A new article in the prestigious journal BMC Neurology suggests that mainstream medicine should stop wasting millions researching a major class of Alzheimer’s dementia (AD) drugs. The authors assert that these drugs don’t work…and never will.
This thought-provoking essay came on the heels of two failed, high-profile clinical trials for AD drugs. The failed trials tested two new AD drugs designed to combat amyloid beta (A-beta).
Amyloid beta is a protein that clumps into brain plaques in AD patients. It disrupts the flow of information across nerve synapses and causes nerve cell death. For years, many brain experts insisted we could treat or prevent AD by targeting these proteins.
But newer evidence suggests that A-beta actually results from stresses on the brain …rather than causes it. So these new A-beta drugs may be trying to target a “fix” that’s too late in the process of dementia. In other words, the drugs attempt to treat AD after the damage is already done.
Where have we seen that before?
It’s not entirely clear whether the drugs in these trials simply fail to reverse A-beta accumulation…or whether reversing A-beta fails to cure Alzheimer’s disease.
Either way, I don’t imagine many mainstream researchers will give up on the A-beta hypothesis any time soon.
Though, it’s encouraging to see at least some experts recognize the writing on the wall. The authors of the BMC article suggest it’s “unreasonable” to continue further attempts at testing these kinds of drugs for AD.
I’d use a stronger word: insanity.
In fact, some attribute Albert Einstein with saying insanity is “doing the same thing over and over again and expecting different results.”
And that’s modern, mainstream medicine in a nutshell.
You see, recent imaging studies show A-beta can accumulate in the brains of patients without dementia. Conversely, a sizeable proportion of patients with clinical dementia do not show accumulation of A-beta.
But rather than expand their view of dementia, a consensus of AD “experts” argue that patients without A-beta don’t technically suffer from dementia in the first place. (When the facts go against them, they just change the rules and definitions.)
Of course, when it comes to dementia, a loss of cognitive function is the biggest symptom, right? And we can easily assess cognitive function clinically, without even considering anything about A-beta. In other words, doctors can diagnose a patient with dementia based on simple cognitive tests. That’s what counts.
We don’t really need to look at A-beta levels. Indeed, the BMC authors argue that doctors should only assess dementia clinically to determine which patients should participate in therapeutic trials.
Furthermore, it may well be that treatments for AD must start before A-beta begins to accumulate in the brain. But these single-minded “experts” will probably exclude all the patients without A-beta from their future trials…because they don’t fit the narrow definition. But these patients are the only ones who might actually benefit from the treatment.
Ah, the irony.
So, in what is perhaps an object lesson in the manifestations of dementia itself, some persistent drug researchers simply get around these new facts by excluding dementia patients without A-beta from yet more drug studies!
Meanwhile, other researchers are now beginning to investigate real possible causes of AD.
The Adaptive Response Hypothesis is a more physiological concept, proposing that dementia develops from exposure to chronic brain-stress stimuli. These stress factors include oxidative stress, metabolic dysfunction (such as insulin resistance), and chronic inflammation. Genetic factors also appear to play a part.
So–effective therapeutic intervention for AD should focus on these stressors as the actual primary causes of the disease…and not on A-beta, which may simply be a byproduct of the process. Indeed, it makes sense to explore the stress factors, as they relate to aging in general.
Finally, some evidence suggests that drugs designed to remove the accumulated A-beta may actually interfere with normal brain function. In fact, in addition to the normal slew of effects, these A-beta drugs appear to cause brain swelling and damage to cerebral blood vessels in many patients.
Dementia is a serious clinical condition. Yet we don’t spend a fraction of the money on researching natural approaches as we do on failed drug approaches to treat it.
Nevertheless, the few clinical trials that have been done on natural approaches have yielded some tremendous breakthroughs.
For instance, clinical trials from this past year show vitamin D and vitamin E can clearly help prevent and reverse dementia. In one remarkable study, vitamin E clearly outperformed a mainstay AD drug. Furthermore, when patients took both vitamin E and the drug, the drug appeared to wipe out any benefits the vitamin would have incurred.
The herbs berberine (discussed earlier this week) and turmeric, which are widely available in dietary supplements, also help preserve brain function. Research shows these herbs may help the brain because they have strong anti-inflammatory and anti-oxidant properties. Also, they support metabolic health by controlling blood sugar. To complete the interdependent circle, the brain seems to benefit from this improved blood sugar control as well.
Meanwhile, the mainstream continues its insanity about dementia. They continue to waste precious time and money…they continue to pursue their illogical hypotheses…and they continue to push studies on failed drugs. All the while, the natural solutions remain readily available from Nature.
P.S. The World Health Organization estimates about 115 million people worldwide will develop dementia in the next 35 years. Some research shows “brain training” may help stave off age-related cognitive impairment. And brain training is now a multi-million dollar industry. But does it really work? In the February 2015 issue of my Insiders’ Cures newsletter I’ll delve into this hot debate. If you’re not yet a newsletter subscriber, now is the perfect time to get started so you won’t miss this important report.
1. “Moving beyond anti-amyloid therapy for the prevention and treatment of Alzheimer’s disease,” BMC Neurology 2014; 14: 169