Dementia has been described as a disorder that deprives people of their identity and—even more chillingly—destroys every faculty that makes them human. The disorder is rarely short-lived: victims endure a relatively swift death of the mind, which is then followed by a long and lingering death of the body, with a gradual loss of all attendant bodily functions. So dementia is quite literally a living death.
It’s the most feared disease of old age not just for individuals, but for society too. From being a rarity half a century ago, dementia is now rapidly becoming the most expensive item in developed nations’ healthcare budgets. In the US alone, 5 million people suffer from dementia, costing the nation an estimated $236 billion in 2016. In the UK, dementia treatment accounted for about a quarter of the total National Health Service (NHS) expenditures in 2014. Those figures are predicted to double in 20 years, but may rise even higher, given that dementia is so difficult to diagnose, especially in its early stages.
In June 2014, in an initiative echoing Richard Nixon’s ‘cancer wars’ of the 1970s, Britain’s Prime Minister David Cameron called for “a global fight-back against dementia [which] now stands alongside cancer as one of the greatest enemies of humanity.”
But, unlike cancer, where new drugs are launched almost every month, dementia drugs are few and far between. Cameron tells us that “losses by pharmaceutical companies [on dementia drug R&D] have reached around $50 billion,” with only “three out of 101 dementia drugs developed between 1998 and 2011 making it to market.”
In fact, five drugs have made it onto the marketplace, one of which was withdrawn in the early 2000s: the notorious Tacrine.
Like most of the current antidementia drugs, Tacrine was a ‘cholinesterase inhibitor,’ which acts by maintaining levels of acetylcholine in the brain. Acetylcholine is a major brain chemical known to be reduced by as much as 90 percent in dementia sufferers; it’s also believed to be heavily involved with memory. So, in theory, a drug with an action that keeps this chemical flowing throughout the brain makes sense.
The theory may be fine, the trouble is the side-effects. After just a decade on the market, Tacrine began to be “no longer actively marketed” after reports of severe liver toxicity. In fact, as many as 60 percent of patients found the side-effects intolerable at high doses. The final nail in Tacrine’s coffin was that it didn’t actually work.1
Since then, three other drugs have appeared, all of which attempt to accomplish the same trick of maintaining acetylcholine in the brain: Pfizer’s Aricept (donepezil); Novartis’s Exelon (rivastigmine); and Shire Pharmaceticals/Janssen’s Reminyl (galantamine).
The problem is, these ‘second-generation’ drugs tend not to work either: even clinical trials funded by the drug companies themselves have failed to show much benefit.
When Oxford University researchers scrutinized the data from 23 separate Pfizer-sponsored Aricept trials, involving more than 5,000 patients at different stages of dementia, the researchers concluded that “the treatment effects are small and are not always apparent in practice.” Add to that the strong likelihood of “a variety of adverse events,” such as nausea, vomiting, diarrhea, muscle cramps, dizziness, fatigue and anorexia, and it’s small wonder there is what the researchers politely call a “debate” over whether Aricept is worth using.2
In an independent two-year clinical trial by Birmingham University, Aricept was tested in over 500 patients with mild to moderately severe Alzheimer’s disease (AD). Again, the drug’s benefits were so small that they were deemed “below minimally relevant thresholds.”3 Said study director Professor Richard Gray, “Patients and their families would probably notice no difference if the drug was stopped.”
Another independent survey of the drug’s value in earlier-stage dementia, or ‘mild cognitive impairment’ as it’s officially known, similarly concluded that Aricept’s “putative benefits are minor, short-lived and associated with significant side-effects.”4
It’s much the same picture with Exelon, where a recent independent analysis of clinical trial data reported that the benefits were “small and of uncertain clinical importance”—plus causing common severe side-effects like diarrhea, nausea and vomiting, and a host of less common ones, including aggression and vomiting blood.5
Reminyl is equally ineffective, producing only “small improvements on cognitive tests,” and its one advantage is “usually mild” side-effects.6
The final drug available is memantine (Ebixa, Maruxa, Nemdatine). Originally claimed to be a breakthrough drug with a new mode of action (it inhibits glutamate, a brain chemical that can destroy brain cells in Alzheimer’s patients), animal studies showed it to be yet another run-of-the-mill anticholinergic drug—albeit a powerful one.
Nevertheless, once again, it was found to have only a “small beneficial effect” and then only in moderate-to-severe AD; it also takes six months to work.7
One indication of the drug companies’ desperation to market dementia drugs happened last July, when Eli Lilly mounted a frenzied PR campaign for their new compound solanezumab. The drug was hailed as a ‘breakthrough’ and ‘miracle’ in the world’s press, even though it claimed merely to slow the progress of mild early-stage dementia.
In fact, the company’s own initial clinical trial showed that the drug was useless, reporting that it “failed to improve cognition or functional ability.”8 However, as a final grasp at straws, the company said the data did reveal a small subset of patients with early-stage mild dementia who may have benefitted, so meriting further clinical trials. But don’t hold your breath: the original data showed that the cognitive benefits were trivial and statistically insignificant.8
Despite this poor showing, these four currently available drugs are still widely prescribed, as observational studies (which are not the same as proper clinical trials) claim to have found benefit, particularly for ‘caregivers.’ As the drugs marginally reduce symptoms of dementia, patients are easier to manage in care facilities.
One consequence of this dismal situation is that institutional caregivers have had to look elsewhere —to conventional psychiatric drugs. They’ve latched onto the so-called ‘antipsychotics,’ drugs like olanzapine, haloperidol and risperidone. All are powerful tranquillizers often used to manage people with schizophrenia and bipolar disorder, yet they’re being widely marketed to dementia care homes for their sedating properties.
Although these sedatives may make life easier for caregivers by reducing patients’ aggression, UK dementia expert Clive Ballard, professor of age-related diseases at King’s College London, says the effects are only “modest” and “need to be balanced against numerous adverse events, including parkinsonism, gait disturbance, accelerated cognitive decline, pneumonia, strokes and a significant increase in mortality risk.”9 In other words, these drugs can kill, and even if they don‘t, they’ll make dementia worse.
A major symptom of dementia is anxiety, for which, yet again, clinicians have reached out to Big Pharma for a solution. Over the past 40 years, antianxiety benzodiazepine drugs such as diazepam (Valium) and lorazepam (Ativan) have been routinely doled out to dementia patients, but with “limited evidence for clinical efficacy,” concluded an Austrian review of 18 reports. Most striking was their discovery that, in many cases, the drugs “accelerated cognitive deterioration”—again, they made dementia worse.10 A contemporaneous French report agreed, finding “an increased risk of dementia in benzodiazepine users” in nine of the 10 studies they reviewed.11
So, the outlook for both dementia sufferers and healthcare budgets is bleak: not only is the conventional medicine chest almost bare, but some of its contents may actually be fueling the disorder.
The wrong target
Why have the billions spent on drug research gone nowhere? Two main reasons have been proposed. First, dementia is notoriously difficult to diagnose: post mortems show that as many as one in four people with suspected dementia may not have had it at all.12 That’s because dementia-like symptoms have a wide variety of causes, including underactive thyroid, depression, vitamin deficiencies, alcohol abuse and diabetes.
The second reason why Big Pharma has failed to find any useful drugs is the recent realization that, not surprisingly, they may have been targeting the symptoms of AD, and not the cause.
For the past 40 years, AD has been thought to result from the development of ‘neurofibrillary beta-amyloid plaques’ in the brain, but this idea is now doubtful: an increasing number of experts speculate that the plaques are a manifestation of the disease, not a cause (see box, page 26). As a result, the search for ‘anti-amyloid’ drugs is not only fruitless but, as Eli Lilly itself acknowledged in their recent drug trial, “might have a deleterious effect on the symptoms, course or signs of Alzheimer’s disease.”8
Although dementia is the most feared disease of old age, it isn’t an inevitable part of growing old. At age 65, women have about a one in six chance of developing Alzheimer’s before they die, while men have about half that risk. Even at age 85, the overall chance is only one in four.
Looked at from this perspective, the vast majority of old people don’t get dementia, so what are they doing right to avoid the dreaded disease?
The good news is you can significantly reduce your dementia risk by making the right lifestyle choices. The latest evidence shows that simple dietary changes can have major benefits.
Food and drink
1) Choose a Mediterranean diet, which more than halves the risk of AD.13
The reason seems to be that three major components of the diet—olive oil, red wine and coffee—have powerful brain-protective effects. Animal tests using oleocanthal, an important component in extra-virgin olive oil, show that it “enhances beta-amyloid clearance,” making it “a potential neuroprotective mechanism against Alzheimer’s disease.”14
A Danish study of over 1,600 seniors found that those who drank wine had about half the risk of dementia as non-drinkers,15 and a French study found that old people who drank up to half a liter of wine a day reduced their dementia risk by as much as 80 percent.16 Surprisingly, any type of alcohol may be of benefit: a German study found that a daily drink of 20–29 g of alcohol (a pint of beer, a double scotch or a third of a bottle of wine) reduced old people’s chances of developing “overall dementia” by two-thirds, and actual AD to almost zero.17
As for the Mediterranean love of coffee, US pharmacologists have tested caffeine on mice and found that it “enhances brain beta-amyloid clearance”; although animal studies don’t always apply to humans, it might explain the “protective effect of caffeine against AD.”18 However, an Italian study warns against taking up extreme coffee-drinking in later life. Its benefits appear to be seen only in people with a lifelong history of downing one to two cups a day.19
A recent US study showed that old people whose diet most closely corresponded to a Mediterranean one (“green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, seafood, poultry, olive oil and wine”) had the greatest protection against “cognitive decline.”20 The mechanisms include “enhancement of neuronal communication via increases in neuronal signaling and decreases in stress signals induced by oxidative/inflammatory stressors,” say Tufts University nutritionists, who recommend “high-antioxidant foods such as berries, Concord grapes, and walnuts.”21
2) Avoid foods that increase the risk of diabetes (such as refined carbohydrates). Population studies show that diabetes is a major risk factor for dementia, more than doubling the risk.22
3) Drink tea. Studies show that tea drinkers have lower estimates of cognitive decline, according to a recent review of the evidence.23 Why? Probably because tea is rich in the polyphenol epigallocatechin-3-gallate (EGCG), a major antioxidant shown to be “neuroprotective.”24 And green tea is thought to be better than black as it contains more EGCG.
4) Eat berries. These fruits contain chemicals such as anthocyanin, caffeic acid, catechin, quercetin, kaempferol and tannin, all shown to be “capable of modulating signaling pathways involved in inflammation, cell survival, neurotransmission, and enhancing neuroplasticity”—in other words, they can all boost brain function.25
5) Take supplements. Low levels of vitamins A, B9 (folate), B12, C and E have consistently been found in AD patients, according to a recent survey of 80 authoritative population studies.26 Low vitamin B12 is related to high levels of homocysteine, a major risk factor for AD.27 AD patients also have low levels of zinc and selenium. But be aware that high levels of these minerals have also been found in AD, so take care not to overdose on them.28
6) Keep challenging your brain. A reduced risk of AD has been found in people with “high job complexity or a cognitively active lifestyle,” “increased mental activity” and “an active and socially integrated lifestyle.”29
7) Keep moving. Studies convincingly show that even moderate regular exercise is good for brain health. An eight-year study tracking 2,509 Californian seniors found that those who exercised moderately to vigorously at least
once a week had a 30 percent lower risk of AD. 30
Modern brain imaging has helped to explain why exercise is so important in AD. One American study found that exercise results in “neurogenesis” (brain cell growth) in the dentate gyrus, an area of the brain crucial for memory function,31 while controlled trials have shown that “the dose of 150 minutes of moderate aerobic exercise per week is sufficient to be cognitively protective.”32 (Here, ‘moderate’ means achieving a heart rate that’s roughly 60 percent of your maximum.)
8) Eat organic and avoid pesticides. A recent study found that people with traces of hexachlorocyclohexane and dieldrin in their blood have more than two times the risk of AD.28 Organochlorine and organophosphate pesticides are similarly hazardous; the effects are seen primarily among highly exposed farmworkers.33
9)Watch out for heavy metals.
Aluminum. At levels above 1,000 ng/L in the water supply, French researchers found a link between aluminum and AD,34 but the hazard of cookware is uncertain.
Lead. People exposed to this well-known neurotoxin tend to suffer from ‘late cognitive deterioration.’35
Mercury. Animal studies have shown that this neurotoxin can cause changes in the brain “similar to those seen in AD.”36 A review of the published evidence base—including clinical trials and population studies—confirms “a decisive role for inorganic mercury in the etiology of Alzheimer’s disease.”37 The biggest source of mercury is dental (amalgam) fillings, although the association between fillings and AD hasn’t been proven due to a lack of adequate studies.38 One theory suggests that people carrying the apolipoprotein E (APOE) gene variant are prone to AD because they cannot detoxify mercury—a situation that can indirectly lead to AD.39
As heavy metals are highly toxic to brain cells, some doctors have tried chelation therapy for AD patients, attempting to chemically ‘grab’ metal from the body’s tissues and blood. But this hasn’t shown success to date in full-blown AD, as it failed to reverse the brain damage caused by the disease.40
Many of the above non-toxic answers to dementia are at least as promising as the latest drugs but, as usual, they are rarely publicized. Scandalously, not one of the many dementia charities recommends any of the options outlined here, despite being supported by published peer-reviewed data. Why is this? Almost certainly because health charities receive massive financial support from Big Pharma—a strategy cynically employed by the industry to promote their products and, by implication, to discourage non-drug solutions.41 This is even more scandalous considering that many prescription drugs are themselves responsible for dementia in the first place (see page 30).
While none of the following has been demonstrated to cure full-blown dementia, all of of them may slow the disease’s progression.
Vitamin E. Doctors in the US found that giving Alzheimer’s disease (AD) patients 2,000 IU/day of vitamin E resulted in “a delay in clinical progression” of more than six months.1 The type most readily assimilated by the body is d-alpha-tocopherol. Derived from plants, it’s only slightly more expensive than the synthetic version—confusingly called dl-alpha-tocopherol—which has been shown not to work in tests.
B vitamins. A cocktail of vitamins B6, B9 and B12 can help prevent ‘brain atrophy’ in the elderly, according to Oxford University researchers. Their six-month trial halved the normal rate of cognitive decline in people aged over 70 with early-stage dementia. One dramatic finding was an up to sevenfold reduction of atrophy in the parts of the brain often associated with AD.2
“This B-vitamin treatment is the first and only disease-modifying treatment that’s worked,” says Oxford professor of pharmacology Dr A. David Smith. “B vitamins lower homocysteine, which directly leads to a decrease in gray matter atrophy, thereby slowing cognitive decline. We have proved the concept that you can modify the disease.”
Suggested daily dosage: 8 mg B9, 0.5 mg B12, 20 mg B6. As with vitamin E, the natural form of B9 (folate) is more beneficial than folic acid, its synthetic look-alike. A nutritional cocktail, comprising folate, vitamin E, B12, S-adenosylmethionine (SAMe), N-acetyl cysteine (NAC) and acetyl-l-carnitine, has recently completed its phase-II clinical trials, where it “improved cognitive performance.”3
Coconut oil. In people with mild dementia, this medium-chain triglyceride has been found to improve cognitive function by raising ketone levels in the brain. Ketones, the end-product of fat-burning, can serve as ‘brain fuel’ when glucose levels, its usual fuel, are low.4 Lab tests have confirmed that coconut oil “attenuates the effects of beta-amyloid” on isolated brain cells.5
Fish oil. Fish oil is a rich source of EPA (eicosapentaenoic acid), DHA (docosahexaenoic acid) and long-chain polyunsaturated omega-3 fatty acids, and there’s evidence that fish-oil supplements can help retard early-stage dementia.6 Souvenaid®, a commercial product containing a cocktail of nutrients such as omega-3, choline, selenium, and vitamins B6, B9, B12, C and E, can also improve symptoms of early-stage dementia, but not more advanced disease.7
Ginkgo biloba. The leaves of this Chinese tree have a well-deserved reputation for improving brain function in general, and are particularly invaluable for controlling dementia. Clinical research shows that 240 mg/day of a standardized extract of Ginkgo can consistently “stabilize or slow decline in cognition, function, behavior, and global change . . . in cognitive impairment and dementia.” It can take up to six months to work, though.8
Curcumin. The active ingredient in turmeric, a curry spice with a long history of medicinal use in India, curcumin is a polyphenol with powerful antioxidant and anti-inflammatory actions. Laboratory tests have found that it “clears and reduces existing plaques” in mice that were artificially given AD.9 Other test-tube studies at the UCLA School of Medicine found that curcumin enhanced the binding activity of macrophages taken from AD patients, suggesting “a safe approach to immune clearance of amyloidosis” from the AD brain.10 Nevertheless, its practical benefit as a real-life treatment is still uncertain, possibly because curcumin is not readily taken up by the body, although doctors in India report several cases of AD patients responding favorably to 100 g/day of turmeric powder given in capsules.11
Exercise. Besides preventing AD, one hour of aerobic exercise three times a week can improve cognitive function, and decrease irritability and depression.12
Homeopathy. Tests on laboratory rats dosed with Lycopodium Clavatum 200C and 1M showed a “beneficial effect” on the animals’ cerebral blood flow, as well as “improvements in learning and memory.”13 While no formal trials have been done with AD patients, success has been reported in individual case reports.14
Acupuncture. A particular technique called ‘acupoint cat-gut implantation therapy’ has been found to “increase cognitive function” in AD patients in a placebo-controlled study by doctors at Beijing’s Capital Medical University.15
Huperzine A. An extract of a type of club moss, huperzine A is widely used in Chinese medicine. A survey of 20 randomized controlled trials concluded that 300–500 mg/day led to “a marked improvement in cognition,” although the quality of some of the research is questionable.16
Cinnamon. Experiments with aging mice (which may not apply to humans) have shown this spice to have powerful antioxidant effects in the brain, including inhibiting the production of beta-amyloid plaques while protecting memory and learning.17
Transcranial magnetic stimulation. Brazilian scientists have recently reported some success with this technique, which directs variable pulsed magnetic fields to the head. TMS was able to improve memory function for a month at a time in people with early-stage dementia.18
What causes dementia?
The prevailing theory of dementia as a disease caused by beta-amyloid plaques in the brain has been challenged by post-mortem evidence. Some people die mentally fully functioning, but with their brains suffused with plaques; others die with full-blown Alzheimer’s disease (AD) symptoms, but with no plaques.1 So something else other than the plaques must be involved in AD.
Two major theories have arisen. One says that AD is a kind of diabetes. As many as 25 years ago, AD patients were found to have abnormal glucose metabolism—a key element of diabetes. Crucially, this abnormality was also found in their brains.2
This ties in with the finding that diabetics have more than double the risk of AD—with even ‘borderline’ type 2 diabetes (blood glucose levels of 7.8–11 mmol/L) carrying an excess risk of developing AD.3
Brain imaging and animal studies have now confirmed the diabetes–AD connection, leading some researchers to argue that AD could be classified as “fundamentally a metabolic disease” that contributes to neural cell damage by affecting glucose and insulin in the brain.4
Indeed, experts such as Professor of Pathology (Neuropathology) Suzanne de la Monte at Brown University, in Providence, Rhode Island, have even suggested that AD should be termed ‘type 3 diabetes.’5
Part two - The Damaged Brain
If you want to prevent dementia, look first to what’s inside your medicine cabinet, says Lynne McTaggart
We may be living longer and better than ever, but by the time we reach our golden years, the chances of us having any awareness of it are rapidly fading. In fact, the chances that any one of us will suffer from dementia sharply increases with every decade. According to one team of researchers, who tracked the incidence of the disorder over time, after the age of 60, your risk of developing dementia doubles every five years. By the time you reach your mid-80s, you face a one-in-four risk of dementia, and by age 90, the odds increase to one in three.1
One reason for this prevalence is simply the ambiguous nature of the term. Virtually every form of mental decline—memory loss and impaired planning, judgment, reasoning and ordinary thought processes—is classified as dementia.
But modern medicine must take the greatest blame for mental decline among the elderly. Despite representing only one-seventh of the population, people over 65 take one-third of all prescription drugs. The average senior takes six drugs at a time, many of which have hugely deleterious effects on the brain.
Evidence is emerging that a large coterie of drugs given for other conditions, such as high cholesterol, depression, inflammation, insomnia, anxiety, heart disease and arthritis—in short, most of the drugs given to us as we get older—all can bring on dementia.
Many of these drugs cause actual damage to the structure of the brain, including loss of brain volume and the fatty parts of brain cells, leading to abnormal tissue accumulation in vital brain regions. Given that some 90 percent of Americans from their mid-50s onward are taking at least one drug regularly, and nearly a third take five or more, it may well be that dementia is largely a drug-induced disease.2 Of the 36 million Americans who take statins, for instance, an estimated 162,000 could be severely cognitively impaired because of the drugs.
One reason why drugs are so rarely identified as a cause is that researchers can’t agree on whether the features of dementia are the cause or the effect of the disorder (see box, page 26). Evidence on the effects of aluminum and mercury on the brain suggest that the physical effects in dementia patients, such as neurofibrillary ‘tangles,’ are the result of toxicity rather than a true cause of dementia. In test-tube studies of human brain cells, minute doses of mercury produced changes identical to those of Alzheimer’s disease (AD).3
In animal studies, professor of medical biochemistry Boyd Haley, and his colleagues at the University of Kentucky, fed rats aluminum, but noted no changes in tubulin levels, while mercury-fed rats displayed diminished tubulin levels similar to those of typical AD patients. Other researchers suggest that the vacuoles seen in certain lesions are filled with toxic materials like aluminum, which the neuron has ‘fenced in’ to protect the rest of the brain.4
Researchers at the University of Pittsburgh have also discovered the fat-binding agent ‘apolipoprotein D’ (apoD) in the brain plaques of AD patients, and many studies have shown that antipsychotic drugs induce apoD production. What’s more, scientists have also found apoD in fat and brain cells following injury, suggesting the agent has a role in cell renewal and repair.
Taken together, the evidence suggests that toxicity, rather than natural cellular degeneration, is one major cause of dementia.
Among drugs with potentially toxic effects, some of the chief offenders are antidepressants, which appear to target the brain’s white matter, causing damage and functional impairment.
White matter is the part that contains bundles of nerve fibers covered with myelin, a white fatty substance that forms an insulating sheath around each fiber. Messages are passed through these neural bundles to areas of gray matter, made up of unmyelinated nerve cells, so that white matter is like a telephone network, responsible for the rapid transmission of nerve impulses and cell-to-cell communication.
A natural aspect of aging is losing neural connections. Each of us enters adulthood with some 176,000 km of white matter, but should expect to lose around 10 percent of these connections with every decade of life. And antidepressants clearly hasten the process. In 2008, researchers at Duke University Medical Center, in North Carolina, published the results of a 10-year study of magnetic resonance imaging (MRI) scans of more than 1,800 patients taken over two time periods—from 1991 to 1994, and from 1997 to 1999. They then compared the findings of 163 patients who had begun taking antidepressants between the first and second scans with those of patients not using such drugs.
The two groups were similar for virtually every condition looked at—diabetes, stroke, heart attacks, hypertension—save one. Those taking antidepressants had more ‘bright spots’ in their white matter on MRI, a feature thought to indicate damaged blood vessels, impaired blood flow, demyelination (loss of neuronal myelin sheath), disintegration of the blood–brain barrier and even more damage to white matter cells.5
Indeed, those taking the drugs suffered a 36 percent incidence of white-matter damage compared with 27 percent in those who had been drug-free over the decade. All types of antidepressants—old or new—hastened the decline. Although the worst offenders were the old-style tricyclics, adverse effects were also seen with all the newer drugs that inhibit serotonin uptake. Overall, 60 percent of patients who used either type of antidepressants showed increased, abnormal white matter brain damage.
Antidepressants also seem to shrink the hippocampus, the part of the brain’s limbic system involved in long-term memory, spatial navigation, learning and mood. Chronic users of antidepressants, particularly SSRIs (selective serotonin reuptake inhibitors) like Prozac (fluoxetine), have smaller hippocampal structures compared with controls.
In one study, the hippocampal volumes of long-time depressed patients taking long-term medication were compared with those newly diagnosed with depression, who had not yet begun taking any drugs, and a group of non-depressed controls. There was no difference in hippocampal size between the just-diagnosed patients and the controls, whereas the long-term medicated had volumes that were 12 percent smaller, on average.6
Most of all, the study demonstrates that it’s the drugs themselves, and not the depression, that’s behind the shrinking brain.
Autopsies of cavaders have also revealed brain damage in long-term antidepressant users. In one Dutch study, 73 percent showed evidence of brain cell death (apoptosis), compared with 33 percent in patients taking long-term steroids and 6 percent in the matched controls.7
Epidemiological studies have also found a greater incidence of dementia among populations using antidepressants. Researchers in Copenhagen did a sweeping study of nearly a third of the entire Danish population, focusing on patients aged over 40 who’d taken antidepressants even just once. Their risk of having dementia was two to five times higher than the non-users.’8 And this study may even have underestimated the risk, as one-fifth of those using antidepressants died during the follow-up.
Medicine is under the illusion that cutting cholesterol in the elderly is good for the brain and that these ‘miracle’ cholesterol-lowering drugs can keep Alzheimer’s at bay.
While it’s true that statins can alter cholesterol metabolism in the brain, this has no bearing on AD. Harvard University researchers, working with other centers in the US, Germany and Spain, gave statins for 12 weeks to patients with mild AD or mild memory loss. They found a “modest but significant” inhibition of brain-cholesterol production, but this had no beneficial effects on their AD whatsoever.9
In fact, the lack of the effectiveness of statins for treating AD was firmly established in 2009, when two reviewers independently analyzed two large-scale randomized controlled trials—the Heart Protection Study 2002 and PROSPER 2002, involving a total of 26,340 patients—and reached a consensus. Their conclusion was that statins given late in life to people at risk of vascular disease won’t prevent either AD or dementia.10 And not a single long-term follow-up study found any evidence of any benefit with statins in delaying cognitive decline.11
Yeon-Kyun Shin, a professor of biophysics at Iowa State University and an expert in brain signaling, has demonstrated that lowering cholesterol through drugs interferes with brain function. In one experiment, Shin showed that having cholesterol present increases the protein function involved in neurotransmitter-release machinery from brain cells by five times.12 “If you try to lower the cholesterol by taking medicine that is attacking the machinery of cholesterol synthesis in the liver, that medicine goes to the brain too. And then it reduces the synthesis of cholesterol, which is necessary in the brain,” he said.
Another major culprit in dementia is that broad class of drugs called ‘antipsychotics.’ The first of these medications (‘neuroleptics’) appeared in the 1950s to help patients suffering from hallucinations, paranoid schizophrenia and other psychoses. But these drugs brought unwanted extrapyramidal (sensorimotor) side-effects like tardive dyskinesia, characterized by muscle stiffness, tics, tremors and other awkward movements.
The arrival of clozapine (Clozaril) introduced the next generation of neuroleptics—which includes olanzapine (Zyprexa), quetiapine (Seroquel) and risperidone (Risperdal)—dubbed ‘atypical antipsychotics’ to distinguish them from their older and supposedly more dangerous cousins. These drugs are supposed to suppress the psychotic and antisocial aspects of schizophrenia without the sensorimotor effects.13 But this newer generation comes with its own laundry list of dangerous, even life-threatening, side-effects, including serious mental deterioration. And there’s no doubt that the antipsychotics can cause or increase the development of dementia,14 which is ironic as these drugs are often given to sedate or calm patients suffering with dementia.
The most compelling evidence comes from autopsy studies comparing patients who used antipsychotic drugs with those who did not. In a study by the Wolfson Centre for Age-Related Diseases at King’s College London, those who’d taken neuroleptics had a 30 percent greater density of amyloid plaques, and a staggering 65 to 367 percent more neurofibrillary tangles than those not using neuroleptics.15
In a similar US study, 102 patients with schizophrenia showed evidence on autopsy of brain deterioration suggestive of Alzheimer’s or some other form of dementia. The signs were seen in 74 percent of those who’d taken antipsychotics, but in only 36 percent
of those who’d died prior to the introduction of
In other words, taking antipsychotics more than doubled the patients’ chances of having dementia.
The worst combination of all is taking an antipsychotic with an antidepressant, which can quadruple the speed at which the disorder develops.17
Another UK study focused on care facilities in the North East of England compared the efficacy of the antipsychotic quetiapine, the cholinesterase inhibitor rivastigmine and a placebo in calming institutionalized patients with dementia. None of the patients in the active-treatment groups were any calmer than those taking the sugar pill placebos, with one significant difference: quetiapine was associated with significantly greater cognitive decline.18
Antipsychotics also appear to shrink the brain’s frontal-lobe volume, the part that deals with cognition, mood and emotions, according to a US study.19 Other studies have found brain size reductions in a variety of areas with both older (haloperidol) and newer (olanzapine) antipsychotic medications.19
A clear association between antipsychotics and cognitive decline is now coming to light. In one painstaking British survey, every case in a dementia register for 1993–1994 was examined, and the patients’ diagnoses and treatments were obtained from medical records or carers and by interviewing the next of kin, then matched with a similar group of elderly patients living in Southeast London.
Of the patients on the register, 13 percent had a past history of psychiatric treatment, and the use of psychiatric drugs was nearly four times greater among those who’d gone on to develop dementia.20
In addition to the major antipsychotic drugs, benzodiazepine tranquilizers and sleeping pills are also responsible for cognitive decline.
One Argentinian study noted that sleeping pills, which are readily handed out without prescription in that country, led to severe memory and cognitive impairment, and delirium.21
Newer studies show this has to do with their effect on brain gangliosides. These molecules, made up of fat and sugar, are largely found in brain lipids and covering every neuron.
They are essential for regulating cell growth, forming neural synapses and responding to foreign invaders like toxins and bacteria. Without gangliosides, we lose the myelin on our nerve cells, or the entire neuron, and may even die.
A series of Yugoslavian studies involving rats (which of course may not apply to humans) demonstrated that chronic doses of Valium (diazepam) led to the loss of 46 percent of cerebellar gangliosides within six months. A month after total drug withdrawal, the animals’ brains had still not fully recovered.22
When the same team carried out a similar study in 2002, they found significantly reduced gangliosides in the hippocampus, cerebral cortex and cerebellum, as well as increases of simple gangliosides in other brain areas.23
These findings are consistent with those of many human neurological diseases, including Alzheimer’s.
A 1993 UK study examining computed tomography (CT) brain scans of long-term benzodiazepine users compared with drug-free controls revealed that the drug users had lower brain-tissue density in their frontal and occipital lobes, as well as in the left caudate nucleus—areas crucial for cognitive function.24
In the US alone, six million patients are being treated for dementia at a cost of $90 billion, or one-third of all Medicare bills. This means that 1 percent of the entire US gross domestic product is being spent on a mostly iatrogenic (doctor-induced) condition.
Medicine has reached the point where it’s chasing its own tail, attempting to mop up with yet more drugs and treatments a vast and costly problem that it has itself, in large part, caused in the first place.
While evidence is mounting that a major toxic insult to the brain is from the mercury in amalgam dental fillings, this effect may well be eclipsed by the dangers we face from the modern medical response to aging.
Keeping bright and alert in old age requires a few simple practices: regular exercise; an antioxidant-rich wholefood diet plus good fats; minimizing toxic exposure to heavy metals; engaging in regular brain workouts (crossword puzzles, reading); and staying connected through a social network.
Now there’s another one to add to the list: avoiding as many prescription drugs as you can.
The chicken or egg dilemma
As an all-purpose catchphrase, dementia could be defined as any condition with an observable abnormality involving nerve or glial cells. On this basis, there are only four types of true dementia:
1) Lewy body dementia, involving movement disorders like those of Parkinson’s disease, with abnormal deposits of ‘Lewy body’ proteins (named after the German neurologist who discovered them) in neurons
2) Vascular dementia, where the brain’s blood supply is cut off or interrupted, usually by large or small strokes, causing nerve cell death
3) Frontotemporal dementia, usually in patients aged under 65, where the frontal or temporal lobes (including the hippocampus) have shrunk
4) Alzheimer’s disease (AD).Alzheimer’s victims are thought to share three specific abnormalities:
• Senile plaques, abnormal clumps of amyloid and other proteins that form around nerve cells in gray matter
• Neurofibrillary tangles, abnormal, twisted bundles of fibers within neurons mostly made up of tau proteins that hamper tubulin formation, a protein needed for healthy neural connections, so messages in the brain aren’t transmitted properly
• Granulovacuolar degeneration (GVD), where neurons develop ‘holes’ (vacuoles), each containing a small, dense protein granule.
Flying out of his head
Far from aiding memory and cognitive function, statins can cause sudden and complete memory loss. This happened when flight surgeon Duane Graveline suffered global amnesia while taking atorvastatin (Lipitor) for the first time. When his family doctor, Jay S. Cohen, took up his case with Pfizer, the drug’s manufacturer, he was sent clinical evidence gathered before the drug’s release showing 4.5 cases of severe cognitive disturbance in every 100 patients taking the drug.
This included impaired, worsened or general lapses of memory, general forgetfulness and short-term memory loss, as well as difficulty concentrating, abnormally slowed or decreased mental activity (thinking), impaired intellect or judgment and even irrational thoughts.
When Graveline and Cohen conducted an online search of MedWatch, the US Food and Drug Administration (FDA) database of reported drug side-effects, they found 662 reports of severe cognitive impairment or serious amnesia associated with Lipitor. Over time, they discovered the complaints became more frequent.1
As MedWatch is thought to be notified of only 2.5 to 5 percent of all drug side-effects, the true incidence of memory problems from statins may be closer to 66,000 or more. In fact, Graveline and Cohen believe that virtually everyone taking these drugs suffers some cognitive damage that may be too mild to be detected because all statins lower levels of coenzyme Q10, which is vital for brain function (see box, page 35).
The pair’s detective work was vindicated by a meta-analysis by Duke University, which found 60 patients with memory loss attributable to statins. Half these patients had noticed cognitive decline within just two months of starting the drugs, and more than half found their memory improved on stopping the drugs, whereas all patients who started taking the drugs again saw a recurrence of their memory problems.
The role of coenzyme Q10
It’s well known that patients taking statins lose coenzyme Q10 (CoQ10) in a dose-related manner, as the drugs block the production of both cholesterol and CoQ10.
CoQ10 participates in cell energy production, and makes cell membranes more resistant to oxygen damage. It’s abundant in the heart mostly because of the huge energy requirements of cardiac cells.
One US review of all studies into the adverse effects of statins emphasized their negative effects on mitochondria, the power packs of all cells in the body, as well as on CoQ10, a “key mitochondrial antioxidant.”1 Others have discovered that statins can inhibit mitrochondrial cells and cause mutations. Scientists now suspect that an array of neurodegenerative diseases are due to such altered mitochondria.
Critics of statins believe that the widespread use of these drugs has caused an increase in ‘statin cardiomyopathy,’ where heart function or heart rhythm is disturbed. Drug manufacturers tacitly acknowledge this effect by offering several drug formulations that combine a statin with CoQ10.
A less well-known problem of blocking CoQ10 is that it interferes with cognition, resulting in memory loss and muddled thinking. In an elderly person, this is usually passed off as age-related dementia, triggering yet another coterie of ‘wonder drugs.