Author Archives: pprincetta

Poor Sleep = Alzheimer’s

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Poor sleep associated with buildup of toxic Alzheimer’s protein

Restful sleep is required for us to store and save our memories. If you are not getting enough sleep each night, you may be at an increased risk of developing Alzheimer’s disease. This is something that I feel equally applies to many other chronic diseases as well.

I previously wrote about the connection between Sugar and Alzheimers with Alzheimers often referred to as Type 3 Diabetes.  I am worried about this for myself and my patients. This article is a continuation of additional information and insights to help us never to get Alzheimers /Dementia to begin with.

I have also mentioned using sleeping medications does not allow the brain to go into the correct and proper REM cycle and therefore you may in fact be sleeping but your brain is not regenerating and rebuilding as intended.

In a recent study published in Nature Neuroscience, researchers at University of California, Berkeley, found evidence that poor sleep, specifically a deficit of deep sleep, is associated with a buildup of the beta-amyloid protein. Excessive deposits of beta-amyloid are the primary suspects in the pathology of Alzheimer’s disease, as this toxic protein ends up attacking the brain’s long-term memory.

This correlation between sleep, beta-amyloid, memory, and Alzheimer’s disease has been growing stronger. Sleep is when our body repairs itself. Quality sleep prevents these toxic proteins from accumulating and destroying brain cells. A buildup of beta-amyloid protein has been found in Alzheimer’s patients as well as in patients with sleep disorders. A study from University of Rochester in 2013 found that the brain cells of mice shrunk during non-rapid-eye-movement (non-REM) sleep to free up space for the cerebrospinal fluid to wash out toxic metabolites such as beta-amyloid protein.

Overall, the results of the new study demonstrated that the more beta-amyloid you have in certain parts of your brain, the worse your memory. In addition, the less deep sleep you get, the less effective you are at clearing out beta-amyloid protein. Researchers do not know yet which of these two factors – the poor sleep or the build-up of beta-amyloid protein – begins the cycle that triggers this cascade.

This is a new pathway linking Alzheimer’s disease and memory loss, which is significant since we can do something about it, since poor sleep is treatable and can be improved by modifying sleep habits. It is important that you go to sleep around the same time every night. When the timing of your sleep is shifted even if the duration of sleep is the same, it’s not going to be as restorative. In addition, avoid watching TV or using your computer before bed. Computer screens (smartphones and laptops) emit light in the blue part of the spectrum. This doesn’t cause a problem during the daytime, but at night, this blue light limits the production of melatonin. As a result, it disturbs your sleep-wake cycle. There are free apps you can install on your computer if you absolutely need to be on your computer at night that adjusts colors in a way that reduces the stimulating effects of blue light at night.

Caffeine and other stimulants can also keep you up and interfere with sleep. It is best to avoid these four to six hours before bedtime. Finally, try to workout earlier in the day. Exercise increases cortisol and can make falling asleep very difficult.

If behavior and lifestyle modifications are not enough, there are nutrients and botanical agents that can significantly promote restful sleep. Melatonin is a hormone whose primary role is in controlling the body’s circadian rhythm. While adequate levels of melatonin are essential for quality sleep, its production declines significantly as we get older, often causing sleep difficulties associated with aging. Thus, supplementing with melatonin has been shown improve sleep quality. In addition, 5-HTP can further support endogenous melatonin production during the night to help with staying asleep.  Inositol is a member of the B vitamin family that promotes relaxation and helps maintain the proper metabolism of serotonin. In addition, L-theanine provides calming neurotransmitter production clinically proven to reduce stress and improve the quality of sleep.

Valerian root, German chamomile, passion flower, and lemon balm are all calming botanicals used for centuries to help with insomnia. They have all been shown to decrease the amount of time it takes to fall asleep as well as improve sleep quality.

However, although taking herbs to aid in sleep is far better than toxic pharmaceuticals, the bottom line is to find out why we are not sleeping well to begin with.

In addition to eliminating sugar and foods that break down into sugar, I highly recommend Meditation twice daily, Qigong and the powerful Mindfulness Technique.  Doing the above is almost a sure shot of getting a good nights sleep.  So take one of these up, practice makes perfect and before a year is out, if not sooner, you will be sleeping beautifully and as such re-setting our brains circuitry.

B12-

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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.

Statins=Diabetes

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Statins: Sugar-Coating the Effects

Statins. They’re as controversial a topic as cholesterol itself. Medical professionals have a love-hate relationship with these drugs, with some regarding them as lifesaving pharmaceutical miracles, and others claiming they represent all that is wrong with modern medicine. Yet, as with all compounds that significantly alter a complex biochemical pathway, statins bring unintended consequences.

There is a growing awareness that statin drug use may be associated with an increased risk for type 2 diabetes. Although the risk may be small, it is significant enough for the FDA to acknowledge that statins may result in elevated blood glucose and hemoglobin A1cstatins, thus conferring an increased risk for type 2 diabetes. The highly respected Mayo Clinic also lists increased blood sugar  among the potential side-effects of statins.

A recent study added more fuel to the fire when the results indicated a clinically significant increase in new diabetes diagnosis among men ages 43-75 who were taking statin drugs. Compared to subjects not taking statins, those receiving statin therapy had a 46% increased risk for type 2 diabetes during the 6-year follow-up, with the risk specified as dose-dependent for those taking simvastatin and atorvastatin. Among the men receiving statin treatment, insulin sensitivity was decreased by 24% and insulin secretion by 12% compared to individuals not being treated with statins, with these effects also being dose-dependent for simvastatin and atorvastatin.

Out of a total of 8,749 subjects, 625 received new diagnoses of type 2 diabetes. However, compared to subjects who remained healthy, those who became diabetic were older, more obese, less physically active, had lower HDL levels, higher fasting blood glucose and HbA1c, and higher triglycerides. So these subjects had greater risk factors for developing type 2 diabetes and metabolic syndrome regardless of whether they were taking a statin or not. This doesn’t negate a potential role for statins in contributing even further to the risk for diabetes, but it’s important to note that these subjects were already at a higher risk.

While a drug intended to lower serum cholesterol levels may seem unrelated to blood glucose regulation, there is, in fact, a biochemical mechanism by which statins may affect pancreatic beta cell function. Statin is a generic name for drugs that inhibit HMG CoA reductase, a key enzyme in the mevalonate pathway. By inhibiting this enzyme, statins do, indeed, reduce the endogenous synthesis of cholesterol. But they also decrease synthesis of many other substances that are produced along the same pathway.

Among these crucial substances are prenylated proteins, formed from farnesyl pyrophosphate and geranylgeranyl pyrophosphate building blocks. These little-known compounds are required for glucose stimulated secretion of insulin. Disruption in synthesis of the precursor molecule, mevalonic acid, by HMG CoA reductase inhibitors, has been shown to inhibit glucose-stimulated insulin secretion from normal rat islet cells. According to one researcher,  “Inhibition of protein prenylation in β-cells results in selective accumulation of unprenylated G proteins…possibly interfering with the interaction of these proteins with their respective effector proteins, which may be required for nutrient-induced insulin secretion.” Other studies support these findings—that inhibition of protein prenylation/isoprenylation (specifically by lovastatin) may adversely affect the ability of the pancreas to secrete insulin in response to rising blood glucose.

The mechanism by which this might occur is that prenylation/isoprenylation seems to be required for intracellular trans location of the “G” proteins involved in the B-cell function. . There might even be a role for protein prenylation in protecting against the death of β-cells, which results in type 1 diabetes. According to researchers, “These post translational modification steps not only play obligatory roles in fuel-induced insulin secretion, but also in cytokine-mediated apoptotic demise of the beta cell.”

As we know, the use of statin drugs is riddled with controversy. The use of total cholesterol levels or even just LDL-cholesterol levels as markers for heart disease risk has been called into question. Amidst this controversy, statins do seem to get the nod for reducing risk for a coronary event in patients with existing coronary disease or at high risk,, as well as those who have already experienced a coronary event (secondary prevention). Some researchers have called for statin prescribing guidelines to be more precisely defined by parameters of gender and age, suggesting that when it comes to treating risk factors for coronary and cardiovascular events, there is no”one size fits all” approach. The use of statin drugs to reduce bio markers associated with heart disease should be weighed against the potential development of other conditions that may lead to increased morbidity and mortality, however unintended these consequences may be.

I have an entire library of information regarding the dangers of statins.
Keep in mind high cholesterol is not a result of low stain levels in the blood

 

What Your Poop and Pee are Telling You About Your Body

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What Your Poop and Pee are Telling You About Your Body

Ever wonder what’s going on inside your body? Sometimes it may seem hard to tell without blood tests, doctor’s appointments and expensive screenings. However, there are numerous ways you can assess your health every day without even leaving your house (or bathroom).

Going to the bathroom might seem like a standard daily task, but it’s actually a reflection of what’s happening inside your body—what your body likes, what it needs, even serious conditions it might be struggling with. Poop and pee are your friends and they’re trying to tell you something! This infographic can help you read the signs.

Vitamin E & the Brain

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Vitamin E & the Brain

Among fat-soluble vitamins, vitamin E often gets sidelined in favor of compounds with better-known functions. People automatically associate vitamin A with vision and eye health, vitamin D with calcium homeostasis and bone health, and vitamin K with proper blood clotting. When vitamin E makes a rare appearance in discussions about health and nutrition, it’s often in the context of infertility, since deficiency of this nutrient is associated with reproductive difficulties  in animals and humans. But with advances in technology, scientists continue to uncover previously unknown and under-appreciated roles for vitamins and minerals. In the case of vitamin E, this nutrient might have a significant role to play in brain health and neurological function.

Results of a recent animal study support a requirement for sufficient vitamin E in order to deliver and maintain adequate levels of DHA and DHA-dependent phospholipids in the brain. Neuronal cell membranes are rich in cholesterol and polyunsaturated fats, which are highly susceptible to oxidation. With vitamin E having an antioxidant function, a deficiency can have dangerous consequences for brain health. In fact, severe vitamin E deficiency can manifest as cerebellar ataxia, demonstrating the importance of this nutrient for proper functioning of the central nervous system. Vitamin E deficiency also results in reduced myelination of spinal cord fibers, and leads to neuropathic and myopathic lesions all of which may have disastrous consequences for cognition and neuromuscular coordination.

A small, double-blind, placebo-controlled crossover study demonstrated that vitamin E supplementation led to improved scores on the Abnormal Involuntary Movement Scale (AIMS) in tardive dyskinesia patients who had had the condition for less than five years. The vitamin intervention was less effective in subjects with more longstanding disease.

The cerebrospinal fluid (CSF) of Alzheimer’s disease patients has been shown to be low in Vitamin E.While this specific finding may play a direct role in disease pathology, it might also simply be a reflection of overall poor nutrient status resulting, in part, from the modern diet, which is high in refined carbohydrates and low in micronutrients. However, considering the important role of vitamin E in the central nervous system, a lower level of this nutrient in CSF may expose neurons to profound free radical damage, leading to memory loss and declining cognitive function. Compared to placebo, patients with moderately advanced Alzheimer’s given 2000 IU of vitamin E per day experienced delayed deterioration of cognitive function. . Other studies indicate vitamin E is more effective in combination with another important antioxidant, vitamin C.

Reviews and meta-analyses of studies involving the use of supplemental vitamin E show mixed results, leading researchers to stress using caution regarding high doses of vitamin E. Some study authors suggest emphasizing food sources of vitamin E, or a multivitamin with around 30 IU of alpha-tocopherol, rather than isolated vitamin E supplements that deliver a higher dose. As is true for the use of any nutritional compound in a healthcare setting, caution should, of course, be practiced when dosing vitamin E. However, the mixed outcomes of studies employing vitamin E may be the result of confounding from the makeup of the supplements themselves. For example, a high alpha-tocopherol preparation may result in different effects than one with a higher fraction of gamma-tocopherol.

While frank vitamin E deficiency is rare, it is not unheard of. Vitamin E Deficiency can result from inborn errors of tocopherol transfer proteins, as well as disorders of lipid absorption, transport, and assimilation. Conditions that affect digestive efficiency, such as celiac disease and Crohn’s  disease, may interfere with proper absorption of fat-soluble nutrients. Biliary insufficiency resulting from compromised liver or gallbladder function may also contribute. An additional cause of vitamin E deficiency (as well as deficiency of many other nutrients) is bariatric surgery. While this can be a lifesaving procedure for many people, altering the anatomy of the digestive tract can have severe consequences for nutrient absorption, and extra care should be given to ensuring sufficient nutrient uptake in the body.

The foods richest in vitamin E are nuts and seeds, whole grains, and vegetable oils, such as corn, soybean, and safflower oils. However, overly large intake of these oils is not recommended, due to the potential for skewing the dietary omega-6/omega-3 fatty acid ratio toward the generally pro-inflammatory omega-6 pathways.

NOTE: GCEL (Glutathione) is 5000 times stronger than Vitamins C & E,

  • Vitamin C has 5 extra electrons to donate
  • Vitamin E has 3 extra electrons to donate
  • GSH has 1 million extra electrons to donate

E-Coli Proliferates in IBD

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Inflammatory Bowel Disease = E-Coli

Researchers at Penn State University identified a mechanism in which Escherichia coli proliferates in inflammatory bowel disease (IBD) during flare-ups.

Some strains of E. coli are normal, healthy bacteria that compose part of the predominant flora in the gastrointestinal tract. In some patients with inflammatory bowel diseases, researchers have found that the healthy E. coli may proliferate during a flare-up and further contribute to the patient’s symptoms and progression of the disease.

There are several types of inflammatory bowel diseases where opportunistic E. coli bacteria proliferates in the gut. IBD, which primarily includes Chrohn’s  nd ulcerative colitis, involves chronic inflammation of all or part of the gastrointestinal tract.

Here is an example of this situation in one of my patients with Chrohn’s  disease.

The mechanisms by which this occurs with E. coli is not well understood. Identifying these mechanisms will help to reduce the E. coli burden on the inflamed gut and prevent chronic diseases often associated with IBD, such as musculoskeletal and dermatological conditions.

Researchers studied the interactions between enterobactin, myeloperoxidase, and lipocalin 2 and how they regulate E. coli in the gastrointestinal tract. Enterobactin (Ent) is a chemical secreted by E. coli that takes iron from host proteins in the body and aids in the growth of E. coli. Myeloperoxidase (MPO) is an antibacterial protein that white blood cells produce to kill bacteria. However, enterobactin inhibits myeloperoxidase from doing this.

Another protein produced by white blood cells, Lipocalin 2 (Lcn2), collects the enterobactin so that the bacteria cannot obtain enough iron for their survival. The researchers found that Lcn2 can counteract the effects of Ent on MPO.

E. coli can be harmful under certain circumstances commonly seen in inflammatory bowel disease. This new study has defined a defense mechanism used by E. coli.

Bacteriophages can be a great option here. They are not very well known but are one of the most abundant naturally-occurring organisms on earth. They can be found everywhere from the soil to drinking water. They only prey on bacteria, never human cells, and the bacteria have a difficult time becoming resistant to them.  Phages are great because they are species specific – meaning different strains attack different bacteria. This makes them harmless to human cells and even to non-targeted bacteria. This is much different than antibiotics that can wipe out all the beneficial bacteria of the gastrointestinal tract along with the harmful bacteria. Phages are classified as prebiotics, and there are specific phages that can infect and inhibit the growth of E. coli only. Lytic phages are completely safe and considered GRAS (through review of published scientific literature, and based on their common use in food).

Alzheimer’s Disease: Type 3 Diabetes?

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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.

Methylation-MTHFR

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Methylation Turns Good Genes On and Bad Genes Off

The topic of methylation has been gaining in popularity. As a result, there has been an increase in the number of practitioners using genomic testing in recent years. One of the most common SNPs tested is MTHFR, which stands for methylenetetrahydrofolate reductase. MTHFR is a key enzyme in the methylation pathway and is responsible for converting folate into its active state. The two main variants that are well understood and tested for are C677T and A1298C. The end results of having one of these SNPs are reduced enzyme activity and a reduced amount of usable folate. The prevalence for the presence of an MTHFR polymorphism is 25% for C677T and 25% for A1298C.

MTHFR is most commonly associated with homocysteinemia, especially in conjunction with low B vitamin status. Homocysteinemia is associated with many cardiovascular disorders such as increased risk of atherosclerosis, stroke, abdominal aortic aneurysm, essential hypertension, and venous thrombosis. Other conditions correlated with MTHFR polymorphisms are increased risk of diabetic depression, schizophrenia, autism, osteoporosis, certain cancers, and pregnancy-related disorders.

Effects of the MTHFR Polymorphisms:

C677T (-/-)A1298 (-/-) C677T (-/-)A1298 (+/-) C677T (-/-)A1298 (+/+) C677T (+/-)A1298 (-/-)
Normalenzyme activity Normalenzyme activity 30-40% reducedenzyme activity 30-40% reducedenzyme activity
C677T (+/-)         A1298 (+/-) C677T (+/+)           A1298 (-/-) C677T (+/+)       A1298 (+/-)
50-60% reduced    enzyme activity 60-70% reduced       enzyme activity 60-70% reduced enzyme activity

The A1298C is associated with a decreased enzyme activity but not to the same degree as the C677T mutation. In the C677T SNP, the enzyme activity is reduced by each mutant allele present. While there are other MTHFR SNPs, they all don’t have an effect on the enzyme activity.

Lifestyle considerations:

  • Exercise
  • Avoid smoking
  • Avoid excess coffee
  • Avoid alcohol (destroys B Vitamins)

Dietary Considerations:

  • Eat an adequate amount of folate-rich green vegetables
  • Follow a Mediterranean/Paleo Diet
  • Avoid foods fortified with synthetic folic acid (see unmetabolized folic acid below)

UnMetabolized Folic Acid

Natural folates are essential for our overall health and function. However, folic acid, the synthetic form, is used in fortified foods and most dietary supplements. Designs for Health does not use any folic acid in their supplement line. Newer research has shown us that the increased intake of synthetic folic acid combined with MTHFR polymorphisms can lead to an accumulation of unmetabolized folic acid in the blood. Unmetabolized folic acid is associated with the development and progression of certain cancers. In addition, an excess of folic acid or unmetabolized folic acid can weaken immune function as well as impair natural killer cells.

Supplements Considerations

It is important to note that there are many patients with MTHFR SNPs that do not have an elevated homocysteine level. Most people with MTHFR may need a separate folate (L-5-MTHF) if they require higher dosing, at 1mg or 5mg of L-5-MTHF. Patients with MTHFR have folate needs that vary quite a bit from patient to patient, so there will not be a one perfect product for them. How impaired the methylation is will be determined by whether the patient has a heterozygous, homozygous, or compound presentation. One patient may have a heterozygous SNP and only need 1mg of L-5-MTHF while another may have a homozygous C677T and require 5-10 mg. Others may have one copy of A1298T and not need any more folate. Keep in mind that some of these patients have developed compensatory ways to counter the SNP and may actually have sufficient folate.

When supporting methylation pathways, it is important consider synergistic nutrientsin addition to folate and vitamin B12. In some of the toughest cases, the patient will not get effective lowering of homocysteine until choline is supplemented. Choline converts to betaine with the help of riboflavin and aids methylation in this step of the pathway. In addition, TMG (trimethylglycine) provides extra methyl groups. The most common block in the homocysteine pathway is the conversion of cystathionine to cysteine, which requires vitamin B6 to activate the cystathionine beta-synthase enzyme. Serine is also needed along with B6 to help convert homocysteine into cystathionine.

N-Acetyl-cysteine supports homocysteine metabolism by mobilizing homocysteine from its binding proteins (albumin). N-Acetyl-cysteine at 600 mg daily has been shown to reduce plasma homocysteine levels.

In addition, when using high doses of folate it is possible to have an imbalance of vitamin B12 as a result, so B12 may need to be assessed and supported. Low dose niacin should also be considered with high doses of folate since this requires a lot of methyl groups during its breakdown in the liver.

Additional Testing for Methylation

Complete blood count – Simply looking at the mean corpuscular volume (MCV) can reveal if someone has a methylation problem. This is one of the first things I look at. Large red blood cells (folate or vitamin B12 deficiency) or anemia can be a sign of impaired methylation.

Plasma Homocysteine – Homocysteine is an amino acid produced as part of the body’s methylation process. The metabolism of homocysteine is highly dependent on in vitamin B12, folate, and vitamin B6. Deficiencies in any of these may be associated with elevated homocysteine levels.

Organic acid testing – Organic acids are products of metabolism that can identify nutrient deficiencies that typically precede any abnormal findings on a CBC or a comprehensive metabolic panel. Methylmalonate (MMA) is a more specific test for a vitamin B12 insufficiency. A person’s levels may be elevated even if you have a normal serum vitamin B12 or homocysteine level. In addition, formiminoglutamate (FIGLU) is a functional marker of folate insufficiency.

For additional information on MTHFR, Folates, B12 and how I treat this problem with my patients, feel free to contact me at [email protected] or 619-231-1778

Constipation Remedies

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Constipation Remedies

Here is a list of remedies for constipation. The best on this list is Grandma’s Power Pudding which was told to me by an old time medical doctor in Atlanta in 1973.

I also like Blackstrap Molasses because it is loaded with minerals especially iron and magnesium

Grandma’s Power Pudding

  • 1 cup applesauce
  • 3/4 cup prune juice
  • 1 cup of unprocessed wheat bran

Mix together in a small storage container; applesauce, prune juice and wheat bran until it forms a pasty pudding. Take one tablespoon every morning followed by a full glass of water. Drink some water throughout the day.

Blackstrap Molasses

One tablespoon of blackstrap molasses before bed should help ease your constipation by morning. Blackstrap molasses is boiled and concentrated three times, so it has significant vitamins and minerals; magnesium in particular will help relieve your constipation

Mint or Ginger Tea

Mint and ginger are both proven home remedies to help alleviate a slew of digestive problems. Peppermint contains menthol, which has an antispasmodic effect that relaxes the muscles of the digestive tract. Ginger is a “warming” herb that causes the inside of the body to generate more heat; herbalists say this can help speed up sluggish digestion. In tea, the hot water will also stimulate digestion and help relieve constipation. Dandelion tea is also a gentle laxative/detoxifier.

Lemon Water

The citric acid in lemon juice acts as a stimulant to your digestive system and can help flush toxins from your body. Squeeze fresh lemon juice into a glass of water every morning, or add lemon to tea; you may find that the refreshingly tart water not only acts as a natural remedy to your constipation but also that it helps you drink more water throughout the day

Raisins

High in fiber, raisins also contain tartaric acid, which has a laxative effect. In one study, doctors determined that panelists who ate 4 1/2 ounces of raisins (one small box) per day had their digested food make it through the digestive track in half the time it took other subjects who did not. Cherries and apricots are also rich in fiber and can help kick your constipation. Eat these fruits with a bowl of yogurt for the added benefits of gut-soothing probiotics.

Prunes

These fiber-rich fruits are a go-to home remedy for getting your digestion back on track. Three prunes have 3 grams of fiber, and they also contain a compound that triggers the intestinal contraction that makes you want to go. Another great dried fruit choice is figs, which may not cause as much bloating as prunes.

**Mix half a glass of prune juice with half a glass of oat milk. Drinking this before you eat or drink anything else in the mornings will help you get rid of constipation for good.

Even having prune juice all by itself can treat constipation easily. Take a glass in the morning and one in the evening while you are suffering from constipation and reduce this intake to half a glass twice a day for maintaining good colon health and avoiding constipation permanently.

Castor Oil

This home remedy for constipation has been handed down for generations. One of the primary uses for castor oil is as a laxative; take 1 to 2 teaspoons on an empty stomach and you should see results in about 8 hours. Why? A component in the oil breaks down into a substance that stimulates your large and small intestines.

Note #1: This information is for those who know they have chronic constipation not related to a specific pathology such as colon cancer or thyroid problems with T4 a & T3

Note # 2: Exercise such as walking and definitely Yoga can be beneficial as well

For additional information regarding constipation, you can contact me directly at [email protected] or 619-231-1778