the spleen to the central nervous system). So, what causes amyloid in an Alzheimer’s patient to become infectious? What turns it into a prion? To answer this question, the author turns to research on fungal and yeast prions.

“Recent findings in the field have shown that the number of nuclei of aggregation could be a factor that affects the infection capacity of amyloid-prone proteins, just as their intrinsic cytotoxicity does.

In both fungal and yeast prions, the number of nuclei of aggregation per cell determines, following Poisson’s law, the probability of prion infectivity. Thus, high numbers of nuclei of aggregation per cell result in an increase in infectivity,” he writes.

He also speculates that cytotoxicity plays a big role, and that “the intrinsic cytotoxicity of each amyloid … could be a key factor in the differentiation between infectious and noninfectious amyloids in humans.”

The following year, 2015, the same author, joined by several others, published a second paper33 in the same journal, titled “Amyloids or Prions? That Is the Question.” “Despite major efforts devoted to understanding the phenomenon of prion transmissibility, it is still poorly understood how this property is encoded in the amino acid sequence,” they write.

According to this 2015 paper, experiments using yeast prions have demonstrated that in order for prions to form, there must exist “intrinsically disordered sequence regions enriched with a particularly high proportion of glutamine and asparagine.”

The Antimicrobial Protection Hypothesis of Alzheimer’s Disease

Other recent studies,34,35,36 meanwhile, suggest the amyloid beta found in Alzheimer’s patients is also an antimicrobial peptide (AMP). AMPs are the primary effector proteins of your innate immune system that target bacteria, viruses and fungi. They also act as mediators of inflammation and play a role in cytokine release, angiogenesis and more.37

In one such study,38 the authors suggest amyloid beta, as an AMP, “utilizes fibrillation to protect the host from a wide range of infectious agents.” Another study39 points out that “Ancient origins and widespread conservation suggest the human A? sequence is highly optimized for its immune role.”

Findings such as these would support the hypothesis that amyloid beta protein might actually be targeting prions and trying to protect the host from infection. In other words, the presence of beta amyloid may not be the actual cause of Alzheimer’s but rather the result of an innate defense mechanism against prion infection, perhaps acquired through consumption of prion-infected meat.

A lot of this is still speculative, but it’s an intriguing idea. And, while slim, there’s some evidence40 (which has yet to be reproduced) that cross-species prion infections could in fact occur. As noted in “The Antimicrobial Protection Hypothesis of Alzheimer’s Disease,” published in the December 2018 issue of Alzheimer’s & Dementia:41

“We explore here a novel model for amyloidogenesis in Alzheimer’s disease (AD). This new perspective on AD amyloidosis seeks to provide a rational framework for incorporating recent and seemingly independent findings on the antimicrobial role of ?-amyloid and emerging experimental, genetic, and epidemiological data, suggesting innate immune-mediated inflammation propagates AD neurodegeneration …

[E]emerging findings are increasingly inconsistent with characterization of A? oligomerization as a nonphysiological and exclusively pathological activity. Recent studies suggest A? is an ancient, highly conserved effector molecule of innate immunity.

Moreover, A? oligomerization and ?-amyloid generation appear to be important innate immune pathways that mediate pathogen entrapment and protect against infection.

NEW AD AMYLOIDOGENESIS MODEL: Recent findings on inflammation-mediated neurodegeneration and the role of A? in immunity have led to emergence of the ‘Antimicrobial Protection Hypothesis’ of AD. In this model, ?-amyloid deposition is an early innate immune response to genuine, or mistakenly perceived, immunochallenge.

A? first entraps and neutralizes invading pathogens in ?-amyloid. A? fibrillization drives neuroinflammatory pathways that help fight the infection and clear ?-amyloid/pathogen deposits. In AD, chronic activation of this pathway leads to sustained inflammation and neurodegeneration.

Mounting data link elevated brain microbe levels with AD. The Antimicrobial Protection Hypothesis reveals how increased brain microbial burden may directly exacerbate ?-amyloid deposition, inflammation, and AD progression.”

Alzheimer’s Is Largely Preventable

It is often believed dementia is a condition that can’t be controlled, but there are many factors you can influence to greatly reduce your risk. It is important to address several factors, however, and not focus exclusively on only one or two.

That said, improving your cardiovascular fitness is an excellent place to start, as I discuss in my previous article, “How to Decrease Your Risk for Dementia by 90 Percent.” When combined with other approaches to resolve mitochondrial dysfunction, it can be highly effective in preventing cognitive decline.

Other strategies to help you reduce your risk of Alzheimer’s disease include eating a ketogenic diet, optimizing your vitamin D and omega-3 levels, eliminating gluten and processed foods, and cyclical (both intermittent and partial) fasting, as detailed in my latest book, “KetoFast.”

You’ll find more details on the lifestyle strategies I believe to be most helpful and important to reduce your risk of Alzheimer’s disease in my previous article, “Link Between Sugar and Alzheimer’s Strengthens.”

To learn more about Alzheimer’s and the tests that can help diagnose it early, see my interview with Dr. Dale Bredesen, author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”

Additionally, one of the most effective and simple strategies for increasing heat shock proteins, which are responsible for refolding the amyloid and tau proteins properly, is near infrared sauna. I personally believe this is a strategy that virtually everyone over 50 should regularly engage in. Please review my engaging interview with Brian Richards below for more details on this valuable therapy.

Ex-Government Physicist Shares What He Knows About ‘Activating’ ESP (Psi) Dreaming

The most astonishing fact about studies within the realm of parapsychology (Psi) is that they are often shunned by the mainstream media and this comes despite the fact that they have extremely high amounts of credibility within the realms of academia. Parapsychology deals with phenomena like pre-cognition, remote viewing, telepathy, mind matter interaction, and more that fall under the label of extra sensory perception (ESP), and the truth is, there is no reason why these topics should not be studied openly within the mainstream. Why is it that they are ridiculed in that realm, but have been studied at the highest levels of government for decades with high amounts of success and credibility? The US/Stanford University STARGATE project is one of many examples that confirm parapsychology’s legitimacy.

These programs usually run and are funded by the black budget. Find out where trillions of our tax dollars are going here.

Dr. Jessica Utts, the Chair of the Department of Statistics at the University of California, Irvine makes a great point on the show Talking Points, further emphasizes my point.

“What convinced me was just the evidence, the accumulating evidence as I worked in this field and I got to see more and more of the evidence. I visited the laboratories, even beyond where I was working to see what they were doing and I could see that they had really tight controls… and so I got convinced by the good science that I saw being done. And in fact I will say as a statistician I’ve consulted in a lot of different areas of science; the methodology and the controls on these experiments are much tighter than any other area of of science where I’ve worked.” (source)

Based on all of my research into the field of parapsychology, the information seems to be shunned away from in mainstream academia simply because it has an association with superstition, spirituality, metaphysics and ‘magic’. This alone, no matter how strong the evidence and how significant the results when studied in a scientific setting, instantly have closed-minded ‘non-believers’ yell out pseudoscience. There is instant condemnation without investigation and sometimes, “protecting against this possibility sometimes seems more important than encouraging scientific exploration or protecting academic freedom. But this may be changing.” Said Cassandra Vieten, PhD and President/CEO at the Institute of Noetic Sciences (source).

One realm within the topic of parapsychology is the study of our dreams and there is no better person to learn about dreams from than than Dale E. Graff.  Graff is an MS in Physics and a life long investigator of Psi phenomena specializing in a variety of extrasensory perception (ESP) topics including remote viewing and precognitive dreaming. He has a scientific background in the aerospace industries and in technical intelligence assignments for the Department of Defense. He was also a director of the STARGATE program mentioned above.

In the lecture below, he answers the following questions: What is Psi dreaming? How can individuals experience Psi dreams? How can Psi dreaming be researched and evaluated scientifically? What can we do with Psi dreaming? How can Psi dreaming be understood relative to other forms of Psi, such as remote viewing and some types of intuition?

He provides information about how Psi dreaming is accomplished, and goes into the evidence and investigations that have shown evidence for the reality of Psi dreaming. He talks about how Psi dreaming may occur and provides exercises to assist in dream recall, among other things.

The Takeaway

A great quote that’s often attributed to Nikola Tesla reads as follows, “The day science begins to study non-physical phenomena, it will make more progress in one decade than in all the previous centuries of its existence.”  This is true I believe, just take a look at quantum physics for example, it really opened up the collective mind about non-physical factors of reality and how it may influence material physical reality. It also demonstrated that matter itself, which makes up all of physical reality, is not really physical at all, that it’s mostly comprised of energy. Just look at the atom, the smallest observable piece of matter, it’s what everything else is made up of. An atom is almost all empty space, more than 99 percent of it to be exact. The kicker? That empty space is not useless, and from what we know now, “empty space” is really not “empty” at all. This is why I’ve always stressed the importance in many of my previous articles of this quote from theoretical physicist John Wheeler:

No point is more central than this, that space is not empty, it is the seat of the most violent physics.”

Another great quote from Tesla:

“All perceptible matter comes from a primary substance, or tenuity beyond conception, filling all space, the akasha, or luminiferous ether, which is acted upon by the life-giving Prana or creative force, calling into existence, in never-ending cycles all things and phenomena.” – Nikola Tesla, Man’s Greatest Achievement, 1907

I go into a deeper discussion regarding non-physical reality within this article if you’d like to learn more: Scientists Call Out “Dark Matter” – Have We Been Wrong About It All Along?

The point is, non-physical reality, and the metaphysical world is not limited to philosophy, but it’s been subjected to rigorous investigation and science. The collective mind seems to be opening up quite rapidly, but just as we look back in the past to some concepts now accepted as truth that were once considered blasphemy, it’s important to remember that this type of resistance still exists today.