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Posted July 7, 2013: by Bill Sardi
The inconceivable is being contemplated – that the intellectual disability among individuals with an inherited developmental disorder (Down’s syndrome) is being partially reversed in animal models of this syndrome with small molecules (example: EGCG from green tea) and may be ready for human application within the next decade, say medical researchers.
Genetic researchers are raising the possibility that certain features of Down’s syndrome, an inherited developmental disorder that affects an estimated 5.8 million people worldwide, can now be reversed or partially corrected by use of small natural molecules. Recent successes in the animal lab provide hope.
Almost all individuals with Down’s syndrome over the age of 40 have changes in their brain characteristic of Alzheimer’s disease at autopsy.
Since 1984 it has been well known that “the typical neuro-pathological features of Alzheimer’s disease, plaques and tangles, appear in virtually all patients with Down’s Syndrome after the age of 40.”
Since Down’s syndrome individuals develop an early form of Alzheimer’s disease, this proposed breakthrough could lead to greater insights how to head off the predicted epidemic of Alzheimer’s memory loss in older adults.
The announcement of this development prompted this health writer to investigate further.
As more and more developmental drugs for Alzheimer’s disease fall by the wayside, even investment magazines say these failures are causing researchers to abandon drug models and look towards vitamins and herbal cures to treat this devastating disease.
So far the various theories involving accumulation of brain plaque (beta amyloid, tau protein) or inhibition of an enzyme (acetycholinesterase) that degrades a key neurotransmitter (acetycholine) involved in memory loss, have been therapeutic dead-end streets.
Could Down’s syndrome children provide clues to the origin of this disease? Maybe.
Down’s syndrome individuals have widely recognizable physical characteristics. These include: short stature; short limbs; stubby fingers; smaller head; a flattened face and nose, a short neck, a small mouth sometimes with a large, protruding tongue, small ears, upward slanting eyes that may have small skin folds at the inner corner; short hands with broad fingers; poor muscle tone and loose ligaments, which suggests weakened connective tissue.
Mentally, Down’s syndrome subjects typically have learning disabilities and developmental delays. Particularly affected is the hippocampus, a part of the brain that is responsible for learning and memory.
Physically Down’s individuals have low muscle tone in infancy, may be born with heart defects, develop leukemia, gastric problems and develop early Alzheimer’s disease.
In good health, a person with Down’s syndrome will on average live to age 55 years or beyond.
The use of vitamin therapy for Down syndrome is not new. A recent study showed no benefit from antioxidant therapy (vitamins C, E, lipoic acid) for Down’s syndrome patients was deemed to be ineffective.
Similarly, an earlier study also showed that antioxidant supplement (folic acid, selenium, zinc, vitamins A, C, E) also proved to be ineffective.
Yes, despite these null studies, it is clear that Down’s syndrome is characterized by premature aging driven by a pro-oxidant state. Antioxidants are still the theoretical antidote.
Another characteristic of Down’s subjects is that they exhibit an impairment in their arteries to respond to changes in blood flow, specifically an inability to dilate (widen) blood vessels with increased blood flow as in exercise or emotional stress. It is believed that increased oxidation degrades a transient gas known as nitric oxide that dilates blood vessels during periods of stress.
Therefore, since it has been demonstrated that injectable vitamin C helps to restore normal dilation (widening) of blood vessels in healthy humans, researchers tested to see if there was the case among Down’s patients.
Intravenous vitamin C only slightly improves dilation of arteries under experimental conditions. But the level of oxidation was not measured and the dosage of vitamin C used, while similar to the dose used in other successful human studies, may not have been adequate nor of sufficient duration to produce a significant effect. Today the dynamics of vitamin C therapy are better known. So don’t rule out vitamin C therapy just yet. It may be beneficial for Down’s sufferers.
Indeed, vitamin C deficiency among Down’s syndrome subjects has been previously described and is associated with increased rates of infection. Supplemental vitamin C has been suggested to prevent chronic infections in Down’s subjects.
But antioxidant therapy only counters the symptoms, not the cause of Down’s syndrome.
The body shape of Down’s syndrome subjects is typically obese. A study conducted over two decades ago showed that their short stature contributed most to their obese state, but it was also noted that the group of Down’s subjects studied consumed ~42% of their calories from fat and 40% from carbohydrates (sugars). A low carbohydrate diet appears to be in order for Down’s individuals.
Over three decades ago it was observed that Down’s syndrome subjects exhibit autoimmune disease, multiple food allergies, gluten intolerance and mal-absorption of vitamins. Researchers then proposed “the most likely mechanism is low vitamin B1 that impairs sufficient release of cAMP.” In one study the frequency of celiac disease was 8% among Down’s syndrome sufferers, much greater than found in the general population. The importance of these digestive disorders in understanding Down’s syndrome becomes clearer with further reading of this report.
It should come as no surprise to learn that a recent survey found gluten intolerant children exhibit greater deficiencies of vitamin B1 (thiamin) and vitamin C. Unexpectedly, thiamin deficiency may be more prevalent even after implementation of a gluten-free diet.
Of further interest, children on gluten-free diets have been found to consume high-sugar diets that are known to block thiamin absorption.
Is a vitamin B1 deficiency implicated in Alzheimer’s disease?
Researchers have suggested “adequate vitamin/mineral supplementation, especially vitamin B1, prior to conception and in the first trimester for mothers at risk for Down’s syndrome offspring, especially older mothers.” A gluten free diet for those with celiac disease or gluten intolerance was also suggested. These suggestions appear to have been largely ignored.
Multiple deficiencies of vitamin and trace minerals have been commonly found among Down’s syndrome subjects and these shortages appear to be life-long. However, there does not appear to be a strong impetus to correct these vitamin and mineral deficiencies among Down’s individuals.
Almost 25 years ago low levels of vitamin B1 were reported among Down’s syndrome subjects who typically develop Alzheimer’s-like symptoms at an early age.
In 1976 one researcher proposed a link between thiamin deficiency and Down’s syndrome. This hypothesis does not seem to have been tested and certainly never disproven.
A report published in The Journal of Orthomolecular Medicine in 1979 convincingly linked (a) the development of Down’s syndrome to shortages of vitamin B1 in pregnancy and (b) improvement in mental function among Down’s subjects with provision of supplemental thiamin. This report suggested correction of vitamin B1 deficiency would “help prevent early senescence as B1 requirements increase with age and Down’s individuals are more prone to dementia such as Alzheimer’s disease.” This forgotten and overlooked report, published over three decades ago, may have pointed to a widespread essential nutrient deficiency as a primary or at least secondary cause of Alzheimer’s disease. Tragically, humanity faces an unprecedented number of new Alzheimer’s patients with no cure in hand.
Tracking down the origins of Alzheimer’s disease becomes more intriguing when we read some very recent scientific reports.
One such report presents the case of a female patient with nervous system problems due to chronically insufficient dietary intake who developed elevated levels of tau protein in her cerebral spinal fluid. Shortly following immediate treatment with thiamin (vitamin B1) this patient clinically improved. Her dementia was resolved. Abnormal tau protein levels may be linked to thiamin depletion!
Another strong association with Alzheimer’s disease is the presence of diabetes. This is also linked to a shortage of thiamin. Read excerpts from a recent paper published in the journal Molecular Cell Neuroscience below:
“Reduced glucose metabolism is an invariable feature of Alzheimer’s Disease (AD) and an outstanding biomarker of disease progression..… The cause of cerebral regional glucose hypo-metabolism remains unclear. Thiamine-dependent processes are critical in glucose metabolism and are diminished in brains of AD patients upon autopsy.
“Further, the reductions in thiamine-dependent processes are highly correlated to the decline in clinical dementia rating scales. In animal models, thiamine deficiency exacerbates brain plaque formation … and impairs memory. In contrast, treatment of AD mice mouse with the thiamine derivative benfotiamine (fat-soluble vitamin B1) diminishes brain plaques, decreases accumulation of tau protein and reverses memory deficits. Diabetes predisposes to AD, which suggests they may share some common mechanisms.
“Benfotiamine diminishes peripheral neuropathy in diabetic humans and animals. In diabetes, benfotiamine induces key thiamine-dependent enzymes of the pentose shunt to reduce accumulation of toxic metabolites including advanced glycation end products (AGE).
“Related mechanisms may lead to reversal of plaque formation by benfotiamine in animals. If so, the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of AD progression.”
Unsurprisingly, it was an 8-week course of benfotiamine (fat soluble vitamin B1) and not thiamin (water soluble vitamin B1) that was found to reverse cognitive (thinking) impairment in laboratory mice, improving both memory and reducing beta amyloid plaque and tau protein levels in mice brains. Researchers now conclude: “benfotiamine may be beneficial for clinical Alzheimer’s disease treatment.”
The positive results of thiamin supplementation are not limited to the animal laboratory. Researchers report: “oral thiamine trials have been shown to improve the cognitive function (thinking ad memory) of patients with Alzheimer’s disease.”
The broader environment that has spawned Alzheimer’s disease can now be characterized.
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