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.