Life-Saving News on Alzheimer’s Disease

My father turned 92 this year, so I thought I’d turn to a different topic.

If there’s anything that puts fear into those over 40, it’s cancer. For those over 60, it’s the mental breakdowns, symbolized most by dementia and Alzheimer’s disease. While many find treatments for cancer, few have been successful with Alzheimer’s disease.

The reason that cancer has been so slippery to treat is that there are so many potential causes (inherited susceptibility, environmental toxins, immuno-suppresion deficiencies, etc.) and so many expressions (malignant, nonmalignant), with so many types (liver, brain, and skin) of the disease. It’s very, very complex.

But Alzheimer’s is a different illness altogether. Alzheimer’s disease (AD) is the most serious form of dementia occurring in the elderly. And it’s the one illness I wouldn’t wish on anyone. But, under the radar, there are some promising treatments that keep making it into the peer-reviewed journals that are worth considering for both prevention and interventions. What I have learned is below. For the surprising news, keep reading…

In more than 90% of cases, Alzheimer’s disease (AD) develops after the age of 65 years, and doubles its prevalence with every successive decade of life; from 10% at 60–70 years to 40% at 80-90 years of age.

To understand what we’re up against in successful treatments for Alzheimer’s disease (AD) we have to take a 3-minute field trip into science behind the disease.

Eleven years ago, the big news in biology was the sequencing of the human genome. At that time, Craig Ventner, the head of the private firm that sequenced the genome surprised everyone by saying, “Human biology is far more complicated than we imagined… genes are absolutely not our fate. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not directly driven by the genetic code.” In short, he is downplaying the “gene to behavior” model and hinting of the field of “New Biology.”

So here’s one of the major scientific players saying PUBLICLY (without directly saying it) that we can’t trust drugs that target genes to fix problems with the body. The major drug companies like Merck, Pfizer and Glaxo-Smith Kline rely on the tireless work of molecular biologists who are trying to make effective “knockout gene” interventions (genes can either be expressed, or be silenced to suppress functions) to solve a problem. Thousands of new drugs are produced, but not without problems. This pathway often has serious issues.

How?

Most of the new drugs produced don’t pass stage II (animal studies) or stage III (safe human trials with efficacy) to make it to market. Those that do make it to the marketplace are fraught with side effects. Nationally, there were 426 drug recalls in the U.S. just three years ago, raising serious questions about the quality of research and production in the United States. In fact, one recall is a disaster if it’s the drug you’re taking. Astonishingly, last year (2010) The Food and Drug Administration initiated more than 1,742 recalls (almost 5 a day!) according to the Gold Sheet, a trade publication on drug quality that analyzes FDA data.

I’m telling you this because I want you to drop any delusions that drug companies can guarantee any quick, safe and effective treatments for Alzheimer’s disease. Almost all of them are going at the problem(s) the wrong way. After a quarter of a trillion dollars spent to cure cancer over the last 40 years, you ought to realize that you can dig all the oil wells you want, but if you’re digging your oil wells in Hawaii, you’re wasting your time.

One of the big pharma drugs for AD is Aricept. It’s an acetylcholinesterase (AChE) inhibitor (it helps make more choline available for better memory function) with some clinical effectiveness for Alzheimer’s disease, but there are adverse effects on peripheral organs (liver, kidneys, etc.). Other drugs approved for the treatment of AD include Tacrine, Donepezil, Rivastigmine and Memantine. These drug companies understand part of the problem, but not all of it.

What?!!!! Aren’t those good drugs? Hang in there with me. We’re going to get to the good stuff.

The “New Biology” is a whole new paradigm for understanding how our brain and body work. Holistic research is going mainstream! There’s a new pack of scientific mavericks from across the country. These pioneers USED to work at the well-known drug companies and they even told the drug companies that all drugs targeting single genes were doomed to fail! What did the drug companies do? They fired them! That’s the mentality of drug company executives.

Here’s what this new understanding is all about. You use Amazon to buy books, right? Well, to organize, track and sell you books, Amazon uses and runs thousands of networked computers. And that’s something that these new maverick biologists drool over. These bio-mavericks actually lease “CLOUD” computer time from Amazon. Why?

The “New Biology” mavericks use very, very fast computers to crunch the data to show diseases are massive network issues (not a single, disconnected gene.) In fact, the databases needed to crunch the numbers and to integrate data in these HUGE genetic and cellular networks are humungous! They use NOT gigabytes or even terabytes of data. Get this: they crunch PETABYTES of data (look it up; it’s a million Gigabytes) of data! Why do you need that much computing power? To sort holistic data! Our bodies have far more complexity than anyone ever dreamed of.

One of those pioneers, Eric Schadt, published a paper in the prestigious journal Nature. (He’s published 118 so far, all in highly reputable, peer-reviewed journals.)
His paper was “A Network View of Disease and Compound Screening.” In short, targeted gene therapy will always have side effects, he says.

Don’t worry about the vague title; I’ll explain it. What he’s telling us is simple.

The old Alzheimer’s thinking was along the lines of, “How do I get rid of those pesky beta-amaloyd plaques?” But it turns out that the plaques may be one of the symptoms, but not the cause of AD. Human biology is WAY more complex. In fact, our whole body communicates with itself far more than we EVER imagined. Eric Schadt says we must treat the “network” in our body (holistic approach) rather than individual receptors or genes.

Why?

What if all our genes, proteins and cells don’t work separately? What if you can’t just target a specific gene that someone thought was responsible for Alzheimer’s? What if genes “talk” to other genes in large social networks? And finally, what if all of these genetic communications (like social networks) could be measured and even predicted? That’s the NEW BIOLOGY! Human biology, at every turn, has turned out to be even more complex that anyone ever thought! It’s social networking INSIDE our body.

Why am I telling you all this?

There are several interventions that have been used lately, each with a different level of effectiveness. Each of these is more holistic. I can tell you that each of them (in low dosages) is completely safe and yet still effective. I cannot (and will not) tell you, or someone you love, to take these, since I am not a medical doctor. You are responsible for your own health. I am merely pointing out what studies have been done. For record, I am only reporting on research here. I am NOT prescribing anything.

PREVENTION

Most of the strategies that you’ll see for Alzheimer’s disease (AD) prevention are commonly known. Researchers look at populations (educators, laborers, males, females, etc.) and determine how often that population gets Alzheimer’s disease. From that data, conclusions are drawn about low or high-risk lifestyles. This may not be the most enlightened approach, but in the absence of other approaches, it is still helpful. Here is what seems to lower your risk. More brain work in your career is better!

Get physical: Find ways to stay active (walks, swimming and yoga are the best). Worry less about WHAT you do for activity and more that you do SOMETHING at all daily.

Location-Lakes: While living near lakes is OK, avoid exposure to life forms near lakes. Some lake areas have 10 to 25 times the expected incidence of cyanobacterial neurotoxins. Possible routes of toxin exposure include inhalation of aerosolized toxins, consuming fish, or ingestion of lake water. (Caller TA, et al. 2009). These are toxic!

Emotions: Rediscover your passion and purpose in life. Do something you care about, do service work and love what you do. Take some travel risks to new destinations. Go to places that take your breath away. In the USA, there are plenty of amazing national parks. Overseas, the choices are endless.

Hard work: Make your brain work hard with new learning 3-5 times a week. Upgrade your reading from the “brain-dead” reading to other types that are more challenging. Sitting around is a risk factor, learning new and challenging things is better for the brain.

Eating Rules: Snack healthy, eat only half portions of your regular meals. Choose greens and proteins over carbs and sugars. Cut your carbohydrate consumption in HALF. The key scientific principle, which forms the basis for these diets, is the relationship between consumption of carbohydrates and the subsequent effect on blood sugar (i.e. blood glucose) and specific hormones. Blood sugar levels in the human body must be maintained in a fairly narrow range to maintain health.

The carbohydrate-rich diets evoke excess insulin secretion from the beta cells in the pancreas, which is meant to stabilize the blood sugar levels. But the constant seesaw and glucose whiplash has serious metabolic health consequences. Alzheimer’s risk goes up! To help regulate blood sugar, a daily teaspoon of cinnamon can support insulin regulation without side effects. Buy a large salt shaker-type container and use it liberally and daily.

Reduce the additives and preservatives and eat natural. A glass of red wine a day is okay, and other alcohol may be consumed, but sparingly. Cold water fish is good such as salmon, mackerel, sardines; cod is a good source of choline, along with whole-grain cereals, legumes, eggs, meat, and royal jelly (all of which contain both vitamin B5, omega 3s and choline.) Turmeric, the bright yellow spice that is a primary ingredient in curry powder, shows great promise against Alzheimer’s disease (29 peer-reviewed studies) due to a variety of actions, including its ability to inhibit and even reverse beta-amyloids. Curry and similar spicy foods may be protective.

FIVE POSSIBLE SUPPLEMENTS

1) Omega-3 fatty acids are neuroprotective during development and aging. Omega 3 supplements have shown positive effects in multiple studies (186 studies) of subjects with very mild AD, especially for early onset conditions. Get Omega 3 as fish oil capsules or liquid. Fish oils support enhanced neurogenesis (the production of new brain cells.) When you raise neurogenesis, this in turn supports learning, memory, mood and weight regulation. This non-prescriptive product (fish oil) may be purchased at a health food store. Get it fresh, the type that smells good and tastes good. Also available in no smell fish oil capsules at health food stores.

2) Lipoic acid (LA) (available in health food stores) is a naturally occurring cofactor for the mitochondrial enzymes. It has properties, which can interfere with the pathogenesis or progression of AD. For example, LA increases acetylcholine (ACh) production by activation of choline acetyltransferase and increases glucose uptake, thus supplying more acetyl-CoA for the production of ACh. In addition, it down-regulates the expression of redox-sensitive pro-inflammatory proteins including TNF and inducible nitric oxide synthase. Furthermore, LA can scavenge lipid peroxidation products to prevent AD. (Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA, Münch G. 2008).

3) Small does of lithium (283 studies found at last count) suggest it may be a neuroprotective agent (it’s available in tablet form at health food stores) and has been shown to reduce the rate of dementia and AD. (Wada A, Yokoo H, Yanagita T, Kobayashi H. 2005).

4) CoQ10 is widely available and very well tolerated with minimal adverse effects, making it an attractive potential therapy. Phase III trials of high-dose CoQ10 in large sample sizes are needed to further ascertain or confirm the effects of CoQ10 in neurodegenerative diseases, but early indications look promising (Spindler M, Beal MF, Henchcliffe C. 2009). It’s available in health food stores.

5) The hormone melatonin may be effective against the famous and pesky plaques found in AD patients. Melatonin interacts with amyloid beta and inhibits its aggregation (Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O’Leary OF, Castren E, Maffei L., 2008). This connection with melatonin, which regulates sleep, is strengthened by the recent research showing that the wakefulness inducing hormone orexin influences amyloid beta, too.

Medications: Take what you absolutely have to take. Ask your doctor if any meds you take can be reduced or eliminated. For example, there are many studies suggesting the statins meds (cholesterol – lowering medications) have significant downsides and minimal upsides. Many are simply regulating a function in areas that other non-prescriptives could also be effective. Avoid taking a medication to prevent a problem.

Environment: At the behavioral level, enriched environments improve learning and memory tasks and reduce anxiety. Enrichment consists of a positive, extended contrast in daily experiences from the typical or usual environment that you might have had. Both animal models of Alzheimer Disease (AD) and human models suggest this may be powerful. Why? Enrichment can reduce the effects of mental and neurodegenerative diseases, stress, aging and development of environmental toxins (Redolat R, Mesa-Greasy P. 2011). Stay social. Invite friends over often. Do neighbor gatherings and host clubs and fund-raisers.

INTERVENTIONS

First, I’m not a medical doctor (and if I was, I might be too worried about lawsuits to suggest alternative interventions anyway.) That means I am not qualified, nor will I suggest any specific treatment. Having said that, I am qualified to share the science and let you make your own decisions. The mainstream medicine will tell you that there is still no single treatment that can successfully stop or reverse the progression of AD. Alzheimer’s is a complex disease that defies simple solutions. However, new research suggests we can slow its progression, and even reverse its pathology, IF you know how.

For now, I’ll mention strategies that are available for over the counter or online purchase. Remember, I am not prescribing these. I am not your doctor. I am only raising awareness. The two “over the counter” interventions are 1) 5-HTP and 2) Galantamine.

1. The first intervention is 5-HTP (hydroxy-tryptophan) with over 937 peer-reviewed studies that explore the relationship to AD. This is the precursor for your brain to make more serotonin. As you know, serotonin supports neurogenesis (new brain cells.) There are currently clinical trials underway to treat AD using fluoxetine (the primary agent in Paxil and Zoloft.) This non-prescriptive product (5-HTP) may be purchased at a health food store.

2. The second intervention is galantamine, with 683 peer-reviewed studies. Galantamine, a natural substance found in certain flowers, has also shown promise in delaying the progression of Alzheimer’s by protecting and enhancing cholinergic function. Although this intervention is available as a FDA-approved prescription drug for the treatment of mild to moderate Alzheimer’s disease, it is also available as the original nutritional supplement that it has been LONG BEFORE a drug company made a prescription out of it and the FDA declared it a “drug.”

In fact, Galantamine, in quality controlled, randomized trials/studies has been documented to have a consistent, albeit sometimes modest, effect on cognition, behavioral symptoms and activities of daily living (ADLs). Although minor adverse effects are commonly reported, the product is generally well tolerated and has a favorable safety profile. This does NOT cure AD, but a modest effect may make a big difference, especially when it’s a loved one’s mind, or even your own, we are talking about. One reputable company that sells Galantamine capsules without a prescription online is Life Enhancement.

Listen, your brain is your life; take good care of it! Share this article!

Your partner in learning,

Eric Jensen

CEO, Jensen Learning Corporation

CITATIONS:
Ago Y. and Yakugaku Zasshi (2010) Beneficial effect of galantamine on sensory information-processing deficits. 2010 Oct; 130(10):1305-10.
Caller TA, Doolin JW, Haney JF, Murby AJ, West KG, Farrar HE, Ball A, Harris BT, Stommel EW. (2009) A cluster of amyotrophic lateral sclerosis in New Hampshire: a possible role for toxic cyanobacteria blooms. Amyotroph Lateral Scler.10 Suppl 2:101-8
Ehninger D, Li W, Fox K, Stryker MP, Silva AJ (2008) Reversing neurodevelopmental disorders in adults. Neuron 60:950 –960.
Fan LY, Chiu MJ. (2010) Pharmacological treatment for Alzheimer’s disease: current approaches and future strategies. Acta Neurol Taiwan. Dec;19(4):228-45.
Greer PL, Greenberg ME (2008) From synapse to nucleus: calcium- dependent gene transcription in the control of synapse development and function. Neuron 59:846 – 860.
Giunta et al. (2010) Fish oil enhances anti-amyloidogenic properties of green tea EGCG in Tg2576 mice. Neurosci Lett 8(471):134-8.
He HY, Ray B, Dennis K, Quinlan EM (2007) Experience-dependent recovery of vision following chronic deprivation amblyopia. Nat Neurosci 10:1134 –1136.
Kavanagh, S, Howe I, Brashear HR, Wang D, Baelen BV, Todd M, Schwalen S. (2011) Long-term response to galantamine in relation to short-term efficacy data: pooled analysis in patients with mild to moderate Alzheimer’s disease. Curr Alzheimer Res Jan 11.
Keller C, Kadir A, Forsberg A, Porras O, Nordberg A. (2010) Long-term effects of galantamine treatment on brain functional activities as measured by PET in Alzheimer’s disease patients. J Alzheimers Dis. Dec 14
Koepsell TD, Kurland BF, Harel O, Johnson EA, Zhou XH, Kukull WA. (2008) Education, cognitive function, and severity of neuropathology in Alzheimer disease. Neurology. May 6;70(19 Pt 2):1732-
Lahiri DK, Chen DM, Lahiri P, Bondy S, Greig NH (November 2005). Amyloid, cholinesterase, melatonin, and metals and their roles in aging and neurodegenerative diseases. Ann. N. Y. Acad. Sci. 1056: 430–4
Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O’Leary OF, Castren E, Maffei L (2008) The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science 320:385–388.
Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA,

Münch G. (2008) Lipoic acid as an anti-inflammatory and neuroprotective treatment for
Alzheimer’s disease. Adv Drug Deliv Rev. Oct-Nov;60(13-14):1463-70
Redolat R, Mesa-Gresa P. (2011) Potential Benefits and Limitations of Enriched
Environments and Cognitive Activity on Age-Related Behavioural Decline. Curr Top Behav Neurosci. Jun 4
Spindler M, Beal MF, Henchcliffe C. Coenzyme Q10 effects in neurodegenerative
disease. Neuropsychiatr Dis Treat. 2009;5:597-610.
Suzuki A, Stern SA, Bozdagi O, Huntley GW, Walker RH, Magistretti PJ, Alberini CM (2011) Astrocyte-neuron lactate transport is required for long-term memory formation. Cell. 2011 Mar 4; 144(5):810-23.
Van Puyvelde K, Mets T. (2011) Galantamine (Reminyl) once daily outcome and satisfaction survey (RODOS) in mild to moderate Alzheimer’s disease: A study in a real life population. Geriatr Gerontol Int Jan 4. doi: 10.1111/j.1447-0594.2010.00674.
Wada A, Yokoo H, Yanagita T, Kobayashi H. (2005) Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases. J. Pharmacol Sci. 2005 Dec;99(4):307-21
Wang XC, Zhang YC, Chatterjie N, Grundke-Iqbal I, Iqbal K, Wang JZ (June 2008). “Effect of melatonin and melatonylvalpromide on beta-amyloid and neurofilaments in N2a cells”. Neurochem. Res. 33 (6): 1138–44
Zhang C, Browne A, Child D, Tanzi RE. (2010) Curcumin decreases amyloid-beta peptide
levels by attenuating the maturation of amyloid-beta precursor protein. J Biol Chem. Sep 10;285(37):28472-8

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