A new study from The University of Texas Medical Branch at Galveston offers important insight into how Alzheimer’s disease begins within the brain.
The researchers found a relationship between inflammation, a toxic protein and the onset of the disease.
The study also identified a way that doctors can detect early signs of Alzheimer’s by looking at the back of patients’ eyes.
“Early detection of Alzheimer’s warning signs would allow for early intervention and prevention of neurodegeneration before major brain cell loss and cognitive decline occurs,” said lead author Ashley Nilson, a neuroscience graduate student. “Using the retina for detecting AD and other neurodegenerative diseases would be non-invasive, inexpensive and could become a part of a normal screening done at patient checkups.”
UTMB researchers have previously found evidence that a toxic form of tau protein may underlie the early stages of Alzheimer’s.
Brain cells depend on tau protein to form highways for the cell to receive nutrients and get rid of waste. In some neurodegenerative diseases like Alzheimer’s, the tau protein becomes a toxic form called tau oligomers and begins clumping into neurofibrillary tangles. When this happens, nutrients can no longer move to where they are needed and the oligomers produce toxic effects leading to the eventual death of the brain cells.
It’s becoming increasingly clear that inflammation within the brain plays an important role in Alzheimer’s development and progression. Inflammation and loss of connections between nerves within the brain happen before the formation of the tangles that are characteristic of this disease.
It’s possible that the tau oligomers may be responsible for this inflammation.
In a recent paper in the Journal of Alzheimer’s Disease, UTMB’s research team detailed their investigation on the relationship between inflammation, toxic tau and Alzheimer’s onset by performing systematic analyses of brain and retina samples from people with Alzheimer’s and a mouse model of Alzheimer’s.
The results demonstrated that the toxic tau may induce inflammation in Alzheimer’s. The toxic tau spreads between connected brain regions, which may initiate inflammation in these new regions. This situation can create a cycle of toxic tau, inflammation and cell death throughout the brain over time.
Beyond determining eye health and corrective lens prescriptions, having an eye exam can alert health care professionals of several different health conditions including diabetic complications, high cholesterol and high blood pressure. Now, UTMB researchers found that retina tissue that they studied can show evidence of toxic tau and inflammation.
“Our findings suggest that the degeneration of nerve cells due to chronic inflammation induced by the tau oligomers may be combated through the combination of anti-tau oligomer and anti-inflammatory therapeutics for the treatment of Alzheimer’s and related diseases,” said senior author Rakez Kayed, associate professor in the UTMB Department of Neurology. “Our is continuing to expand our understanding of neurodegenerative diseases.”
Ian: This article piqued my interest because (apart from my own brush with dementia back in 20111) I have been researching the properties of molecular hydrogen, which may be produced by infusion in our water filter invention, or through a special form of magnesium tablet. One of three major reported benefits to the use of molecular hydrogen infused in water has been support for our natural anti-inflammation process and healing. The other two major reported benefits are selective antioxidant abilities and anti allergenic ability.
(To learn more go to the Molecular Hydrogen Foundation).
So far molecular hydrogen looks like many other products touted as anti inflammatory. But there’s a big difference. H2 is the smallest molecule in the universe. It passes through the body with ease. And unlike all other supplements, it also passes through the blood-brain barrier, accessing the brain. This barrier is a natural defence to preserve the brain’s integrity against anything that may harm it, and as such is a marvellous piece of design. But just take a look at this video, (the sound is rough) to see what happened to an old friend when we gave him a bottle of molecular hydrogen generating tablets! (here’s a link to our UltraStream and another link to the H2 producing tablets.
ASHLEY N. NILSON, KELSEY C. ENGLISH, JULIA E. GERSON, T. BARTON WHITTLE, C. NICOLAS CRAIN, JUDY XUE, URMI SENGUPTA, DIANA L. CASTILLO-CARRANZA, WENBO ZHANG, PRAVEENA GUPTA, RAKEZ KAYED. TAU OLIGOMERS ASSOCIATE WITH INFLAMMATION IN THE BRAIN AND RETINA OF TAUOPATHY MICE AND IN NEURODEGENERATIVE DISEASES. JOURNAL OF ALZHEIMER’S DISEASE, 2016; 1 DOI: 10.3233/JAD-160912
This story highlights the crossover diagnosis that I am hearing about more often. And it’s exacerbated by the prevailing attitude of the established medical fraternity to Lyme disease. The US is ahead of us here in Australia where it’s not even considered a ‘real’ disease. So I was not surprised at this article about Kris Kristofferson.
Six years ago I was suffering all of the symptoms of early onset Alzheimers. I won’t detail my experience, but if anyone is interested it’s all in the video below.
I have a closer friend whose partner suffered as much through the misdiagnosis of her Lyme’s disease as she did from the disease. Spending over $100,000 with various practitioners, but traditional and alternative, she went through a living hell not only of disease but also of the feeling of complete loss of control as diagnosis after diagnosis failed her.
We eventually gave her a bottle of I LOVE H2. She was a fitness fanatic, but of course in her state she was not even capable of her reputation as ‘The runner” that she had earned at the gym with her marathon treadmill sessions.
She’s back and running today. We can’t claim to be a part of her healing because I LOV E H2 is simple a sports supplement, but what we can say was that when she came in to see us, we just didn’t recognise this beautiful, glowing new woman.
Here’s a comment I just received from my friend, her partner on this article.
“Thanks for that Ian. Until my partner was clinically diagnosed as having Lyme Disease she simply thought she was “losing it” emotionally, mentally and physically. It’s so easy to classify a person with all these weird symptoms and expressions as simply hyperchondriac, especially because of the amount of anxiety, depression and endless fatigue that come with such a shut down of the endocrine system.”
The Body Brain Barrier is a membrane that prevents anything that shouldn’t get to our brain passing through it.
It’s essential in protecting the brain from toxins of all forms but is so efficient that it also prevents drugs entering the brain. This has inhibited the formulation of many Alzheimers drug strategies that rely on direct brain contact.
Of course we now know that there are amy things we don’t wnat to get into our brain; one big one being EMF from our mobile phones. damage is easily seen in the brain; whether it is directly caused by the phones is still being fiercely debated. That the brain suffers oxidative damge is not in dispute.
So imagine something with proven selective antioxidant and anti inflammatory abilities. Now imagine that ‘something’ can easily penetrate the brain body barrier.
Now imagine that same something that easily passes out of the brain via the skull if it encounters nothing in the brain it can assist with.
Wow. That’s molecular hydrogen, and a huge number of studies are indicating ita vast number of therapeutic capabilities, including Alzheimers’.
Here’s a video of a discussion with George,a friend of mine, and here’s a list of over sixty scientific studies on the same subject.
..and while we make no claims about the ability of our products to work this way, we do sell products that may assist your body by facilitating its ability to access molecular hydrogen. Learn more here.
A large, multi-center study led by the UC Davis School of Medicine for the first time has shown that people as young as their 40s have stiffening of the arteries that is associated with subtle structural damage to the brain that is implicated in cognitive decline and Alzheimer’s disease later in life.
A collaboration of UC Davis, the Framingham Heart Study and Boston University, among others, the study found that, among young healthy adults, higher aortic “stiffness” was associated with reduced white matter volume and decreased integrity of the gray matter, and in ages much younger than previously described.
“Effects of Arterial Stiffness on Brain Integrity in Young Adults from the Framingham Heart Study,” is published online in the American Heart Association journal Stroke.
“This study shows for the first time that increasing arterial stiffness is detrimental to the brain, and that increasing stiffness and brain injury begin in early middle life, before we commonly think of prevalent diseases such as atherosclerosis, coronary artery disease or stroke having an impact,” said Pauline Maillard, UC Davis Department of Neurology and Center for Neuroscience and the study’s lead author.
“These results may be a new avenue of treatment to sustain brain health,” she said.
The study also noted that elevated arterial stiffness is the earliest manifestation of systolic hypertension.
“Measures of arterial stiffness may actually be a better measure of vascular health, and should be identified, treated and monitored throughout the lifespan,” Maillard said.
The large study involved approximately 1,900 diverse participants in the Framingham Heart Study, who underwent brain magnetic resonance imaging (MRI), as well as arterial tonometry.
The tests measured the force of arterial blood flow, the carotid femoral pulse wave velocity or CFPWV — the reference standard for noninvasive measurement of aortic stiffness — and its association with subtle injury to the brain’s white and gray matter. The research found that increased CFPWV was associated with greater injury to the brain.
The reasons this is so are complex, and more study is needed, Maillard said. However, with age high blood pressure causes the arteries to stiffen, further increasing blood pressure as well as increasing calcium and collagen deposits, which promotes atrophy, inflammation and further stiffening, decreasing blood flow to vital organs including the brain and promoting brain atrophy.
“Our results emphasize the need for primary and secondary prevention of vascular stiffness and remodeling as a way to protect brain health,” early in life, Maillard said.
Ian: A truly frightening possibility that the scientists admit to having no immediate answer. me? I’m taking Vitamin K2 to ensure my calcium goes where it should rather than accreting on my blood vessels. And I’m taking molecular hydrogen every day because I’ve experienced the clarity of mind. H2 crosses the body/brain barrier with ease in its quest for free radicals and inflammation.
Alzheimer’s disease may cause us to forget faces, where we left familiar objects… even where we are… because our brains cannot find where we put those memories!
At least that’s what a new study suggests.
The study, reported in Nature1, challenges the assumption that Alzheimer’s prevents the brain from making new memories. It also suggests that brain stimulation may temporarily improve memories in early stages of the disease.
This new research enhances earlier work by lead author Susumu Tonegawa, a neuroscientist, and his colleagues at MIT in Cambridge. Last year, they showed that in certain types of amnesia, memories were stored but could not be retrieved2.
It’s hard to detect what is a stored and what is a retrieved memory . The only way to test a memory is to ask a patient to recall it.
Memories can be manipulated in mice, so Tonegawa and colleagues tested their theory using two strains of mice with mutations in genes linked to Alzheimer’s disease.
These mice develop amyloid protein clusters, or plaques, in their brains and eventually lose their memories — just like humans. The team were able to demonstrate this memory loss by placing the mice in a box in which they received an electric shock. (Ouch) Normal mice learned to fear the box, but the mutant mice did n’t. They had no memory of being shocked.
The researchers engineered the mutant mice to make a light-sensitive protein in neurons in the part of the brain that encodes short-term memories. Then they placed the mice back into the box, shining a light onto the animals’ brains to force the modified neurons to fire. This caused the mice to recall the memory of being shocked, and the animals froze — suggesting that the memory had been encoded in the first place. And yet… the next day, the mice had again forgotten their fear of the box.
Next, the scientists pulsed the light, mimicking a process that occurs naturally as a memory is accessed repeatedly over time. This strengthened the connections between the hippocampus and another brain region called the entorhinal cortex, a connection that serves as long-term memory storage. With the memories now firmly embedded, the mice remembered to be afraid of the box, even when the light was off.
Can you get what this means? It means that the memories seemingly obliterated by Alzheimers may not be.
When the team dissected the mouses’ brains, they found that the pulsing stimulation had created new connections between the hippocampus and the entorhinal cortex — connections that are lost as Alzheimer’s disease progresses. Don’t get too excited yet.. the researchers expect that the technique may only work for a few months in mice, or two to three years in humans, before the disease erases any gains.
This theory about how Alzheimer’s affects the brain agrees with symptoms seen in patients. Our hippocampus appears to be particularly vulnerable to the ravages of Alzheimer’s, so a person with the disease first forgets new memories, like where he left his car. As Alz worsens, more of the brain is destroyed, causing us to forget long-term information such as family members’ names.
“It’s a beautifully executed study,” says Itzhak Fried, a neurosurgeon at the University of California Los Angeles. But he cautions that the findings may not translate to human brains, because mice do not develop amyloid plaques in the same way as humans do. And… it’s impossible to test whether the memory-retrieval hypothesis holds true in humans, because researchers haven’t worked out how to stimulate human brains using light.
Yet another study that tells us that care of the brain is perhaps our most important self-health regimen. My own experience with what looked starkly like early onset Alzheimers came unbidden and -I have to admit – not because I was in any way abusing my brain. I wasn’t taking drugs, drank very moderately.. I was (at that time) vegetarian, so the only possible culprit I can think of is carbs and sugar.
I have learned a great deal since I posted our Coconut Oil Video almost a million views ago. I’ve learned that I am still susceptible. If I go ‘off the rails’ and indulge in either sugar or carbs, it takes only a couple of days before words seem to disappear from my vocabulary and I get ‘foggy’. We use coconut oil in all our cooking so I am still getting plenty, but the carb/sugar effect is clear. I’m also taking H2 every day in water in the form of our I LOVE H2 tablets, mainly because of another study using H2 on Alzheimers.
It appears from the study that H2 that “It is also suggested that the major findings of this study is that hydrogen rich saline was able to improve long-term potentiation, learning, and memory most likely by reducing inflammation and oxidative stress.”
Here’s a video of a discussion between myself and an old friend comparing notes on memory loss, coconut oil and H2. The studies are only mouse studies, but for me, with the constant reminder of memory loss – and possible worse – always close at hand, I’m happy to use everything I can to avert Alzheimers even when it’s only shown to be beneficial in some poor mousies.
As readers know I have had my own relationship with Alzheimers.
That’s why I think this article may be of interest to the people that have seen our video on my journey.
This article was co-written by Smita Patel, DO, FAASM, and Anne Marie Fosnacht, MPH, CPT
The rate of Alzheimer’s disease (AD) continues to soar due, in part, to the successful aging of the largest generation ever to walk the earth.
Limited by a dearth of successful pharmacological agents, more and more physicians are shifting from a treatment paradigm to one of prevention. Here at the NorthShore Center for Brain Health we believe that getting enough sleep–7 or more hours nightly–is a way to help prevent AD.
Prevention necessitates intervening on modifiable risk factors. Evidence is mounting that lifestyle factors, such as diet, daily activity, education, and social engagement–combined with non-modifiable factors such as family history and genetics–play a significant role in the ontogeny of Alzheimer’s disease in patients over time.
Recent clinical trials in Spain and Finland have shown that eating a Mediterranean diet, or receiving healthy-eating counseling and assistance are associated with improvement in cognitive function.
Exercise training has been shown to increase the size of the hippocampus, the memory center of the brain, and to improve memory.
Epidemiologic studies suggest that people with more years of education can tolerate changes associated with neurodegeneration longer than those with less education, effectively delaying onset of cognitive dysfunction.
Cohort studies have found that social engagement is associated with larger brain volume.
Non-modifiable risk factors include a family history of dementia and having a certain variant (APOE4) of the apolipoprotein allele, which is responsible for cholesterol transport and mediation in the brain. Individuals with 1 copy of APOE4 have a 2- to 4-fold increased risk of AD while those who have inherited 2 copies have 10-fold increased risk.
While disturbances in the sleep cycle and altered circadian rhythms are common symptoms of dementia and Alzheimer’s disease, sleep quality throughout one’s lifetime is gaining momentum as a possible factor associated with eventual development of AD.
Helping patients achieve better sleep may help reduce their risk of developing the disease.
While experimental studies in humans are rare, there are animal models of sleep-related causation. The results of these studies are compelling. In 2009, Kang and colleagues reported that beta amyloid dynamics were found to be regulated by the sleep-wake cycle in mice.
In 2013, Xie and colleagues reported that in mice sleep was associated with naturally-occurring flushing/removal of exogenous AB from the brain by cerebrospinal fluid. Others have found that deprivation of sleep exacerbates neuronal injury and tau phosphorylation.
Recently, key cross-sectional studies have shown an association between Alzheimer’s and sleep variables in humans.
Spira and colleagues found that self-reported short sleep duration and poor sleep quality were associated with increased AB burden as seen in PET amyloid imaging. Similarly Ju and colleagues reported that greater amyloid burden was associated with poor sleep efficiency and wakefulness episodes.
Observational studies also offer compelling data linking sleep to Alzheimer’s risk. Virta et al. report that among 2,300 middle age Finnish twins, self reports of too much (>8 hrs) sleep was associated with 1.8 times higher odds of developing AD. Hahn and colleagues found that self reports of decrease in depth of sleep were associated with 70 to 100% greater odds of having AD 9 years later.
While the exact mechanisms by which sleep duration and quality affect development of Alzheimer’s and dementia are still enigmatic, more and more research show they are firmly associated.
Educating patients on the impact of sleep on their brain health and helping patients achieve high quality sleep can be important steps in mitigating the risk of neurodegeneration.
- Bryan D. , Thomas G., Brian C., et al., Association of social engagement with brain volumes assessed by structural MRI, Journ Aging Research, vol. 2012, Article ID 512714, 9 pages, 2012. doi:10.1155/2012/512714
- Di Meco A., Joshi Y., Practico D., Sleep deprivation impairs memory, tau metabolism, and synaptic integrity of a mouse model of Alzheimer’s disease with plaques and tangles. Neurobiol Aging 2014; 35: 1813-1820.
- Donix, M., Small, G., Bookheimer, S. Family history and APOE-4 genetic risk in Alzheimer’s disease. Neuropsychology Review, September 2012, vol 22, issue 3, 298-303.
- Erickson, K., Voss M., Prakash R., et al. Exercise training increases size of hippocampus and improves memory. PNAS 2011. Vol. 108. 3017-3022.
- Hahn E., Wang H., Andel R., Fratiglioni L., A change in sleep pattern may predict Alzheimer’s disease. Am J Geriatr Psychiatry 2013. Doi: 10.1016/j.jagp.2013.04.015.
- Ju Y., McLeland J., Toedebusch C., et al. Sleep quality and preclinical Alzheimer’s disease. J. AM Med Assoc Neurol 2013; 70:587-593.
- Kang J., Lim M., Bateman, R., et al. Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle. Science 2009; 326:1005-119.
- Kivipelto M., Solomon A., Ngandu T. et al. The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER): study design and progress. Alzheimers Dement, 2013 Nov; 9(6):657-65. doi: 10.1016/j.alz.2012.09.012. Epub 2013 Jan 17.
- Rothman S., Herdener N., Camandola S., Texel S., Mughal M., Cong W., et al. 3xTgAD Mice Exhibit Altered Behavior and Elevated Abeta After Chronic Mild Social Stress. Neurobiol Aging 2012; 33: 830 e831-812.
- Spira A., Gamaldo A., An Y., et al. Self-reported sleep and beta-amyloid deposition in community-dwelling older adults. J Am Med Assoc Neurol 2013; 70:1537-1543.
- Stern, Yaakov. Cognitive Reserve in ageing and Alzheimer’s Disease. The Lancet Neurology, Volume 11, Issue 11, 1006-1012.
- Valls-Pedret C, Sala-Vila A, Serra-Mir M, et al. Mediterranean diet and age-related cognitive decline: A randomized clinical trial. JAMA Intern Med. Published online May 11, 2015. doi:10.1001/jamainternmed.2015.1668.
- Virta J., Heikkila K., Perola M. et al. Midlife sleep characteristics associated with late life cognitive function. Sleep 2013; 361533-1541.
- Xie L., Kang H., Xu Q., et al. Sleep drives metabolite clearance from the adult brain. Science 2013; 342:373-337.
- Watson, N. et al. Recommended amount of sleep for a healthy adult: A joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society. Sleep 2015, Vol. 38, No. 6, 843-844.
Brain health: the second most important component in maintaining a healthy lifestyle (according to a 2014 AARP study).
As we age we can experience a range of cognitive issues from decreased critical thinking to dementia and Alzheimer’s disease. In the March issue of Food Technology published by the Institute of Food Technologists (IFT), contributing editor Linda Milo Ohr writes about eight nutrients that may help keep your brain in good shape.
1. Cocoa Flavanols:
Cocoa flavanols have been linked to improved circulation and heart health, and preliminary research shows a possible connection to memory improvement as well. A study showed cocoa flavanols may improve the function of a specific part of the brain called the dentate gyrus, which is associated with age-related memory (Brickman, 2014).
See the research here
2. Omega-3 Fatty Acids:
Omega-3 fatty acids have long been shown to contribute to good heart health are now playing a role in cognitive health as well. A study on mice found that omega-3 polyunsaturated fatty acid supplementation appeared to result in better object recognition memory, spatial and localizatory memory (memories that can be consciously recalled such as facts and knowledge), and adverse response retention (Cutuli, 2014). Foods rich in omega-3s include salmon, flaxseed oil, and chia seeds.
3. Phosphatidylserine and Phosphatidic Acid:
Two pilot studies showed that a combination of phosphatidylserine and phosphatidic acid can help benefit memory, mood, and cognitive function in the elderly (Lonza, 2014).
Where do you get it? Look here.
4. Walnuts: A diet supplemented with walnuts may have a beneficial effect in reducing the risk, delaying the onset, or slowing the progression of Alzheimer’s disease in mice (Muthaiyah, 2014).
Citicoline is a natural substance found in the body’s cells and helps in the development of brain tissue, which helps regulate memory and cognitive function, enhances communication between neurons, and protects neural structures from free radical damage. Clinical trials have shown citicoline supplements may help maintain normal cognitive function with aging and protect the brain from free radical damage. (Kyowa Hakko USA).
Ian: I’ve been on this for a few years. Does it work for me? Along with everything else, yes!
6. Choline: Choline, which is associated with liver health and women’s health, also helps with the communication systems for cells within the brain and the rest of the body. Choline may also support the brain during aging and help prevent changes in brain chemistry that result in cognitive decline and failure. A major source of choline in the diet are eggs.
Where to get it.
7. Magnesium: Magnesium supplements are often recommended for those who experienced serious concussions. Magnesium-rich foods include avocado, soy beans, bananas and dark chocolate.
Where to get it:
8. Blueberries: Blueberries are known to have antioxidant and anti-inflammatory activity because they boast a high concentration of anthocyanins, a flavonoid that enhances the health-promoting quality of foods. Moderate blueberry consumption could offer neuro cognitive benefits such as increased neural signaling in the brain centers.
9. Coco Oil! I can’t ignore this one for it was coconut oil that gave me back my brain. See my original story here.
Is it possible? Just by adding more spinach, kale, collards and mustard greens to your diet can you help slow cognitive decline?
New research just in says YES! The research also examined the nutrients responsible for the effect, linking vitamin K consumption to slower cognitive decline for the first time.
Ian: This is great news for us and er.. vindicating. For a long time now I have questioned where the benefits of our so-called alkalizing vegetables comes from. Is it the alkaline minerals? Is it the phytonutrients? Is it the vitamins?
“Losing one’s memory or cognitive abilities is one of the biggest fears for people as they get older,” said Martha Clare Morris, Sc.D., at Rush University Medical Center and leader of the research team. “Since declining cognitive ability is central to Alzheimer’s disease and dementias, increasing consumption of green leafy vegetables could offer a very simple, affordable and non-invasive way of potentially protecting your brain from Alzheimer’s disease and dementia.”
Researchers tracked the diets and cognitive abilities of more than 950 older adults for an average of five years and saw a significant decrease in the rate of cognitive decline for study participants who consumed greater amounts of green leafy vegetables.
People who ate one to two servings per day had the cognitive ability of a person 11 years younger than those who consumed none.
Ian: I LIKE this study. We see many studies that are published with very small subject numbers, but this one has almost 1000 subjects.
When the researchers examined individual nutrients linked with slowing cognitive decline, they found that vitamin K, lutein, folate and beta-carotene were most likely helping to keep the brain healthy.
Ian: K? Or K2? I have K2 for my bone building. It facilitates the transfer of Calcium to the bones and without it Calcium is either peed out or used by the body to combine with cholesterol and form plaque.
“Our study identified some very novel associations,” said Morris, who will present the research at the American Society for Nutrition (ASN) Annual Meeting during Experimental Biology 2015. “No other studies have looked at vitamin K in relation to change in cognitive abilities over time, and only a limited number of studies have found some association with lutein.” Other studies have linked folate and beta-carotene intake with slower cognitive decline.
To conduct the study, Morris’ research team gathered data from 954 participants from the Memory and Aging Project, which aims to identify factors associated with the maintenance of cognitive health. The participants, whose age averaged 81, reported their daily food and beverage intake by answering a detailed 144-item questionnaire at the beginning of the study. The researchers computed the total daily nutrients by combining the nutrient content for each food consumed with the number of servings eaten each day. They followed participants for 2 to 10 years, assessing cognition annually with a comprehensive battery of 19 tests and adjusted for age, sex, education, smoking, genetic risk for Alzheimer’s disease and participation in physical activities when estimating the effects of diet on cognitive decline.
“With baby boomers approaching old age, there is huge public demand for lifestyle behaviors that can ward off loss of memory and other cognitive abilities with age,” said Morris. “Our study provides evidence that eating green leafy vegetables and other foods rich in vitamin K, lutein and beta-carotene can help to keep the brain healthy to preserve functioning.”
In addition to green leafy vegetables, other good sources of vitamin K, lutein, folate and beta-carotene include brightly colored fruits and vegetables.
Ian: So this benefit is quite separate from the alkalizing benefits of leafy greens. I’m also interested in the reports I’m getting of the effect of molecular hydrogen on Alzheimers. There are already scientific studies, and now we are getting actual user stories.
This report is wonderful news.
The above story is based on materials provided by Federation of American Societies for Experimental Biology (FASEB).
Turmeric has been used in India for over 5,000 years, which is probably why even today both rural and urban populations have some of the lowest prevalence rates of Alzheimer’s disease (AD) in the world. A recent study on patients with Alzheimers’ found that less than a gram of turmeric daily, taken for three months, resulted in ‘remarkable improvements.’
Alzheimer’s Disease: A Disturbingly Common Modern Rite of Passage
A diagnosis of Alzheimer’s disease (AD), sadly, has become a rite of passage in so-called developed countries. AD is considered the most common form of dementia, which is defined as a serious loss of cognitive function in previously unimpaired persons, beyond what is expected from normal aging.
A 2006 study estimated that 26 million people throughout the world suffer from this condition, and that by 2050, the prevalence will quadruple, by which time 1 in 85 persons worldwide will be afflicted with the disease.
Given the global extent of the problem, interest in safe and effective preventive and therapeutic interventions within the conventional medical and alternative professions alike are growing.
Conventional drug-based approaches amount to declaring chemical war upon the problem – a mistake which can result in serious neurological harm, as evidenced by the fact that this drug class carries an alarmingly high risk for seizures, according to World Health Organization post-marketing surveillance statistics.
What the general public is therefore growing most responsive to, is using time-tested, safe, natural and otherwise more effective therapies that rely on foods, spices and familiar culinary ingredients.
Remarkable Recoveries Reported after Administration of Turmeric
Late last year, a remarkable study was published in the journal Ayu entitled “Effects of turmeric on Alzheimer’s disease with behavioral and psychological symptoms of dementia.” Researchers described three patients with Alzheimer’s disease whose behavioural symptoms were “improved remarkably” as a result of consuming 764 milligrams of turmeric (curcumin 100 mg/day) for 12 weeks. According to the study:
“All three patients exhibited irritability, agitation, anxiety, and apathy. Two patients suffered from urinary incontinence and wonderings. They were each prescribed turmeric powder capsules and started recovering from these symptoms without any adverse reactions in clinical symptoms and laboratory data.”
After only 3 months of treatment, the patients’ symptoms and the burden on their caregivers were significantly decreased.
The report describes the improvements:
“In one case, the Mini-Mental State Examination (MMSE) score was up five points, from 12/30 to 17/30. In the other two cases, no significant change was seen in the MMSE; however, they came to recognise their family within 1 year treatment. All cases have been taking turmeric for more than 1 year, and re-exacerbation of BPSD was not seen.”
This study illustrates just how powerful a simple natural intervention using a time-tested culinary herb can be.
Given that turmeric has been used medicinally and as a culinary ingredient for over 5,000 years in Indian culture, even attaining the status of a ‘Golden Goddess,’ we should not be surprised at this result. Indeed, epidemiological studies of Indian populations reveal that they have a remarkably lower prevalence of Alzheimer’s disease relative to Western nations, and this is true for both rural and more “Westernised” urban areas of India.
Could turmeric be a major reason for this?
Turmeric’s Anti-Alzheimer’s Properties.
The GreenMedInfo.com database now contains a broad range of published studies on the value of turmeric, and its primary polyphenol curcumin (which gives it its golden hue), for Alzheimer’s disease prevention and treatment. While there are 114 studies on Turmeric, 30 of these studies are directly connected to turmeric’s anti-Alzheimer’s disease properties.
Two of these studies are particularly promising, as they reveal that curcumin is capable of enhancing the clearance of the pathological amyloid–beta plaque in Alzheimer’s disease patients, and that in combination with vitamin D3 the neurorestorative process is further enhanced. Additional preclinical research indicates curcumin (and its analogs) has inhibitory and protective effects against Alzheimer’s disease associated β-amyloid proteins.
Other documented Anti-Alzheimer’s mechanisms include:
- Anti-inflammatory: Curcumin has been found to play a protective role against β-amyloid protein associated inflammation.
- Anti-oxidative: Curcumin may reduce damage via antioxidant properties.
- Anti-cytotoxic: Curcumin appears to protect against the cell-damaging effects of β-amyloid proteins.
- Anti-amyloidogenic: Turmeric contains a variety of compounds (curcumin, tetrahydrocurcumin, demethoxycurcumin and bisdemethoxycurcumin) which may strike to the root pathological cause of Alzheimer’s disease by preventing β-amyloid protein formation.
- Neurorestorative: Curcuminoids appear to rescue long-term potentiation (an indication of functional memory) impaired by amyloid peptide, and may reverse physiological damage by restoring distorted neurites and disrupting existing plaques.
- Metal-chelating properties: Curcumin has a higher binding affinity for iron and copper rather than zinc, which may contribute to its protective effect in Alzheimer’s disease, as iron-mediated damage may play a pathological role.
Ian: here’s the thing: turmeric breaks down to molecular hydrogen, and the benefits of turmeric in this article are identical to what h2 users experience. So the question becomes: Turmeric or H2 water?
Dehydration common among UK care home residents
Research recently published in the Journal of the Royal Society of Medicine concludes…
“patients admitted to hospital from care homes are commonly dehydrated on admission and consequently appear to experience significantly greater risks of in-hospital mortality”.
The researchers were from Barnet and Chase Farm Hospitals NHS Trust, the University of Oxford and the London School of Hygiene & Tropical Medicine.
They reviewed “over 20,000 patients aged 65 years and over admitted to a London hospital trust for the first time between January 2011 and December 2013”, and looked at sodium levels.
“After adjustment for a number of possible explanatory factors, including age and dementia, the risk of high sodium levels was still over five times higher for those admitted from care homes”. The lead researcher, Dr Anthony Wolff, said “High sodium levels in care home residents should raise questions about adequate support for drinking”.
Ian: My worst nightmare is going to an old people’s warehouse. This article reinforces my nightmare.
A new report from Science Daily tells us that diabetes in midlife determines a high probability of cognitive decline 20 years later. So.. we’re looking at a nation of senior morons! Ouch!
And yet diabetes is SO unnecessary!
The study is a rather personal message for me because I experienced what we believe to be incipient Alzheimers’ some 5 years ago. Believe me, it was seriously scary to try to put a sentence together and see GAPS where words used to be, to go to the supermarket and completely forget why you went there, and to lose motor responses sufficient to be banned from the kitchen because I smashed so many things. Our video about my recovery has now hit a quarter of a million views and you’ll see it here.
How am I today? Well, coconut oil was just the beginning. I still consume as much orgainic coco oil as I can but I’ve also experienced that ANY carbs or sugary foods have an effect on my mental clarity, which ties in with this study in that diabetes is the result o9f high sugar and carb intake. It ties in perefectly with our new alkaline diet and that’s why we are revising and updating our old Alkaline Defence Program. It was put together back in 2006 and there’s so much new science since then tying in alkalinity, carb intake, fats and more. I’m madly trying to get it completed by Christmas so stay in touch for your copy – free to blog readers.
I received this report today. I’ve seen a number of reports on turmeric recently all raving about its antioxidant and anti inflammation effects, which, as I’ve pointed out, accurately parallels the effects of hydrogen rich water.
“”We found that this modest addition to breakfast improved working memory over six hours in older people with pre-diabetes,””
Now this new report tells us that just one gram of Turmeric improves memory. It made me recall a study by leading Japanese researcher on H2. Just look at the abstract. It’s some years old and you can multiply the numbers by at least two, and it’s awesome!
“Effects of molecular hydrogen on various diseases have been documented for 63 disease models and human diseases in the past four and a half years.
Most studies have been performed on rodents including two models of Parkinson’s disease and three models of Alzheimer’s disease. Prominent effects are observed especially in oxidative stress-mediated diseases including neonatal cerebral hypoxia; Parkinson’s disease; ischemia/reperfusion of spinal cord, heart, lung, liver, kidney, and intestine; transplantation of lung, heart, kidney, and intestine.
Six human diseases have been studied to date: diabetes mellitus type 2, metabolic syndrome, hemodialysis, inflammatory and mitochondrial myopathies, brain stem infarction, and radiation-induced adverse effects.
Two enigmas, however, remain to be solved. First, no dose-response effect is observed. Rodents and humans are able to take a small amount of hydrogen by drinking hydrogen-rich water, but marked effects are observed. Second, intestinal bacteria in humans and rodents produce a large amount of hydrogen, but an addition of a small amount of hydrogen exhibits marked effects. Further studies are required to elucidate molecular bases of prominent hydrogen effects and to determine the optimal frequency, amount, and method of hydrogen administration for each human disease.”
For me, the comment that you need only ingest small amounts to have an effect are borne out by our own observations of our customers. No-one knows why. It just works.
In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants displayed subjective or objective improvement in their memories beginning within three to six months after the program’s start.
The study’s approach is personalized to the patient, based on extensive testing to determine what is affecting the plasticity signaling network of the brain. As one example, in the case of the patient with the demanding job who was forgetting her way home, her therapeutic program consisted of some, but not all of the components involved with Bredesen’s therapeutic program, and included:
(1) eliminating all simple carbohydrates, leading to a weight loss of 20 pounds;
(2) eliminating gluten and processed food from her diet, with increased vegetables, fruits, and non-farmed fish;
(3) to reduce stress, she began yoga;
(4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day;
(5) she took melatonin each night;
(6) she increased her sleep from 4-5 hours per night to 7-8 hours per night;
(7) she took methylcobalamin each day;
(8) she took vitamin D3 each day;
(9) fish oil each day;
(10) CoQ10 each day;
(11) she optimized her oral hygiene using an electric flosser and electric toothbrush;
(12) following discussion with her primary care provider, she reinstated hormone replacement therapy that had been discontinued;
(13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime;
(14) she exercised for a minimum of 30 minutes, 4-6 days per week.
The results for nine of the 10 patients reported in the paper suggest that memory loss may be reversed, and improvement sustained with this therapeutic program, said Bredesen. “This is the first successful demonstration,” he noted, but he cautioned that the results are anecdotal, and therefore a more extensive, controlled clinical trial is needed.
See the full study report here
In 2014, the World Health Organization (WHO) published a report entitled “Tobacco Use & Dementia,”3, 4 based on a comprehensive scientific review of tobacco use, exposure to secondhand smoke, and incidence rates for all types of dementia, including Alzheimer’s.
The report found that smokers have a 45 percent higher risk of developing dementia than non-smokers, and concluded that 14 percent of all Alzheimer’s cases worldwide may potentially be attributed to smoking.
These risks hold true across nearly every income level and geographic boundary—including US, China, India, and Latin America. Smokers with dementia also die earlier than non-smokers with dementia.
Ian: My strongest memory of my dear old Dad was his hacking cough from his ‘roll-your-owns’. And yes, Alzheimers’ got him.
Today I was sent a new report on Turmeric says a compound in turmeric promotes stem cell proliferation and differentiation in the brain.
The findings suggest aromatic turmerone could be a future drug candidate for treating neurological disorders, such as stroke and Alzheimer’s disease. Here’s the study.
Research shows that turmeric has powerful anti-inflammatory, anti-tumor, and antioxidant properties. Inflammation, if left untreated, can become a chronic health issue. And unlike aspirin or ibuprofen, turmeric’s curcumin reduces inflammation naturally, without damaging the liver or kidneys.
Healthier Talk reports:
“It has been found especially helpful in treating conditions like arthritis, sports injuries, irritable bowel syndrome, Crohn’s disease, tendonitis and various autoimmune diseases. Some research even suggests that curcumin may also help those suffering asthma, inflammatory bowel disease and, yes, even cancer.”
We’ve looked at Turmeric closely mainly because of its reported ability to create molecular hydrogen in the body. In fact the benefits of molecular hydrogen evidenced in all the new scientific studies seem to parallel everything published about Turmeric. Erica, our inhouse naturopath, makes the point that the difficulty of using Turmeric. It seems its absorbability is rather poor.
Obesity, as we know, creates all sorts of problems. But now there’s a new one! Dementia.
Science Daily reports:
“Early to mid-life obesity appears to be linked to heightened risk of dementia in later life, researchers report. There is a threefold risk for those with severe obesity in their 30s, the observational study indicates.
Estimates suggest that almost 66 million people around the globe will have dementia by 2030, with the numbers predicted to top 115 million by 2050.
There is growing evidence that obesity is linked to dementia, but the research indicates that risk may be heightened or lowered, depending on age. And as yet, no study has looked at the age related effect of obesity on dementia risk across the whole age range in the population of one country.
So the researchers decided to do this, using anonymized data from hospital records for the whole of England for the period 1999-2011. Data in which obesity had been recorded were then searched for any subsequent care for, or death from, dementia.
During the study period, 451 232 of those admitted to hospital in England were diagnosed with obesity, 43% of whom were men.
The analysis revealed an incremental decrease in overall risk of hospital admission for dementia the older a person was when a diagnosis of obesity was first recorded, irrespective of gender.
For those aged 30-39, the relative risk of developing dementia was 3.5 times higher than in those of the same age who were not obese. For those in their 40s, the equivalent heightened risk fell to 70% more; for those in their 50s to 50% more; and for those in their 60s to 40% more.
People in their 70s with obesity were neither at heightened or lowered risk of developing dementia, while those in their 80s were 22% less likely to develop the disease, the findings indicated.
There were some age differences between the risk of developing vascular dementia or Alzheimer’s disease, with those in their 30s at greater risk of both. A diagnosis of obesity in the 40s through to the 60s was associated with an increased risk of vascular dementia, while the risk of Alzheimer’s disease was lower in those diagnosed with obesity from their 60s onwards.
This is an observational study, so no definitive conclusions can be drawn about cause and effect. But the findings confirm smaller published studies from elsewhere which report an increased risk of dementia in young people who are obese, but a reduced risk in older obese people, say the researchers.
They venture that a possible explanation for the particularly high risk found in early to mid-life may lie in the fact that heavier weight is associated with diabetes and cardiovascular risk factors, which are themselves linked to a heightened risk of dementia.
And it would seem that if people can stave off significant weight gain until at least their 60s, or survive long enough with obesity, they may have a lower risk of developing dementia, they suggest.
“While obesity at a younger age is associated with an increased risk of future dementia, obesity in people who have lived to about 60-80 years of age seems to be associated with a reduced risk,” they conclude.
And now for the common garden variety ways obesity can ruin our lives…
As your body mass index rises, so does your risk for coronary heart disease(CHD). CHD is a condition in which a waxy substance called plaque (plak) builds up inside the coronary arteries. These arteries supply oxygen-rich blood to your heart.
Plaque can narrow or block the coronary arteries and reduce blood flow to the heart muscle. This can cause angina. or a heart attack. (
Obesity also can lead to heart failure. This is a serious condition in which your heart can’t pump enough blood to meet your body’s needs.
High Blood Pressure
Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps blood. If this pressure rises and stays high over time, it can damage the body in many ways.
Your chances of having high blood pressure are greater if you’re overweight or obese.
Being overweight or obese can lead to a buildup of plaque in your arteries. Eventually, an area of plaque can rupture, causing a blood clot to form.
If the clot is close to your brain, it can block the flow of blood and oxygen to your brain and cause a stroke. The risk of having a stroke rises as BMI increases.
Type 2 Diabetes
Diabetes is a disease in which the body’s blood glucose, or blood sugar, level is too high. Normally, the body breaks down food into glucose and then carries it to cells throughout the body. The cells use a hormone called insulin to turn the glucose into energy.
In type 2 diabetes, the body’s cells don’t use insulin properly. At first, the body reacts by making more insulin. Over time, however, the body can’t make enough insulin to control its blood sugar level.
Diabetes is a leading cause of early death, CHD, stroke, kidney disease, and blindness. Most people who have type 2 diabetes are overweight.
Abnormal Blood Fats
If you’re overweight or obese, you’re at increased risk of having abnormal levels of blood fats. These include high levels of triglycerides and LDL (“bad”) cholesterol and low levels of HDL (“good”) cholesterol.
Abnormal levels of these blood fats are a risk factor for CHD. For more information about triglycerides and LDL and HDL cholesterol, go to the Health Topics High Blood Cholesterol article.
Metabolic syndrome is the name for a group of risk factors that raises your risk for heart disease and other health problems, such as diabetes and stroke.
You can develop any one of these risk factors by itself, but they tend to occur together. A diagnosis of metabolic syndrome is made if you have at least three of the following risk factors:
- A large waistline. This is called abdominal obesity or “having an apple shape.” Having extra fat in the waist area is a greater risk factor for CHD than having extra fat in other parts of the body, such as on the hips.
- A higher than normal triglyceride level (or you’re on medicine to treat high triglycerides).
- A lower than normal HDL cholesterol level (or you’re on medicine to treat low HDL cholesterol).
- Higher than normal blood pressure (or you’re on medicine to treat high blood pressure).
- Higher than normal fasting blood sugar (or you’re on medicine to treat diabetes).
Being overweight or obese raises your risk for colon, breast, endometrial, and gallbladder cancers.
Osteoarthritis is a common joint problem of the knees, hips, and lower back. The condition occurs if the tissue that protects the joints wears away. Extra weight can put more pressure and wear on joints, causing pain.
Sleep apnea is a common disorder in which you have one or more pauses in breathing or shallow breaths while you sleep.
A person who has sleep apnea may have more fat stored around the neck. This can narrow the airway, making it hard to breathe.
Obesity Hypoventilation Syndrome
Obesity hypoventilation syndrome (OHS) is a breathing disorder that affects some obese people. In OHS, poor breathing results in too much carbon dioxide (hypoventilation) and too little oxygen in the blood (hypoxemia).
OHS can lead to serious health problems and may even cause death.
Obesity can cause menstrual issues and infertility in women.
Gallstones are hard pieces of stone-like material that form in the gallbladder. They’re mostly made of cholesterol. Gallstones can cause stomach or back pain.
People who are overweight or obese are at increased risk of having gallstones. Also, being overweight may result in an enlarged gallbladder that doesn’t work well.
Overweight and Obesity-Related Health Problems in Children and Teens
Overweight and obesity also increase the health risks for children and teens. Type 2 diabetes once was rare in American children, but an increasing number of children are developing the disease.
Also, overweight children are more likely to become overweight or obese as adults, with the same disease risks.
Hmmm, perhaps dementia is one way of getting out of the pain of ‘normal’ obesity!
New evidence shows that sugar, a highly processed diet and nitrates in food and fertilizers may be the cause of our Alzheimer’s epidemic.
Every 68 seconds, another person in the US develops Alzheimer’s disease, making it the sixth leading cause of death and one of the fastest-growing illnesses in the West (affecting 5.4 million American adults, and 26 million worldwide). Governments in the US and UK are so concerned about what has been labelled the ‘silver tsunami’-
the swell of Baby Boomers from the 1950s moving into older age, and the implications on society of a projected trebling of cases of dementia (to 135 million) by 2050-that health members from all the G8 leading nations met recently in London to coordinate efforts to find a successful treatment by 2025.
November is National Alzheimer’s Awareness Month and the serious issues of cognitive health will be in the spotlight in the coming weeks. The medical community agrees that cognitive impairment (CI), ranging from mild to severe, is almost epidemic in the U.S. as the Baby Boomer generation is aging and living longer. Scientists believe one reason is that the human brain begins shrinking after age 25. Structural changes and loss of brain synapses lead to rapid decline in cognitive health.
The solution is still unclear, however the good news is that the human brain has a greater degree of plasticity than scientists previously believed, and new studies, specifically those made in nutritional research, show that magnesium deficiency in adults may play a more important role in CI, and more seriously, Alzheimer’s Disease (AD), than previously thought.
The results of one medically significant study spearheaded by Dr. Guosong Liu, one of the world’s leading cognitive health researchers, suggest that elevation of brain magnesium through dietary intake exerts substantial positive effects on brain synapes in a mouse model of AD, actually restoring ageing brains to their youthful conditions. The study is the first to show a mechanism for reversing cognitive decline in advanced stage AD mice, and is also the first to show an effective long-term treatment in AD mice. More exciting, though, are the implications of this study for the potential for treating AD in humans.
Commenting on his work, Dr. Liu said, “The body of our peer-reviewed and published work underscores that magnesium threonate can help maintain healthy brain activity. There is no doubt that magnesium threonate has dramatic effects in preventing synapse loss and reversing memory decline in mice with Alzheimer’s disease.
Furthermore, he states, “There is no question that cognitive impairment is a major fear and health issue for the nation. People are living longer and they want to take steps to maintain the quality of their physical and mental health. Cognitive impairment can affect a person’s memory, language, perception, ability to plan and carry out tasks, and judgment. A recently concluded double blind, placebo-controlled human study, the ‘gold standard’ of science, demonstrates that dietary supplementation of Magtein, patented magnesium threonate, can significantly enhance human cognitive functions and decrease symptoms of cognitive impairments.” The study is expected to be published in a leading peer-reviewed journal in 2014.
Dr. Peter Osborne, a Board Certified doctor of clinical nutrition, said, “Healthy cognitive function begins with a solid nutritional foundation. We know magnesium is essential to maintaining healthy brain functions. We know 50 million Americans are magnesium deficit because people do not eat enough foods that contain magnesium. We know that as we age our bodies naturally lose magnesium. For example, drinking coffee or caffeinated products increases the loss. This deficit must be replaced by taking a nutritional supplement. I use Magtein with my patients as a valuable part of my treatment protocols.”
According to the Centers for Disease Control and Prevention, estimates show that approximately 20% of people ages 55 and older will experience some form of cognitive impairment. The number and growth of the ageing population in the U.S. is unprecedented. Two factors — longer life spans and aging baby boomers — will combine to double the population of American’s aged 65 years or older during the next 25 year to about 72 million. By 2030, older adults will account for roughly 20% of the U.S. population.
I was quite impressed with this ‘map’ of decline into Alzheimers particularly because it clearly demonstrates the focus now being placed by the scientific research community on causation. You will see near the top of the map the two big ones; Insulin imbalance and glucose increase. Under glucose increase we see free radical activity and AGE’s.
Most of my readers know that I have had a bout with incipient Alzheimers’. We posted a video on YouTube about it – and it has reached over 170,000 viewers.
Here’s one viewer’s response.
“Thank you for sharing your touching story with us. I have had my grandmother on coconut oil for the last 2 months and on a Paleo diet for the past week and she has improved dramatically! Her mood is better and she remembers everything! Before she used to forget people’s names, colors and even the name of places and things and she would get terrified because her mother died of Alzheimer’s. The paleo diet has improved her stomach problems and she has more energy too.”
And here’s the video for those of you who haven’t seen it.