Sep
28
2013

Sleepless Nights

Sleeping problems (insomnia) are very common. About 10% of the population suffers from chronic insomnia; 30% of the population suffers from occasional sleep problems. In a large outpatient population of a clinic consisting of 3500 patients who had at least one major clinical condition, 50% complained of insomnia, 16% had severe symptoms, 34% had mild symptoms (Ref.1). Insomnia is more common among women, and older people as well as in people with medical or psychiatric illnesses. Long-term studies have shown that the same insomnia problems persist throughout many years. It is not possible to offer a simple remedy for insomnia, because insomnia is a complex problem. Here I will discuss some of the causes of insomnia and also discuss some of the treatment options.

Symptoms of insomnia

The person who suffers from insomnia will usually state that they have problems falling asleep. Worries of the day suddenly circulate through their thoughts and they toss and turn nervously looking at the clock from time to time and getting more and more anxious that they cannot sleep. Others fall asleep OK, but in the middle of the night they wake up perhaps to visit the restroom, but then they cannot go back to sleep. Others wake up 2 hours before their normal alarm clock time and they feel their stomach rumbling making it impossible to fall back to sleep. Older people with chronic diseases and general poor health suffer more from insomnia. In this setting insomnia may be more related to the underlying disease rather than old age. Psychiatric disorders also are associated with more insomnia. Treat the underlying psychiatric illness, and the insomnia disappears.

Although insomnia is a sleep disturbance during the nighttime, people who are affected with this complain of daytime fatigue, of overstimulation, yet they catch themselves making frequent mistakes, and their inability to pay attention gets them involved in accidents and falls. Longitudinal studies have shown (Ref. 1) that people with chronic insomnia are more likely to develop psychiatric disease, such as major depression,  anxiety disorder and alcohol and substance abuse. Unfortunately these disorders can by themselves again cause insomnia, which reinforces chronic insomnia. Insomnia leads to poorer social and physical functioning, affects emotions, leads to a lack of vitality and physical endurance, contributes to worsening of pain and can affect general and mental health.

Research about insomnia

Much has been learnt from sleep studies using polysomnography monitoring during a full night’s sleep. These studies have been used mainly as a research tool. In such studies eye movements, brain wave activity, muscle activity, chest movements, airflow, heart beats, oxygen saturation and snoring (with a microphone) are all simultaneously recorded. This way restless leg syndrome, sleep apnea, snoring, seizure disorders, deep depression etc. that can all lead to insomnia can be diagnosed and separated from insomnia. The stages of sleep (wakefulness, stage 1 to 3 sleep and the REM sleep stage) can also be readily measured using polysomnography (Ref.2). According to this reference the majority of insomnia cases do not need this complex procedure done.

Sleepless Nights

Sleepless Nights

Causes of insomnia

Traditionally insomnia cases are classified into primary insomnia and secondary insomnia. Secondary insomnia is caused by all of the factors discussed below. When they are dealt with, we are left with cases of primary insomnia.

The following medical conditions can cause insomnia: heart disease, pulmonary diseases like asthma and chronic obstructive pulmonary disease (COPD); gastrointestinal disease like liver cirrhosis, pancreatitis, irritable bowel syndrome, ulcers, colitis, Crohn’s disease; chronic kidney disease; musculoskeletal disease like arthritis, fractures, osteoporosis; neurodegenerative disease like MS, Parkinson’s disease, Alzheimer’s disease; endocrine disease like diabetes, hyper- or hypothyroidism, adrenal gland fatigue and insufficiency; and chronic pain conditions. Also, psychiatric conditions like major depression, schizophrenia and anxiety disorders can cause insomnia.

This list in not complete, but it gives you an idea of how complex the topic of insomnia is.
The physician who is seeing a patient with insomnia needs to rule out any of these other causes of insomnia to be certain that the only condition that is left to treat in the patient is insomnia itself. The other diagnoses have to be dealt with separately or else treatment of insomnia will fail.

Ref. 1 points to a useful model of how to think about causation of insomnia: there are three points to consider, namely predisposing, precipitating, and perpetuating factors. Let’s briefly discuss some of these.

Predisposing factors

We are all different in our personal make-up. If you are well grounded, chances are you are not susceptible to insomnia. Anxious persons or persons who have been through a lot of negative experiences in life will have personality traits that make them more prone to insomnia. Lifestyle choices such as late nights out, drinking with the buddies in a bar (extreme circadian phase tendencies) will have an impact on whether or not you develop insomnia.

Precipitating factors

A situational crisis like a job change or the death of a loved one can initiate insomnia.  However, there could be a medical illness such as a heart attack, a stroke or the new diagnosis of a psychiatric illness that has become a precipitating factor. Sleep apnea and restless leg syndrome belong into this group as well as would the stimulating effect of coffee and caffeine containing drinks. Jet lag and nighttime shift work can also be precipitating factors.

Perpetuating factors

Daytime napping to make up for lost sleep the night before can undermine sleep initiation the following night, which can lead to a vicious cycle. Similarly, the use of bedtime alcoholic drinks leads to sleep disruption later that night and can become a perpetuating factor, if this habit is maintained. Even the psychological conditioning of being anxious about whether or not you will fall asleep easily or not the next night can become a perpetuating factor.

I will return to this classification and the factor model of causation of insomnia when we address treatment options.

Drugs that can cause insomnia

One major possible cause for insomnia  can be side effects from medications that patients are on (would belong to the ‘perpetuating factors’ among causes). Physicians call this “iatrogenic insomnia”. The antidepressants, called selective serotonin reuptake inhibitors (SSRI’s) like Prozac are particularly troublesome with regard to causing insomnia as a side effect. Other antidepressants like trazodone (Desyrel) are used in small doses to help patients with insomnia to fall asleep. Some asthmatics and people with autoimmune diseases may be on prednisone, a corticosteroid drug. This can cause insomnia, particularly in higher doses; so can decongestants you may use for allergies; beta-blockers used for heart disease and hypertension treatment; theophylline, an asthma medication and diuretics. Central nervous stimulants like caffeine or illicit drugs can also cause insomnia. Hormone disbalance in general and hyperthyroidism specifically as well as Cushing’s disease, where cortisol levels are high will cause insomnia.

Treatment of insomnia

So, how should the physician approach a patient with insomnia? First it has to be established whether there is secondary insomnia present due to one of the predisposing, precipitating or perpetuating factors. In other words, is there secondary insomnia due to other underlying illnesses? If so, these are being addressed first. Lifestyle choices (staying up late every night) would have to be changed; alcohol and drug abuse and overindulging in coffee or caffeine containing drinks needs to be dealt with. Cognitive therapy may be beneficial when mild depression or anxiety is a contributing factor to insomnia.

The remaining insomnia (also medically termed “primary insomnia”) is now being treated.

The following general points are useful to get into the sleeping mode (modified from Ref. 3):

  1. Ensure your bedroom is dark, soundproof, and comfortable with the room temperature being not too warm, and you develop a “sleep hygiene”. This means you get to sleep around the same time each night, have some down time 1 hour or so before going to bed and get up after your average fill of sleep (for most people between 7 to 9 hours). Do not sleep in, but use an alarm clock to help you get into your sleep routine.
  2. Avoid caffeine drinks, alcohol, nicotine and recreational drugs. If you must smoke, don’t smoke later than 7PM.
  3. Get into a regular exercise program, either at home or at a gym.
  4. Avoid a heavy meal late at night. A light snack including some warm milk would be OK.
  5. Do not use your bedroom as an office, reading place or media center. This would condition you to be awake.  Reserve your bedroom use only for intimacy and sleeping.
  6. If you wake up at night and you are wide awake, leave the bedroom and sit in the living room doing something until you feel tired and then return to bed.
  7. A self-hypnosis recording is a useful adjunct to a sleep routine. Listen to it when you go to bed to give you something to focus on (low volume) and you will find it easier to stop thinking.

Drugs and supplements for insomnia

1. In the past benzodiazepines, such as diazepam (Valium), lorazepam (Ativan), fluorazepam (Dalmane), temazepam (Restoril), triazolam (Halcion) and others were and still are used as sleeping pills. However, it was noted that there are significant side effects with this group of drugs. Notably, there is amnesia (memory loss), which can be quite distressing to people such as not remembering that someone phoned while under the influence of the drug, you promised certain things, but you cannot remember the following morning what it was. Another problem is the development of addiction to the drugs with worse insomnia when the drugs are discontinued. Many physicians have stopped prescribing benzodiazepines.

2. There are non-benzodiazepines drugs that are used as sleeping pills (hypnotics), such as Zaleplon (Sonata), Zolpidem (Ambien) and Eszopiclone (Lunesta).  They seem to be better tolerated.

3. Ramelteon, a melatonin agonist, is available by prescription in the US. It probably is the best-tolerated mild sleeping pill and works similar to melatonin, but is more expensive. Chances are that your physician likely would prescribe one of the non-benzodiazepines drugs or Ramelteon for you as they do not seem to be addicting.

4. However, there is an alternative: Many patients with insomnia tolerate a low dose of trazodone (Desyrel), which is an antidepressant with sleep restoring properties. A low dose of 25 to 50 mg at bedtime is usually enough for insomnia. This allows the patient to fall asleep within about 30 minutes of taking it, and sleep lasts through most of the night without a hangover in the morning. Many specialists who run sleep laboratories recommend trazodone when primary insomnia is diagnosed. However, this is still a drug with potential side effects as mentioned in the trazodone link, but 50 mg is only ¼ of the full dose, so the side effects will also be less or negligible.

5. I prefer the use of melatonin, which is the natural brain hormone designed to put us to sleep. Between 1 mg and 6 mg are sufficient for most people. We know from other literature that up to 20 mg of melatonin has been used in humans as an immune stimulant in patients with metastatic melanoma with no untoward side effects other than nightmares and some tiredness in the morning. A review from the Vanderbilt University, Holland found melatonin to be very safe as a sleeping aid. There are several melatonin receptors in the body of vertebrates (including humans), which are stimulated by melatonin.

6. Other natural methods are the use of L-Tryptophan at a dose of 500 mg at bedtime, which can be combined with melatonin. It is the amino acid contained in turkey meat, which makes you tired after a Thanksgiving meal. GABA is another supplement, which is the relaxing hormone of your brain, but with this supplement tolerance develops after about 4 to 5 days, so it is only suitable for very short term use. Herbal sleep aids are hops, valerian extract and passionflower extract. They are available in health food stores.

Conclusion

A lack of sleep (insomnia) is almost a given in our fast paced lives.

When it comes to treatment, all of the other causes of secondary insomnia need to be treated or else treatment attempts would fail. What is left is primary insomnia. This is treated as follows:

We need to review our sleeping habits, lifestyles and substance abuse. Remove what is detrimental to your sleep. Start with the least invasive treatment modalities such as self-hypnosis tapes, melatonin, L-Tryptophan or herbal extracts. Should this not quite do the trick, asks your doctor for advice. The non-benzodiazepines drugs or Ramelteon would be the next level up. It may be that an alternative such as low dose trazodone would be of help. Only, if all this fails would I recommend to go to the more potent sleeping pills (keep in mind the potential for addiction to them).

References

1. David N. Neubauer, MD (John Hopkins University, Baltimore, MD): Insomnia. Primary Care: Clinics in Office Practice – Volume 32, Issue 2 (June 2005)  © 2005, W. B. Saunders Company

2: Behrouz Jafari, MD and Vahid Mohsenin, MD (Yale Center for Sleep Medicine, Yale University School of Medicine, New Haven, CT, USA): Polysomnography. Clinics in Chest Medicine – Volume 31, Issue 2 (June 2010), © 2010 W. B. Saunders Company

3. Jean Gray, editor: “Therapeutic choices”, 5th edition, Chapter 8 by Jonathan A.E. Fleming, MB, FRCPC: Insomnia, © 2008, Canadian Pharmacists Association.

Last edited Sept. 28, 2014

Aug
17
2013

Postpartum Depression

Recently there has been a lot of publicity around the topic of postpartum depression (PPD). Typically the reports originate from a case where depression led to catastrophic consequences. It is sad that it often takes a tragedy before a problem like this is publicly more acknowledged. But sadly reports are often one-sided and are missing vital information about pre-existing risk factors. The family doctor often misses the diagnosis of postpartum depression. There is often denial on behalf of the mother and family. The mother is getting no support from support groups, even though there are such groups.

Swift treatment often not given

And swift treatment that would be available is often not given. The results are finally making headlines. Once a mother is desperate and deeply depressed (“psychotic depression”) she is capable of killing the baby, herself and others who are close. PPD affects 15% of mothers (Ref.1); a small percentage of them may have postpartum psychosis, which is the most severe form of PPD.

Risk factors for postpartum depression

Ref. 1 reviews  several risk factors that can lead to postpartum depression. For instance, a history of a major depressive episode or anxiety attack during the pregnancy predisposes a young mother to develop PPD. However, there may also have been a history of dysphoria (intense feeling of discontent) before her periods in the past; stressful events during the pregnancy or right after birth. Often there is poor social support or a marital conflict. Other factors are low income, young maternal age or immigrant status with deprivation. A lack of support from the partner can also be a major factor.

Up to 85% of women experience postpartum blues within the first 10 days after the delivery of the baby. Symptoms such as mood swings, fatigue, confusion, tearfulness, mild elation and irritability are common during these initial days following her delivery.

Progesterone levels decreased up to 3 months

Researchers found a decrease in progesterone levels following delivery for at least one month, sometimes up to 3 months. This leads to sleep problems (insomnia), which coupled with the baby crying in the middle of the night causes more sleep disruption. Electroencephalography studies documented abnormal brain wave patterns in women following the birth of a child.

Only 1 in 500 mothers after birth develop what physicians call “postpartum psychosis”, which is a recognized psychiatric emergency.  The symptoms here are extreme mood swings with confusion, poor judgment, disordered thoughts (“delusions”), paranoia (where they think that someone is after them or it is the baby’s fault that they feel that way).

Erratic behavior and impaired functioning

Erratic behavior and impaired functioning are also part of this symptom complex. It is this state that needs to be monitored in a psychiatric unit as it is associated with a high suicide and homicide rate. A psychiatrist with experience in treating PPD needs to treat the patient.

Urbanization leads to a lack of support, which is particularly devastating to new mothers who need all the support they can get. This is reflected in a higher percentage of PPD in urban areas versus the percentage of PPD in more rural areas where there is more family support.

 

Postpartum Depression

Postpartum Depression

Hormone changes with postpartum depression

Some people do not understand why a woman who just had a baby would not be happy and content. Most women are. However, the stress from the pregnancy and from childbearing can be too much on her system. There can be a point where the hormones no longer are in balance and the young mother loses her coping mechanisms.

Serotonin concentrations in the brain of women during pregnancy are at a higher level due to higher estrogen levels that slow down the degradation of serotonin. Serotonin is the brain hormone that makes you feel good. Estrogens and progesterone are very high during the pregnancy, but this changes right after the baby’s delivery and during the time of recovery in the first few days and weeks. Studies showed that there was a 15% higher thyroid autoantibody rate in postpartum depression patients in comparison to controls without depression.

Patients with higher thyroid autoantibody rates respond to thyroid

Patients with thyroid autoantibodies associated weakly with postpartum depression and responded favorably to thyroid replacement therapy. Progesterone levels were much lower in patients with depression and in patients without depression following delivery. The reason for this likely is the fact that with the delivery the placental source of natural progesterone disappeared. Researchers replaced progesterone in a group of patients, but they die not observe any significant improvement of PPD. However, they did not explain whether the progesterone replacement involved bioidentical hormones or synthetic hormones.

Dr. Michael Platt described a case of a postpartum woman who was hypothyroid as well (Ref.2). She responded to hormone replacement with thyroid hormones and progesterone by shedding 60 pounds (she always had a weight problem) over 10 months changing from a size 20 to a size 4. She was able to wean herself off the anti-depressants.

Breast feeding women on bioidentical progesterone

In breast feeding women this could be a significant difference as women on bioidentical progesterone can breast feed and will positively influence their breast-fed child’s brain development (brain cells have a lot of progesterone receptors, which are stimulated by progesterone).

A recent Canadian study involving pregnant women and women after delivery of their babies showed that there was a significant drop of progesterone levels in saliva samples for several weeks, particularly with breast feeding. The authors explained that the lack of ovulation with a lack of progesterone synthesis in the ovaries was responsible for this. It takes several weeks for most women to regain regular menstrual cycles. It would follow from this that there is room for bioidentical progesterone replacement in the first few months of the postpartum period until the ovaries have resumed their normal cyclical hormone activity.

Conventional treatment for postpartum depression

With baby blues the symptoms are much less severe (in comparison to PPD) and are starting 2 to 3 days after childbirth, resolving spontaneously within 10 days after delivery. PPD occurs within 3 months following delivery and responds to treatment with antidepressants and psychotherapy such as cognitive behavioral therapy.  Breast feeding needs to be stopped, as it is known that metabolites of the antidepressants end up in breast milk. Typically, a less toxic antidepressant is used like paroxetine (Paxil), otherwise citalopram (Celexa), and fluoxetine (Prozac). In the rare cases where PPD is so severe that psychotic symptoms are present (postpartum psychosis) hospitalization is mandatory (Ref.3). Some of these cases may require electroconvulsive therapy (ECT) and/or lithium treatment for mood stabilization. Thyroid hormone therapy has also shown a beneficial effect in treating antidepressant-resistant cases of PPD (Ref.4).

Alternative treatment of postpartum depression

Although review texts of the treatment of PPD mention that estrogen replacement in postnatal women with PPD was beneficial, there is a warning that this could cause blood clots and anticoagulant measures would have to be combined with this to prevent deep vein thrombosis. Researchers suggested progesterone replacement, which is a treatment modality where blood clots are no danger. However, there are no formal trials yet, so most medical professionals ignore this suggestion. Here is forum of women who have taken postpartum progesterone with positive effects.

Dr. Katherina Dalton published a trial involving 30 PPD patients with a positive response rate of 95% when treated with natural progesterone.

Bioidentical progesterone treatment reduces symptoms of postpartum depression

Before treatment patients were suffering from an average of 7.57 symptoms, after the treatment only 2.1 symptoms remained. (Figures with details regarding this study under the above link).

There are many descriptive observations without controls like this where natural progesterone creams are part of a holistic approach to treating PPD. Dr. Mercola describes here how useful natural progesterone therapy can be. He also cautions that the woman should take bioidentical progesterone cyclically to mimic nature’s biorhythm to allow progesterone receptors to recover in between treatments.

There are many websites that have useful information about natural progesterone cream treatment for PPD, such as this.

Conclusion

It is common sense that a woman may need natural progesterone following a delivery. She just gave birth to her placenta, which was a virtual progesterone factory. It  protected her body and the baby’s brain all throughout the pregnancy. If women decided to use natural progesterone for 3 to 6 months, this would make a big difference.  The majority of women would not experience the baby blues or PPD. Eventually regular menstrual cycles return, the patient’s own ovarian progesterone production resumes and there no longer is a need for progesterone cream until after the birth of the next child or at the arrival of menopause. Medicine is full of examples where common sense was applied for effective treatment options despite missing randomized studies.

Natural progesterone treatment of PPD

Natural progesterone treatment of PPD is one such example. Physicians used bioidentical progesterone intuitively, but it worked in many patients. The progesterone receptors do not distinguish whether or not researchers did a clinical trial. But they do not like the synthetic versions of progesterone, as they block the receptors leading to progesterone deficiency.  The physician can combine natural progesterone treatment with traditional treatments of PPD.

More information on postpartum depression: http://nethealthbook.com/mental-illness-mental-disorders/mood-disorders/postpartum-depression/

References

1.Teri Pearlstein, MD, Margaret Howard, PhD, Amy Salisbury, PhD and Caron Zlotnick, PhD: “Postpartum depression” : American Journal of Obstetrics and Gynecology – Volume 200, Issue 4 (April 2009)

2. Dr. Michael E. Platt: The Miracle of Bio-Identical Hormones; 2nd edition, © 2007 Clancy Lane Publishing, Rancho Mirage, Ca/USA (p.53-55).

3. Bope & Kellerman: Conn’s Current Therapy 2013, 1st ed.© 2012 Saunders

4. Jacobson: Psychiatric Secrets, 2nd ed. © 2001 Hanley and Belfus

May
18
2013

Treatment For Alzheimer’s Failed, But Prevention Succeeds

Recently another news story about a failed drug against Alzheimer’s disease (AD) went through the news media as shown in this link.

Donepezil, galantamine, rivastigmine and memantine are the most common drugs used to attempt to treat Alzheimer’s as this review explains. None of these drugs are a real breakthrough with regard to truly curing AD, as the drugs only achieve a few months of delay in the eventual deterioration of the AD patient’s symptoms. On the other hand there is an overwhelming accumulation of data in the last few years showing that many different factors can prevent AD and dementia. Below I am reviewing all these preventative factors and steps.

Genetic and epigenetic factors in Alzheimer’s disease

Early onset Alzheimer’s disease occurs between 30 and 60 years of age. It is due to a genetic predisposition (mutations on genes of chromosomes 1, 14 and 21). Only about 5% of all AD cases are caused this way. The remaining 95% of Alzheimer’s cases are due to late-onset Alzheimer’s disease. Here the causation is due to a combination of genetic, environmental and lifestyle factors. One genetic risk factor in this group is important, namely the apolipoprotein E gene (APOE), which is located on chromosome 19. There are several forms of APOE as this review explains. It also states that there is so much variation between the various APOE forms and even the worst form of this does not necessarily mean that the person who has this will come down with late-onset Alzheimer’s disease. So APOE is presently only used in research projects. Your doctor will only order genetic tests in people who have a strong family history of early onset AD.

There is another genetic marker, the CYP46 gene that was found to be present in some late-onset AD patients. If it is combined in a patient with the APOE gene, there is a much higher chance of developing AD as this review shows.

Epigenetic factors are probably more important than genetic factors for most cases of late-onset AD, as this review explains. Another review came to the same conclusion.

What are epigenetic factors? Exercising, replacing missing hormones, using a calorie restricted, only 15-20% fat containing diet; and taking supplements as listed below that will keep harmful genes in the “off” position and protective genes in the “on” position. Taking these preventative steps is probably more powerful than using any of the presently available medications mentioned above.

Treatment For Alzheimer’s Failed, But Prevention Succeeds

Treatment For Alzheimer’s Failed, But Prevention Succeeds

Exercise, diet, control blood pressure

As already mentioned, these are some of the powerful epigenetic factors that will prevent AD down the road. Controlling blood pressure has long been known to improve cognitive function. It is now evident that there seems to be a problem with microcirculation in brain tissue before it comes to neurodegenerative changes of AD and the underlying deficiency in nitric oxide production in the lining of the diseased arteries. Other research has shown that a lack of nitric oxide (NO) production is also the underlying problem with hypertension.

Green vegetables such as kale, spinach, also cabbage varieties and red beets are a source of nitric oxide and have also been shown to prevent AD at the same time.

Add to this exercise and you have a winning combination for the prevention of AD. You guessed right: exercise increases NO production from he lining of your arteries. When people age their lining of the arteries does not produce as much NO as in younger years. However, there is a supplement available, Neo40 Daily, that can be taken twice a day to compensate for this.

Here is another report about a 30% to 40% reduction in the incidence of AD when people do regular, simple exercises.

More good news about fruit and vegetables: tomatoes, watermelons, pink guava, pink grapefruit, papaya, apricot and other fruit all contain lycopenes, which have been shown to prevent AD.

Recently a new testing tool in combination with a PET scan of the brain has been developed, which may help the treating physicians to assess improvement or deterioration of an AD patient objectively using this method. However, this is still considered to be only a research tool at this time.

Supplements to prevent Alzheimer’s disease

The following brain-specific nutrients play a part in the prevention and treatment of AD (according to Ref.1):

1. B-vitamins: they are important to support the energy metabolism of brain cells.

2. Vitamin C: this has antioxidant properties and prevents brain cells and supportive glia cells from oxidizing.

3. Vitamin E in the form of mixed tocopherols: together with vitamin C has been shown to prevent Alzheimer’s disease

4. Phosphatidylserine (PS), with an intake of up to 300mg/day: counteracts and prevents memory loss.

5. Coenzyme Q10 (ubiquinone), 100mg/day (it would be safe to take 400 mg per day, which is also cardio protective): stabilizes the mitochondria of brain cells and heart muscle cells. It is a powerful neuroprotective agent and supports ATP production (energy metabolism of brain cells).

6. Ginkgo (Ginkgo biloba), at a dose up to 240mg/day: increases micro vascular circulation, neutralizes free radicals from oxidation and improves short-term memory.

7. Omega-3 fatty acid and DHA, 1500mg/day: has anti-inflammatory properties.

Other nutrients that hold promise are:

8. Huperzine A, 100 to 200mg/day: natural anticholinesterase inhibitor, derived from the Chinese club moss, surpasses donezepil according to studies by doctors in China

9. Vinpocetine, 2.5 to 10mg/day: comes from the periwinkle plant, increases cerebral blood flow and stimulates brain cell metabolism

10. Turmeric extract (curcumin) is very beneficial in reducing tau protein deposits in AD.

All these statements and dosages are cited from Ref.1.

Hormones to prevent Alzheimer’s disease

According to Ref. 1 there are certain hormones that can prevent AD: DHEA, pregnenolone, estrogen (bioidentical estrogen only).

  1. DHEA is persistently low in AD patients and replacement with DHEA at 50 mg daily has shown improvements in muscle strength and energy of AD patients.
  2. Pregnenolone has been shown to be a powerful memory enhancer in animals and humans alike.
  3. Estrogen, if taken as bioidentical estrogen cream (Bi-Est) can improve brain function. Estrogen is a strong epigenetic switch that keeps a woman mentally younger for longer, but has to be balanced with bioidentical progesterone cream to prevent breast cancer and uterine cancer. A study showed that estrogen replacement early in menopause will cut down on the heart attack rates, but it is also known, particularly when given as bioidentical hormone cream to prevent AD.
  4. In addition progesterone has been described to be of value in the aging woman to preserve brain metabolism.
  5. Testosterone is known to protect against Alzheimer’s disease in the aging male.
  6. Melatonin at a starting dose of 1 mg to 3 mg at bedtime often helps to restore the disturbed sleep pattern, but also augments the effects of the other hormones (Ref.1).

Removal of toxins, particularly mercury

Mercury is extremely toxic in minute amounts and affects brain cells preferentially. Intravenous vitamin C/glutathione treatments as described in this blog will remove mercury from your system including the brain.

It may take 20 to 30 such treatments in weekly intervals followed by a maintenance program every two to three weeks to remove mercury from the body.

Other heavy metals can accumulate in the brain as well and must be removed. This is described here in more detail.

Conclusion

There have been major breakthroughs in prevention of Alzheimer’s disease and dementia over the past few years, many unnoticed by the media. The search is still on for an effective drug that would treat AD when it is present. However, this may be 10 or 15 years away and we cannot afford to wait that long. Instead I suggest that people should embrace the concept of preventing AD by using as many of the factors described above. Both at the 2011 and the 2012 Anti-Aging Conferences in Las Vegas several speakers pointed out that a combination of several preventative factors will be much more effective than one factor alone and they estimated that about 80% of AD could be prevented this way.

References

Ref.1. Rakel: Integrative Medicine, 3rd ed., Copyright © 2012 Saunders, An Imprint of Elsevier. Chapter 9 – Alzheimer Disease. Integrative Medicine: “Kirtan Kriya, Telomeres, and Prevention of Alzheimer Disease”, by Dharma Singh Khalsa, MD

Last edited Dec. 18, 2014

Dec
29
2012

Avoid Mistakes by Looking at the Brain Carefully

Introduction

In mid December 2012 I attended a conference, which taught me to avoid mistakes by looking at the brain carefully. Doing this avoids missed diagnoses and treatment failures. In midf December 2012 I attended a medical conference in Las Vegas. The American Academy for Anti Aging Medicine organizes this annual event and provides fascinating topics. It gives information about the newest diagnostic methods and presents treatment options that reach beyond the borders of conventional medicine. One morning lecture, which took place on December 14, 2012 was given by Dr. Daniel Amen. It was an unforgettable session for the large audience, which filled the main auditorium. Dr. Amen is a psychiatrist, and he explained in detail the importance of a correct diagnosis for psychiatric problems. One diagnostic tool is the SPECT scan.

SPECT scan as a tool for psychiatric patients

It is not just some sophisticated scanning method that shows interesting images of the brain. But it provides detailed information, which part of the brain has an abnormality. As a result, a trained specialist will be able to classify, which treatment option would yield the best result to help the patient who may have a form of depression or other psychiatric disorder. A pill such as Prozac is not the miracle cure for all forms of depression! Detailed scan information prevents treatment failures. This can make a big difference in a patient’s life as he/she can lead a healthy and productive life.  However, contrast this to a patient who did not receive help, is in an institution, hurt others, killed in a rage or took his own life.

Look At The Brain To Avoid Missed Diagnoses and Treatment Failures

Avoid Mistakes by Looking at the Brain Carefully

Application of SPECT scans

The SPECT scan depicted here is from a patient who suffered from Lyme disease, but his treating physicians at first did not believe him. It was only after the abnormal SPECT scan on the left that further more sophisticated tests did prove Lyme disease was present and extensive antibiotic treatment cured the lad (normal SPECT scan on the right).

A case of a “conduct disorder”

Mental problems present in frightening ways, as the lecturer explained in the case of a young boy with behavioral changes that were terrifying to his family. Previously an easy-going lad, he turned into a challenge for his family and his teachers. He bounced from specialist to specialist. They diagnosed him with various conditions. The specialists stated that he was manipulative and attention-seeking. They also assumed that he was hyperactive and had a learning disability. The term conduct disorder also came up for discussion. But nothing of that helped to improve the situation. The parents felt like they were losing their child that was on a downhill course and on a destructive path.

SPECT scan helped to solve the “conduct disorder”

Finally, a SPECT scan did reveal a previously overlooked condition: the boy had a cyst on the frontal lobe of his brain. It looked like a trench that prevented the frontal brain to communicate with the rest of the brain.  He did need surgery in order to remove the enlarging cyst (pull down to see images), which was not an easy surgical procedure. However, the scan result led to the identification of the problem. This patient – in the meantime a young adult – is no longer troubles with psychiatric problems. He holds a job, has good interpersonal relationships and functions like any normal individual of his age group. Overlooked, undiagnosed and not properly treated mental disease robs people of their ability to lead full and productive lives. Patients with mental illness also represent a large number of the prison population.

Distorted mind of shooters

The lecturer briefly stopped and mentioned that we may have heard of the tragic and unfathomable events in a Connecticut school. A 20-year old shooter killed 20 (we all know this now as the Sandy Hook Elementary School shooting in Connecticut). A somber silence settled over the audience. As most of them had been attending conference lectures all morning, they had not heard about the school shooting and would see the shocking details on the news channels only later that day. For a whole nation December 14, 2012 will be etched into memory as a day of horror, of evil, lives destroyed and hearts broken.

Importance of detecting  and treating mental disorder early

For those who attended this lecture they will be reminded permanently that mental disorders need effective diagnoses and persistent treatment. Mental illness was hiding  behind closed doors in the past. It  was a source of embarrassment and shame, and denial was common in order to keep a pleasant facade. The consequences can be a source of terrible suffering.  This starts with the patient and his family. But as seen a few days earlier it reaches into the community and beyond.

More information on mental illness: http://nethealthbook.com/mental-illness-mental-disorders/

 

May
01
2008

Tree Pollen Connected With Mood Disorders

Seasonal affective disorder (SAD) does have its grip on people who react to a lack of sunlight in the winter month. As a result depression in the winter season is not uncommon. Some people just report it as feeling “down” and “tired” or report a lack of energy. Despite all the reports about SA, epidemiological studies have shown that the rate of depression is not the highest in dreary months like January or February but it spikes in the months of April and June. Dr.Teodor Postolache, a psychiatrist at the University of Maryland made a recent presentation at a meeting of the American Acadamy of Allergy, Asthma and Immunolgy delving into the reason for this finding. He compared the exposure of tree pollen which triggers a cytokine release to a tsunami.Virtually no outdoor allergens are present in the winter months, but with the release of tree pollen people who are vulnerable to allergies are exposed to massive amounts of allergens. The released cytokines may affect brain function and behaviour, resulting ultimately in changed cortisol levels and an altered serotonin metabolism. After breathing the cytokines are already released in the nose and they can continue their action in the prefrontal brain area where the centers for mood, anxiety and impulsivity are located. Dr. Postolache and his colleagues confirmed that individuals with a history of allergy and asthma had a 2.5 fold of suicide compared to controls and those with allergic rhinitis had a 1.7 fold higher risk.

Tree Pollen Connected With Mood Disorders

Tree Pollen Connected With Mood Disorders

For the first time it could also be demonstrated that cytokine levels in suicide victims were significantly elevated in the orbitofrontal cortex, the brain area that affects mood. Intranasal corticosteroids in the form of nosedrops can bring significant relief to allergy sufferers, and Dr. Postolache and his team will examine the benefits of intranasal corticosteroids closer  in a clinical study. Whereas systemic corticosteroids have shown a negative impact on mood disorders and depression, the local application of a nasal spray or drops is geared to abolish the pathways from the nose to the brain for the inflammatory cytokines.

More information on seasonal rhinitis: http://nethealthbook.com/ear-nose-and-throat-diseases-otolaryngology-ent/nose-problems/allergic-rhinitis/

Reference: The Medical Post, April 1, 2008, page 1, 34

Last edited November 3, 2014

Sep
01
2007

Emotional Distress Impairs Cognitive Function

Stress has been linked to numerous medical conditions, such as heart disease, stomach problems and muscle spasm. Stress also has been quoted as a silent killer.

Research in the field of Alzheimer’s has shown that negative emotions and chronic distress are associated with increased vulnerability to this disease.

Study author Dr. Robert Wilson of the Rush’s Alzheimer’s disease Center in Chicago has found that people most prone to psychological distress were 40% more likely to develop mild cognitive impairment (MCI) than the group that is least distress prone.

Dr. Wilson stated that these individuals would not necessarily see a psychiatrist to help them deal with their negative emotions. It becomes clear, however, that persistent negative emotional states truly impact the physical well being, and also the cognitive status. For this reason more medical attention should be given to an older patient with emotional problems and even mild depression.

Emotional Distress Impairs Cognitive Function

Emotional Distress Impairs Cognitive Function

It can become a treatment challenge, if there are personality traits or deeply entrenched behavior patterns that may not respond well to treatment. By understanding the biological link between chronic distress and loss of cognitive function in old age, early intervention can be a way to delay symptoms or to prevent disease onset.

More information on Alzheimer’s: http://nethealthbook.com/neurology-neurological-disease/alzheimers-dementia-and-delirium/

Reference: The Medical Post, August 7, 2007, page 53

Last edited November 3, 2014

Aug
01
2007

Nicotine Addiction Found More Often in Impulsive Behavior

Why do major depression and nicotine addiction often occur together in middle aged people? This is what Dr. Qiang John Fu, assistant professor of community health in biostatistics at Saint Louis University School of Public Health, asked himself and he conducted a study involving 3,360 pairs of middle-aged, predominantly Caucasian twins to find out. Twin studies are a powerful tool to sort out environmental factors from genetic factors. In this particular study the twins had served in the Vietnam war and 45% were fraternal, the rest were identical twins. With identical twins 100% of the genes are identical while the fraternal twins share about half of the genes.

The researchers found that a group of twins who were addicted to nicotine also had a behavioral disorder, called conduct disorder. This can be well defined with psychological tests and is characterized by behaviors such a stealing, fighting, vandalizing, running away from home and drug addiction (including addiction to nicotine). They were also the ones who were much more vulnerable to develop major depression.  As published in the June issue of Twin Research and Human Genetics Dr. Fu, MD, PhD, the lead researcher explained that he found a set of genes that are responsible for the development of major depression and for addiction to nicotine.

Nicotine Addiction Found More Often in Impulsive Behavior

Major depression and nicotine addiction are linked through a gene

These individuals attempt to self-treat depression with cigarette smoking. Linked with this can also be the conduct disorder mentioned above.  These findings may lead to newer approaches in terms of treatment.

Reference: June issue 2007 of Twin Research and Human Genetics

Last edited December 5, 2012

Mar
01
2007

Check For Vitamin B12 Deficiency In Elderly

Elderly patients frequently are seen at the doctor’s office because they are “feeling poorly”. Concerned family members mention that there is lack of energy, and mental impairment may also be present. Immediately there may be the question, whether these are symptoms of Alzheimers disease. The other observation may be that the older person is not eating properly. Family physicians will order laboratory tests including vitamin B12 levels. If a deficiency is shown, patients will be advised to take a vitamin supplement, and they may receive injections of vitamin B12.
The unfortunate fact is that vitamin B 12 levels are notoriously unreliable in the diagnosis of deficiency. As early as 1988 a publication in the New England Journal of Medicine showed that neuropsychiatric disorder due to vitamin B12 deficiency can be present in a patient who had normal blood levels and no other findings. It does take some other avenues to detect the deficiency. The blood can be tested for the metabolite called MMA (methylmalonic acid) which is raised with vitamin 12 deficiency. A second test is the measurement of HTC (holotranscobalamin), which is the fraction of vitamin B12 bound to the plasma protein transcobalamin, which delivers the vitamin to the tissues of the body.
Dr. Cherie McCracken and colleagues from the department of psychiatry at Liverpool University, England studied 42 men and 42 women ages 69 to 93.They were tested for cognitive functions like orientation, language, attention and memory. In addition researchers took measurements of the MMA and HTC, the tests mentioned above. None of the test persons had dementia due to the selection criteria, but 31% were cognitively impaired. Mental scores indicating cognitive impairment were associated with increasing age and MMA, and the areas of language comprehension, language expression and ideation practice (translating an idea into an action) were affected.

Check For Vitamin B12 Deficiency In Elderly

Check For Vitamin B12 Deficiency In Elderly

The reason for the correlation of MMA with impairment of brain function can be explained by the fact that MMA is toxic to the oxidative function of mitochondria. The process is like a chain reaction: when mitochondria are poisoned, the nerve cells will lack energy for proper function.
Despite this sophisticated interplay of blood levels and cell function in the brain, the message that comes from the researchers is very simple. The MMA has to be ordered as a test in elderly persons, and the next important step is supplementation with vitamin B12 to prevent deterioration in mental functioning.

More information about:

1. Causes of dementia: http://nethealthbook.com/neurology-neurological-disease/alzheimers-dementia-and-delirium/dementia/

2. Pernicious anemia: http://nethealthbook.com/anemia/anemia-from-deficient-red-blood-cell-production/megaloblastic-macrocytic-anemia/

Reference: The Medical Post, January 16, 2007, page 27

Last edited November 2, 2014

Mar
01
2007

Depression Increases Stroke Risk

Strokes have been observed mainly in the aging population, and various lifestyle factors play a role in the risks. It is generally well known that smoking is one of them. High blood pressure that is left untreated will have a stroke as a consequence. Even though in the past the development of a stroke was more commonly seen in older patients, it has become something to be reckoned with for patients that are middle aged.
While some risk factors are the same in all the age groups, researches scrutinized the age group under 65 for additional risk factors. The one that stands out is depression.
Margaret Kelly-Hayes Ed.D. and her colleagues evaluated data from the Framingham Heart Study, looking at 4,120 participants aged 29-100 years who were followed for 8 years. In the course of their research they checked for symptoms of depression by administering the Center for Epidemiological Studies Depression Scale (CES-D). If patients were taking medication for depression they were included in the study. In participants under 65 with depressive symptoms the stroke risk was found to be four times higher than in the population of the same age group without depressive symptoms.

The findings were commented on by Dr. Francisco Javier Carod-Artal, of the Sarah Hospital in Brasilia, Brazil. He found that a growing body of evidence suggests that biological mechanisms underlie a bidirectional link between depression and many neurological illnesses. Mood disorders can influence the development of disease.

Depression Increases Stroke Risk

Depressed patients 4 times more at risk of getting stroke

Pinpointing exactly why depressive symptoms are increasing the risk for strokes is a challenge. Dr. David Spiegel from Stanford (Cal.) University was interviewed and he believes that the problem is environmental as well as biologic. People who are depressed may smoke more, avoid social contact, may lack self care and neglect taking blood pressure medication.
In any event it is important to treat depression, and to take care of all the known steps in stroke prevention.

More information about:

1. Stroke prevention: http://nethealthbook.com/cardiovascular-disease/stroke-and-brain-aneurysm/stroke-prevention/

2. Depression: http://nethealthbook.com/mental-illness-mental-disorders/mood-disorders/depression/

Reference: MD Consult News, January 29, 2007

Last edited November 2, 2014

Aug
01
2006

Do Not Mix Migraine Medications With Antidepressants

Headache medications that are available over the counter in the local drugstore are ineffective when it comes to a migraine headache, and migraine sufferers have received great help from medications that are targeting a migraine attack. They are non-narcotic prescription drugs, some of which have to be injected. They are available under names like Amerge, Axert, Frova, Imitrex, Maxalt, Relpax or Zomic, and the medication group is known in pharmacists’ language as “triptans”.
The medications are generally well tolerated, but the FDA has issued a warning.
In combination with another medication group, life threatening side effects can occur.
Any patient who is receiving medication for the treatment of depression in the form of a Selective Serotonin Reuptake Inhibitor (SSRI’s) is strongly warned, not to take any of those listed triptans for migraine. The anti depressive drugs are Celexa, Fluvoxamin, Paxil, Prozac and Zoloft. Two other medications, namely Effexor and Cymbalta are Selective Serotonin/Norepinephrin Reuptake Inhibitors (SSNRI’s), and they carry the same risk when taken in combination with the triptans.
The combination of the two medications can lead to a dangerous condition known as Serotonin syndrome. It occurs when the body has too much serotonin, a chemical found in the nervous system. Serotonin syndrome symptoms may include restlessness, hallucinations, loss of coordination, fast heartbeat, and rapid changes in blood pressure, increased body temperature, overactive reflexes, nausea, vomiting, and diarrhea. Serotonin syndrome may be more likely to occur when starting or increasing the dose of a triptan, SSRI or SNRI.

Do Not Mix Migraine Medications With Antidepressants

Do Not Mix Migraine Medications With Antidepressants

It is up to the prescribing physician to carefully weigh the advantages against the serious side effects, and it can be a difficult choice, as both conditions, migraine as well as depression, need to be treated effectively. Any patient who has to take both medications has to be closely watched. The patient also has to be alert to any side effect.

Reference: FDA/Center for Drug Evaluation and Research, July 19, 2006

Link to chapter on migraines in Net Health Book: http://nethealthbook.com/neurology-neurological-disease/common-causes-headaches/migraine-headache/

Last edited Nov. 1, 2014