B12 – the Vitamin for All Ages

We have long appreciated the role of particular vitamins in contributing to the physical structure of the body. There’s vitamin D for healthy bone turnover, and vitamin C for hydroxylation of proline and lysine, required for the synthesis of collagen. Vitamin B12 is another of these key factors, and it contributes to the building and maintenance of myelin, the protective covering that surrounds neurons. Severe B12 deficiency results in a number of signs and symptoms that affect multiple body systems. Among these are the hematological changes categorized as pernicious and megaloblastic anemias, decreased methylation and elevated homocysteine, and compromised neurological function. The last of these is especially concerning, because some of the adverse effects may be irreversible, even upon repletion of B12 stores.

One group commonly at risk for B12 insufficiency is the elderly. Many older people may be taking stomach acid blocking medication, which will inhibit the body’s ability to absorb this vitamin. Additionally, due to decades of guidance from government nutrition authorities to reduce consumption of foods rich in saturated fat and cholesterol, people may be avoiding some of the primary dietary sources of B12, including red meat (liver, in particular), egg yolks, and shellfish. (Older people might also steer clear of these foods if they find them more difficult to chew, and reduced stomach acid will make them harder to digest, as well.)

It is especially troubling that older people may be deficient in this nutrient, because B12 is critical for healthy cognitive function. It is well known that a B12 deficiency can result in memory loss, disorientation, and dementia. It would be tragic if some older patients were misdiagnosed as having Alzheimer’s disease when the cause of changes in their cognition and behavior was actually a vitamin deficiency. Researchers say that low vitamin B12 status “is an important risk factor for loss of brain volume in older community-dwelling adults. These findings suggest that plasma vitamin B12 status may be an early marker of brain atrophy and thus a potentially important modifiable risk factor for cognitive decline in the elderly.” (Emphasis added.)

Compared to patients with other types of dementia, Alzheimer’s disease patients have lower levels of B12 in their cerebrospinal fluid. The resulting reduced availability of methyl groups is believed to lead to decreased synthesis of myelin, membrane phospholipids, and the neurotransmitter  —all of which would have disastrous consequences for cognitive function. After recognizing that elevated plasma homocysteine was associated with cognitive decline in older adults, researchers who set out to determine whether it was insufficient folate or insufficient B12 that was responsible, found that it is B12 that influences healthy cognition. A doubling of holotranscobalamin (bioavailable or “active” B12) concentration was associated with a 30% slower rate of cognitive decline, whereas a doubling in homocysteine or methyl-malonic acid (markers for B12 insufficiency) was associated with greater than 50% more rapid cognitive decline.

Other groups that may be at risk for low B12 status are vegetarians and vegans, since the most concentrated sources of this nutrient are animal proteins. Lacto-ovo vegetarians may get sufficient amounts from eggs and dairy products, but those who avoid animal-sourced foods altogether may have difficulty remaining nutrient replete without careful supplementation. Children of strictly vegetarian parents have experienced developmental difficulties resulting from decreased myelination due to B12 deficiency. These include severe psychomotor retardation, frontoparietal cranial atrophy, and the more general catch-all, “failure to thrive.” Most disturbing is that even when hematological signs of deficiency are corrected, there may be some degree of long-lasting neurocognitive defects later in child development. Researchers familiar with B12 deficiency in infants emphasize that strict vegetarian parents should be made aware that some of the resulting compromises in development during fetal and neonatal life may be irreversible, and, thus, it would be wise to take precautions to ensure adequate maternal B12 levels during pregnancy and breastfeeding.

 NOTE: Many of you have heard me talk about “Aunt Sadie” who beginning in the 1950’s gave B12 injections to our entire family and everyone else who lived in the neighborhood.  She had a booming B12 practice.

Alzheimer’s Disease: Type 3 Diabetes?

Alzheimer’s Disease: Type 3 Diabetes?

It is no coincidence that we are witnessing a skyrocketing increase in the incidence of Alzheimer’s disease (AD), which parallels those of metabolic syndrome, type 2 diabetes, and obesity. All of these are, in part, outcomes related to carbohydrate intolerance and the mismatch between our biological makeup and our modern diet and lifestyle. In fact, the connections between glucose, insulin dysregulation and Alzheimer’s disease are so strong that many researchers now commonly refer to AD as “type 3 diabetes

The blood-brain-barrier is a powerful border that carefully regulates the entry of fuel substrates and nutrients from the periphery. However, it is not capable of protecting the brain from the deleterious effects of an onslaught of refined carbohydrates, oxidized vegetable oils, and nutritionally empty processed foods. The brain is an intensely energy-hungry organ, and anything that impedes its use of glucose—such as peripheral and/or central insulin resistance—will have disastrous consequences for cognitive function. Alzheimer’s disease is the end stage manifestation after a significant number of neurons have “starved to death” due to a loss of their ability to metabolize glucose.

Although the outward manifestations of AD—such as memory loss, confusion, and disturbing behavioral changes—are easy to observe, there are also physiological factors that can be measured and quantified. One of the earliest and most profound observable biochemical changes in the AD brain is a reduction in the rate at which the brain uses glucose, called the cerebral metabolic rate of glucose (CMRglu). This can be measured in vivo, with AD patients showing upwards of 45% reduction in CMRglu compared to healthy, age-matched controls. Some researchers see this decline in glucose usage by the brain as the predominant abnormality in AD

Interestingly, the decline in CMRglu can be observed in people at risk for AD (based on family history or genotype) as early as in their 30s or 40s, long before overt signs of AD have manifested. Thus, the decreased CMRglu can be seen as a kind of “canary in the coal mine”—an early warning sign that something is going awry in the brain. The extent of the reduction in CMRglu is tied to AD severity. A longitudinal study using PET scan to measure CMRglu.  in people age 50-80 showed that reduced hippocampal CMRglu at baseline predicted progression from normal cognitive function to AD, with the greatest reductions at baseline correlating with the quickest development of full-blown AD.

At baseline, hippocampal glucose metabolism in people who progressed from healthy to AD was 26% below that of people who did not develop AD, and the annual rate of decline averaged 4.4%. In people who progressed from normal to mild cognitive impairment (a precursor to AD), CMRglu was 15% reduced at baseline, with an annual rate of decline at 2.4%. The rate of decline for people who had normal CMRglu at baseline and did not develop AD was just 0.8%. Assuming the rates of decline were somewhat constant, extrapolating backward indicates that the decline may have started as early as 20 years before overt signs of AD were present. At baseline, despite the already decreased CMRglu in some subjects, all subjects were cognitively normal. This suggests that a starting point of reduced glucose usage in the brain and a stronger rate of continued decline might be one of the first triggering events in AD. The brain may be able to compensate for years before damage is so widespread that overt symptoms are observable. The normal forgetfulness and foibles we associate with “just getting older”—Where did I leave my keys? Don’t I have an appointment somewhere this week?—might be the earliest indicators that the brain is struggling to fuel itself.

An interesting potential contributor to the reduced CMRglu is peripheral and/or central insulin resistance. Plasma concentration of insulin is positively correlated with AD severity.  When neurons become insulin resistant, they are afflicted by the same pathology that occurs in the periphery—an inability to properly metabolize glucose, causing glucose to accumulate in extracellular spaces for an extended period of time. This results in rampant glycation and the formation of advanced glycation end products (AGEs). These AGEs add insult to injury by forming cross-linkages with each other that may alter the shape of neuronal synapses and impede cellular communication and nerve impulse transmission in the brain, with cognitive abnormalities being an obvious consequence. With hyperinsulinemia affecting 40% of people over age 80, it’s no surprise to find a link between insulin dysregulation and a condition that preferentially strikes older individuals. Moreover, hyperinsulinemia has been found to be and independent risk factor for AD.

The beta-amyloid (Aβ) plaques often implicated as a cause of AD may, in fact, be a result of peripheral hyperinsulinemia. In addition to the reduced CMRglu, the presence of insoluble Aβ plaques is one of the defining signatures of AD pathology. However, Aβ is a normal product of protein degradation, and there is no evidence that AD patients overproduce Aβ. Rather, the problem seems to be that Aβ isn’t cleared away as it should be, which results in these small, otherwise soluble peptide fragments aggregating into insoluble plaques. (These plaques are then subject to glycation and blocking synapses, adding yet another obstruction to neuronal communication.)

A fascinating thing to note is that what is responsible for clearing away Aβ in a timely manner—before it dwells long enough to form plaques—is insulin degrading enzyme (IDE), the same enzyme that clears away insulin. However, the affinity of IDE for insulin is so high that even small amounts of insulin completely the degradation of AB. One study demonstrated that peripheral infusion of insulin in older subjects increased the level of AB in cerebrospinal fluid within 120 minutes, and this also correlated to decreased memory function. Thus, the formation of Aβ plaques is facilitated by hyperinsulinemia. Adding yet another piece of evidence to the theory that Aβ plaques are an effect of AD pathology, rather than its cause, is the fact that the decline in CMRglu precedes the formation of the plaques. Therefore, the presence of Aβ plaques is not likely the triggering factor. (They may exacerbate disease severity, but they are not the initial event in its initiation.)

Considering the connections between impaired glucose metabolism, chronically elevated insulin, and Alzheimer’s disease, the phrase “type 3 diabetes” is viable.

Sleep Study Questionnaire

 Sleep Study Questionnaire

The purpose of this brief questionnaire is to accrue information now that may prevent us getting Alzheimer’s/Dementia in the future.

Alzheimer’s is now being referred as Type 3 Diabetes!!

Through the use of MRI’s andf other state of the art diagnostics, the above problems actually begin to show up in our 30s.

All of the questions below are approximates—please answer as such

  1. What time do you go to sleep at night  ____________
  2. Do you wake up during the night  ___________
  3. If so how many times do you wake up during the night  ______________
  4. Do you take Ambien, Xanax, Diazepam’s, Melatonin etc. to help provoke sleep  ______________
  5. If yes to the above, do you use every night or just some nights _____________
  6. Have you ever been officially diagnosed having sleep apnea  _______________
  7. Would you say that overall and in general, you get a good night’s sleep  ______________
  8. On a level of 1-10 how would you honestly rate your stress levels  ___________

Fluorides Shocking Facts

Fluoride’s Shocking Facts

All European countries (other than Ireland) wisely banned fluoride from their drinking water decades ago.  Recent data shows that 72.4% of the US population is relegated to consume this poison from faucets and showerheads.  Ireland’s mandatory fluoride law exposes the dangers of this toxic agent—the citizens of this small nation endure one of the highest levels of neurological disease in the world.

Fluoride is a poison, affecting almost every organ in the body. It is as poisonous as arsenic and more poisonous than lead.  Historically, the Roman Empire’s demise was precipitated from lead poisoning via water. In spite of this, worldwide chemical lobbyist and their array of   ill-informed dentists propagate the use of this vile killer.

Empirical research from top universities has revealed:

  • Fluoride alters immune response by inhibiting antibody formation
  • Cancer is one disorder that is linked to fluoride consumption as is reported by the environmental protection agency (EPA)
  • Fluoride disrupts the synthesis of collagen and leads to the breakdown of collagen in bone, tendon, muscle, skin, cartilage, lungs, kidney, trachea and arteries
  • Fluoride promotes bone fractures
  • Fluoride plays a role in sleep disorders by accumulating  in the pineal gland and reducing melatonin (melatonin is necessary for sound sleep)
  • Fluoride encourages learning disabilities
  • Fluoride leads to dementia and other nerve degeneration disorders
  • Fluoride induces thyroid and glandular disease
  • Infertility is directly related to fluoride
  • Birth defects are accelerated by fluoride due to the alteration of brain function and hormones in the fetus
  • Fluoride promotes premature aging and decrease fertility
  • Animal kidneys fail at a much higher level when consuming tainted water
  • Environmental degeneration of our soil is one of fluoride’s top legacies

Prozac/Paxil Facts—Fluoride is the key ingredient in many psychotropic drugs! Prozac is 94.8% FLUORIDE!

Charts of Sodium Fluoride Content in our Food

Let’s speed up the fluoride detox

  1. Iodine supplementation has been clinically demonstrated to increase the urine excretion of sodium fluoride from the body, by changing it to the calcium fluoride form. During this process calcium is robbed from the body, another reason for taking effective calcium and magnesium supplements. Lecithin is recommended as an adjunct to using iodine for excreting fluoride.
  2. Vitamin C

There are many good organizations working to abolish fluoride’s destructive history. One example is the Fluoride Action Network.  Use any search engine (Google) in your part of the world to learn more

Additional Informational Links:   

Detox Tips – Long Term n Easy

Acetyl-Glutathione & Intracellular Detoxification

By Jack Tips (Ph.D, CCN)

Clinical nutritionists have long recognized the premier importance and vast significance of the molecule, glutathione (GSH), in human health.  It is the body’s most important antioxidant/detoxifier, and protects the cells from free radical damage incurred during mitochondrial production of adenosine triphosphate (ATP) energy. Other cellular free radical protectors are the enzymes catalase and super-oxide dismustase. Simply put, if glutathione levels drop, the body is prone to cancer, wasting disease, autism, hepatitis, cataracts, Alzheimer’s, Parkinson’s COPD, asthma, schizophrenia, bipolar and aging—just to cite a few conditions bearing numerous medical references

Raising glutathione levels in the cells has been a challenge.  Glutathione can be put into a supplement, but it’s difficult to get it through the intestines into the bloodstream.  Once in the bloodstream, it’s difficult to get supplemental GSH into the cells as degradation occurs in the bloodstream.  Studies showed taking supplemental GSH does not raise blood levels.  Thus oral supplements were deemed  to assist in the gastrointestinal tract; perhaps some help in the blood, but not enter the cells where it’s needed.  Intravenous GSH administration became the most effective way to push GSH into the cells.

Recently, a new form of GSH became available—one that demonstrates it can be absorbed through the G.I. tract and survive degradation in the bloodstream, cross cell membranes and thus favorably impact the cells, as well as help prevent cancer.  It is acetyl-glutathione featured in Systemic Formulas’ GCEL.

S-Acetyl Glutathione is an alternative frm of the reduced GSH. Several studies have shown that this precursor of GSH is well absorbed and more stable throughout the digestive tract than the reduced       L-glutathione and has a positive effect on many oxidative stress bio-markers.  S-Acetyl  Glutathione enters the cell directly and once inside the cell it is converted to GSH by the cytoplasmic thioesterases that remove the acetyl group thus rapidly raising Intracellular GSH levels.

Because of GSH ability to promote detoxification from within the cells, its supplementation can flood the detox pathways and cause large amounts to enter the small intestines via gall bladder excretion via the bile.  To prevent resorption from the intestines, practitioners utilize BIND (Toxin Elimination), a superactived charcoal, to absorb and bind toxins so they cannot be resorbed.  Together GCEL and BIND assist the body in “removing the cause” of inflammation, hormone resistance, cell membrane damage, and errant cell metabolic processes.

NOTE: In clinical practice, detoxification proponents often employ the 60 Day Systemic Detoxification Program to help the body clear out the interfering toxin backlog, improve liver function, open detoxification pathways, and impact cellular metabolism with protective antioxidants.  Then boosting GSH to drive the detoxification effort into the cellular processes offers the body an amazing opportunity to rejuvenate its cellular functions from which a more optimal health can be restored.  Systemic’s Intracellular Detoxification program provides state of the art true cellular detoxification support that serves the brain, cells, and innate healing processes.