Tag Archives: Memory Loss

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.

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

 

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.