Nov
28
2021

Marijuana and Uncontrolled Vomiting

By | Abdominal Pain, addiction, chronic pain, heart attack, marijuana, schizophrenia

Marijuana was considered safe in the past, but now marijuana and uncontrolled vomiting suddenly make the news. Recently there also were reports of marijuana causing heart attacks and schizophrenia.

Abdominal pain with cannabis hyperemesis syndrome

Cannabis hyperemesis syndrome or cannabinoid hyperemesis syndrome (CHS) is a relatively new disease entity. It occurs in people who use marijuana daily for several years. But people affected by this condition often do not realize that it is an overdose of marijuana that brings on the nausea and vomiting of CHS. When they started marijuana use, they may have used intermittent doses of marijuana to treat nausea and vomiting. In intermittent doses marijuana may have been helpful, however constant use is a different story! During several years of use of marijuana, patients never had abdominal pains or vomiting, until one day CHS started.

Possible mechanisms regarding marijuana and uncontrolled vomiting

The body has its own endocannabinoid system with cannabinoid receptors that are distributed throughout the body. There are two cannabinoid receptors, CB1 and CB2. In the central nervous system, there are mainly CB1 receptors, in the rest of the body CB2. It appears that stimulation with intermittent small doses of marijuana suppresses nausea and vomiting in the hypothalamus area. However, constant stimulation of CB2 receptors in the gut with higher doses of marijuana are the cause of CHS. When a person develops cannabis hyperemesis syndrome, the only permanent cure is to stop marijuana use completely. This eliminates the CB2 receptor stimulation and allows the body to heal the gut. Researcher believe that Tetrahydrocannabinol, or THC is more powerful than the endocannabinoids. THC overwhelms the CB1 and CB2 receptors. When people who were cured of CHS restarted marijuana, their symptoms of nausea and abdominal pain returned.

In some people hot bath and hot showers help uncontrolled vomiting

Researchers noted that people reported how sometimes having a hot shower or a hot bath stopped the vomiting. The hypothalamus controls both body temperature and vomiting. A hot bath may send a signal to the hypothalamus, which interrupts the vomiting for a period of time. But with continued use of marijuana the vomiting reoccurs.

Increased strength of marihuana preparations

Dr. Wang, an associate professor of pediatrics at the University of Colorado Anschutz Medical Campus in Aurora, Colorado noted: “It’s been well documented that the amount of THC that now comes in cannabis is increasing substantially. In the ’90s the average was like 4% or 5%. Now in Colorado, it’s anywhere from 15% to 20%.” This means that THC causes more and more toxicity in patients.

In Colorado medical marijuana was legal since 2009 and recreational marijuana was legal since 2014. Dr. Wang researched the cannabis hyperemesis syndrome in Colorado. He found over 800,000 cases of vomiting in Colorado between 2013 and 2018. This was an increase of 29% from the time before marijuana became legal.

Symptoms of cannabis hyperemesis syndrome

The 5 most common symptoms of cannabis hyperemesis syndrome are continuous nausea, repeated vomiting, abdominal pain, weight loss because of decreased food intake and dehydration from fluid loss. Many people have several showers a day because it diminishes their nausea.

Three phases of cannabis hyperemesis syndrome

The cannabis hyperemesis syndrome often presents in 3 stages: the prodromal phase, the hyper emetic phase, and the recovery phase.

During the prodromal phase symptoms consist of nausea and abdominal pain early in the morning. The eating pattern is still normal in this phase. Some people increase their marijuana consumption as they hope to treat the nausea this way. This phase can last for months or years.

During the hyper emetic phase all of the 5 symptoms mentioned above can occur. This phase often continues until the patient gives up all marijuana consumption. This is when the recovery phase starts.

In the recovery phase the patient returns to a normal eating pattern. All of the symptoms gradually disappear. This phase lasts between days to months. But if the patient starts marijuana again, the symptoms return very quickly.

Treatment of cannabis hyperemesis syndrome

Patients who have severe vomiting require treatment in a hospital. The doctor starts intravenous fluids to treat dehydration. Some medicine to stop vomiting helps in the beginning. The physician must convince the patient to completely stop marijuana use, which helps to treat nausea and abdominal pain. Antacid medication like proton-pump inhibitors is useful to treat stomach lining inflammation. Frequent hot showers help to tone down nausea and vomiting. Hot showers seem to work via the hypothalamic brain center, which is responsible both for nausea/vomiting and heat perception. The physician may prescribe small amounts of benzodiazepams to treat anxiety.

By avoiding marijuana in any form THC, which is a powerful stimulus for CB1 and CB2 receptors gets washed out of the system. This allows the endocannabinoid system to rebalance itself. As long as the patient stays away from marijuana there is usually a complete recovery.

Marijuana and Uncontrolled Vomiting

Marijuana and Uncontrolled Vomiting

Conclusion

Since marijuana is legal in many jurisdictions the cannabis hyperemesis syndrome (CHS) occurs more and more often. Emergency teams at hospitals are kept busy treating these types of patients. It appears that CHS develops in patients who use marijuana regularly and use it in higher concentrations. Nausea and vomiting are the most common symptoms. Some patients can cope for a period of time by taking frequent hot showers. But eventually this home remedy does no longer work. A brief hospital stay may help the patient to recover from this syndrome. The patient needs to stay away from marijuana products to recover from CHS completely, otherwise there will be a relapse.

Oct
16
2021

Marijuana Causes Schizophrenia and Heart Attacks

By | addiction, heart attack, marijuana, schizophrenia, Substance abuse

Two new studies showed that marijuana causes schizophrenia and heart stacks. Marijuana use has been increasing significantly in the general population since the 1990’s. Initially many believed that marijuana would be harmless. But increasingly there are medical publications showing the opposite.

In the following I present data how the use of marijuana causes these two documented side effects, heart attacks and schizophrenia.

Schizophrenia increased since the 1990’s

A July 21, 2021 study from Denmark included all people of Denmark who were older than age 16 from January 1, 1972 to Dec. 31, 2016. The number of participants were 3 ,595 ,910 women (50.0%) and 3 ,590 ,924 men (50.0%). The total number of individuals in the study were 7,186 ,834.

Here are the figures of the percentages of cannabis related schizophrenia cases in Denmark according to the study:

  • 1995: 2% of all schizophrenia cases related to cannabis use in Denmark
  • 2000: 4% of schizophrenia cases due to cannabis use
  • 2010: 8% of all schizophrenia cases from cannabis use

The researchers found that the risk of coming down with schizophrenia heightens with increased cannabis use. Heavy users are more likely to develop schizophrenia than light users.

Cannabis use disorder

One subgroup of cannabis users are people with a cannabis use disorder. They use cannabis, but they become tolerant to it. This requires a higher dose of cannabis to achieve satisfaction. But they are unable to reduce cannabis. They spend more and more time to obtain cannabis, use it and recover from the effect. They give up other activities in favor or cannabis and they continue the use despite negative consequences. Researchers found that this group of individuals had the highest risk to develop schizophrenia. The authors of the Danish study found that patients with cannabis use disorder over the past 2 decades have increased their risk for developing schizophrenia by 3- to 4-fold. They feel it is because of the increase in use and the increase in potency of cannabis.

Heart attacks increased with cannabis use

A Canadian study assessed a cross-sectional study of 2017 and 2018.

The study in question was the American Behavioral Risk Factor Surveillance System survey of US adults. The authors zeroed into young adults (aged 18–44 yr.) with recent cannabis use and a history of a heart attack. Among 33,173 young adults there were 4,610 respondents with recent cannabis use (17.5%). 61 respondents among the recent cannabis users reported that they had a heart attack, which is 1.2%. In comparison non-cannabis users had a heart attack rate of only 0.8%. The adjusted odds ratio for cannabis users compared to non-users was 2.07. This means that the probability of getting a heart attack when using cannabis was 2.07-fold higher when compared to non-users. Also, the investigators found that a history of a heart attack had a probability of being due to cannabis use with a probability of 2.31-fold.

Cannabinoid receptors

Researchers found endogenous cannabinoids in the brain that function as messenger molecules. They need to activate their targets, the cannabinoid receptors, called CB1 and CB2. CB1 receptors are found mainly in the central nervous system. CB2 receptors are located mainly in the immune system. Reproductive organs have their own cannabinoid receptors. The lining of the uterus contains only CB1 receptors. Ovaries and testicles both use CB1 and CB2 receptors. Tetrahydrocannabinol (THC) from smoking or ingesting marijuana is the main psychoactive compound in cannabis. It stimulates these cannabinoid receptors also. But compared to the body’s own cannabinoids THC is much stronger. This leads to more pronounced effects that concern many physicians.

The overwhelming response of the cannabinoid receptors to THC leads to a blunting of the signals of the body’s own cannabinoids. This causes a breakdown in communication between neurons and body cells.

Marijuana Causes Schizophrenia and Heart Attacks

Marijuana Causes Schizophrenia and Heart Attacks

Conclusion re. marijuana causes schizophrenia and heart attacks

Legislators in Canada and many of the states in the US legalized the use of marijuana. As a result, the cannabis use in the younger age group of adults (between 18 to 44 years) has increased significantly. This means that more and more people are exposed to THC from cannabis, which overstimulates the body’s own endocannabinoid system. As explained this leads to a breakdown of communication between neurons and body cells. In time diseases like heart attacks and schizophrenia can develop, a fact overlooked by the media and the public. The overuse of marijuana leads to more than a 2-fold risk to get a heart attack and a 3- to 4-fold risk of coming down with schizophrenia. These are the facts right now. But with further increased use of cannabis researchers will likely find many other diseases that THC can trigger.

Oct
28
2017

Take Enough Vitamin D3

By | Arthritis, Cardiovascular disease, Diabetes, Heart Disease, Inflammation, Multiple sclerosis, schizophrenia, Stroke

Many people supplement with 300 to 400 IU of vitamin D3, but do they take enough vitamin D3? There is a simple way of finding out: ask your doctor to order a 25-hydroxyvitamin D blood test.   This will show whether the gut absorbed enough of the essential vitamin. It will also show whether or not your vitamin D3 capsules or tablets were strong enough. It is now generally accepted that a good range of the vitamin D blood level is between 50 and 80 ng/ml. Unfortunately many Americans who come down with various diseases have blood levels of less than 30 ng/ml. Here are some facts about what a lack of vitamin D3 can cause.

Increased risk of mortality with lower vitamin D levels in ICU patients

  1. A New England Journal study from 2009 reported about 1100 patients in Intensive Care Units (ICU). Their average vitamin D blood level was only 16 ng/ml. They tracked the mortality rates depending on the vitamin D blood level. Insufficient vitamin D levels showed an association with a mortality rate of 45%. An intermediate level had a mortality rate of 35%. And a satisfactory level of vitamin D had a mortality of only16%. Between the low level of vitamin D and the normal level there was a 3-fold difference in mortality!
  2. Another study from 2015 repeated the mortality study with 135 ICU patients. Researchers correlated Vitamin D blood levels with mortality rates of patients. When vitamin D levels were below 12 ng/ml, there was a mortality rate of 32.2%. Patients with higher levels of vitamin D had a mortality rate of 13.2%. The authors concluded that vitamin D blood levels were an independent risk factor for mortality. Patients less than 12 ng/ml had a 2.4-fold higher risk of dying than patients with normal vitamin D levels.

Do patients with multiple sclerosis take enough vitamin D3?

Perhaps one of the earliest results of vitamin D3 research was the following observation. More than 90% of patients with multiple sclerosis were deficient in vitamin D blood levels. Their levels were below 20 ng/ml. Other researchers showed that vitamin D could directly tone down the aggressiveness of the immune cells of MS patients. These were the ones that attacked the myelin sheath. As a result of this knowledge it is important for MS patients to take high enough vitamin D3 supplements. When they reach good vitamin D blood levels their MS is better controlled.

Canada as a northern country has 291 MS patients per 100,000 people. Contrast this to 110-140 MS patients per 100,000 people in the northern US (between the 37th parallel and the US/Canadian border). In addition south of the 37th parallel there are only 57-78 cases of MS per 100,000 people. Researchers have concluded that the less sun light people get, the higher the rate of MS in the population will be. However, instead of sun exposure you can supplement with vitamin D3 capsules to get the blood vitamin D levels up to the range of between 50 and 80 ng/ml.

Do stroke patients take enough vitamin D3?

Strokes are very common. About 6.8 million Americans survive a stroke and live with various disabilities. 15% die shortly after their stroke. 40% are left with moderate to severe disabilities. Many require special care.

  1. Studies have shown that patients with the lowest level of vitamin D have the poorest functional outcomes. Moreover, for every 10 ng/ml decrease in vitamin D levels the odds of a healthy recovery 3 months after the stroke fell by about half. This was independent of age and the initial stroke severity.
  2. In another 2015 study from South Korea 818 stroke patients took tests to evaluate whether they had adequate vitamin D blood levels. There was a clear division between those whose levels were higher than 10 ng/ml or lower. When the vitamin D level was higher, there was a 90% better recovery from their stroke after 3 months. In comparison those whose vitamin D levels were below 10 ng/ml had poor recovery rates. Experts say that vitamin D levels should stay in the range between 50 and 80 ng/ml. This will prevent numerous diseases.

Do diabetics take enough vitamin D3?

  1. Vitamin D3 can silence diabetes genes in connection with the right diet and cofactors of zinc and magnesium. A Mediterranean diet can stabilize the metabolism and fight inflammation. Zinc and magnesium are important cofactors in enzymes necessary to prevent diabetes. Vitamin D3 and omega-3intake are helping to control inflammation and preserve beta cells in the pancreas in diabetes patients. This is important for continued production of insulin.
  2. A Chinese research team found that vitamin D3 protects beta cells in the pancreas from dying off. The finding was that vitamin D3 receptors in the insulin producing cells prevented the dying off of these cells, as long as there was enough vitamin D available. Insulin production by the pancreas remained effective. And insulin is vital for long-term survival of diabetes patients. The key for diabetes patients is to take adequate doses of vitamin D3 to protect their insulin producing beta cells.
  3. A 2015 Italian study showed that micro vascular complications in diabetes patients were high, if the vitamin D3 blood levels were low. If patients had high levels of vitamin D3, there were no complications such as retinopathy or nephropathy. But if levels were below 20 ng/ml, damages were significant in the capillaries of the eyes and kidneys.

Do patients with inflammatory conditions take enough vitamin D3?

What do the lining of the arteries, the inflamed joints, a degenerative meniscus and heart attacks and strokes have in common? It is the inflammation that changes the body chemistry. It gets even more complicated, because the extra calories that we consume get stored as visceral fat. This is done automatically when you eat too much sugar and starchy foods. When the glycogen stores are full, any surplus sugar gets metabolized by the liver into triglycerides, fatty acids and LDL cholesterol and gets stored as body fat. The most active fat is the visceral fat between our guts and around our body organs. This produces interleukins and other inflammatory cytokines that circulate in the blood causing inflammation in all our arteries. Interleukin-6 is an inflammatory cytokine. High interleukin-6 levels contribute to causation of various cancers.

This 2015 study from Seattle University followed 218 obese postmenopausal women with a body mass index of larger than 25.0 for 12 months. Both received weight loss intervention and either 2000 IU of vitamin D3 daily or a placebo pill. Both groups lost about 5 to 10% of weight in 12 months. However, the interleukin-6 level of the vitamin D3 group had a reduction of 37.3%. This was in stark contrast to the placebo group where the interleukin-6 level reduction was only 17.2%. This type of research shows the incredible power of vitamin D3. This likely is the reason why several cancer frequencies can show a reduction with regular vitamin D3 supplementation.

Attention deficit disorder and vitamin D3

  1. Other research compared a group of 37 children with attention deficit hyperactivity disorder (ADHD to 37 normal children. Blood levels of vitamin D were 19.11±10.10 ng/ml in the ADHD group and 28.67±13.76 ng/ml in the normal group. Other researchers have found similar findings, establishing that very low vitamin D levels have a connection with ADHD.
  2. A prospective study from Spain involving 1,650 mother-child pairs investigated the effect of mother’s vitamin D level during her pregnancy with the risk for ADHD by the time the child was 4 to 5 years old. Schoolteachers followed the standard test procedures to establish the ADHD diagnosis. The study showed that for every 10-ng/ml increment of the mother’s blood vitamin D level during her pregnancy the children had 11% less ADHD-like symptoms. The authors cautioned that it takes mega doses of vitamin D3 to reach these kinds of results. The usual 400 IU of vitamin D3 per day will not achieve the desired increase of vitamin D3 levels, but amounts of 5,000 IU to 8,000 IU are necessary to achieve this.

Schizophrenia and vitamin D3

A 2014 Meta analysis found that low vitamin D levels have an association with a 2.16-times higher probability of having schizophrenia than controls with normal vitamin D levels. Another study examined whether those patients who had an acute psychosis would have lower vitamin D blood levels than schizophrenia patients in remission or control patients without schizophrenia. Studies compared 40 patients with an acute psychosis to 41 patients in remission and 40 healthy controls. Patients with an acute psychosis had extremely low vitamin D blood levels, while patients in remission had much better vitamin D levels. Healthy controls had the best vitamin D levels.

Absorption and metabolism of vitamin D3

Magnesium plays a central role in activating vitamin D3. This publication points out that magnesium is also necessary for absorption of vitamin D3 in the gut. The activation of vitamin D3 is also partially responsible for vitamin D absorption. Both vitamin D3 and magnesium play an important role in bone and calcium metabolism. The fact that every body cell has vitamin D3 receptors shows how important it is for the maintenance of the body. Many researchers say that vitamin D3 qualifies as a hormone because of the specific effects on cells via vitamin D3 receptors.

Take Enough Vitamin D3

Take Enough Vitamin D3

Conclusion

Vitamin D3 is an important signaling hormone and vitamin that regulates the body’s calcium absorption and is responsible for bone metabolism. Research has shown that the lack of vitamin D3 causes several unrelated diseases, like rickets, multiple sclerosis, and schizophrenia. But other diseases, where a lack of vitamin D3 was present, were diabetes, attention deficit disorder and strokes. When patients with elevated inflammatory markers take vitamin D3 their interleukin-6 levels dropped by 37.3%. To achieve this, patients needed to consume at least 2000 IU. We all should have our vitamin D blood level measured from time to time. It should be between 50 and 80 ng/ml. Too many Americans are deficient in vitamin D3 and come down with the diseases mentioned! Prevention and supplementation go hand in hand. You can prevent a lot of diseases this way.

 

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Sep
28
2013

Sleepless Nights

By | Health, Hormones, Insomnia, Mental Health, Pain, Prevention, Sleep apnea, Substance abuse, Vitamins and supplements

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

Oct
02
2003

Schizophrenia Gene Discovered

By | Mental Health

In the not too distant future new tests and new anti-psychotic drugs (“designer drugs” rather than “trial and error drugs”) for schizophrenia will likely be developed in the US because of the following new findings.

At the 19th International Congress of Genetics in Melbourne/Australia (July 2003) the Nobel Prize laureate Dr. Susumu Tonegawa, who had won the 1987 Nobel Prize for Medicine, reported about his new discovery of a gene that controls schizophrenia. This has already been studied extensively in mice by the research team that he is heading (from the Howard Hughes Medical Institute of Technology (MIT) in Cambridge/Mass).

Together with other colleagues from other Centers (Duke University, Rockefeller University and Columbia University College of Physicians and Surgeons) they have developed an animal model, a “schizophrenic mouse”, that is defective for the schizophrenia gene. Researchers had found that an enzyme called “calcineurin” was missing in schizophrenic families where genetic defects could be located in one particular gene. Subsequently this type of gene was also shown to be important for the normal brain metabolism in mice. The detection of a mouse model for schizophrenia has made it much easier to do ground-breaking research in the field of schizophrenia. Dr. Tonegawa said that the existing drugs for schizophrenia were developed by trial and error. In some patients these drugs do not work, in many others they have serious side-effects. He stated further that in future there will be a new class of anti-psychotic drugs with minimal side-effects as they will specifically normalize the calcineurin production.

Schizophrenia Gene Discovered

Anti-psychotic designer drugs

This in turn will normalize the derailed brain metabolism. In schizophrenics it is in this area where the psychotic behavior originates due to a lack of normal calcineurin production. This enzyme is found not only in brain tissue, but also in immune cells such as the T lymphocytes throughout the body. Because of this connection a future modern treatment for schizophrenia will likely normalize the brain metabolism, but also have beneficial effects on the entire immune system.

Here is a link to a review of schizophrenic disorders

Last edited October 26, 2014