Later school start times are

associated with more sleep and better performance in

high school students.

Gideon P. Dunster1, Luciano de la Iglesia1, Miriam Ben-Hamo1, Claire Nave1, Jason G. Fleischer2, Satchidananda Panda2, Horacio O. de la Iglesia1,3*

Most teenagers are chronically sleep deprived. One strategy proposed to lengthen adolescent sleep is to delay secondary school start times. This would allow students to wake up later without shifting their bedtime, which is biologically determined by the circadian clock, resulting in a net increase in sleep. So far, there is no objective quantitative data showing that a single intervention such as delaying the school start time significantly increases daily sleep. The Seattle School District delayed the secondary school start time by nearly an hour. We carried out a pre-/post-research study and show that there was an increase in the daily median sleep duration of 34 min, associated with a 4.5% increase in the median grades of the students and an improvement in attendance. 

Is Vitamin D3 Worth Giving to Our Patients with Mild Cognitive Impairment?

Jonathan Silver, MD reviewing Hu J et al. J Neurol Neurosurg Psychiatry 2018 Oct 2Improvements in cognition and lipid levels were seen after 1 year of supplementation in a study from China.Many patients with mild cognitive impairment (MCI) progress to Alzheimer disease. No preventive intervention is proven, although we tell our patients to have a healthy diet, get sleep, and exercise — and multiple supplements are advertised for “brain health.” In a randomized, placebo-controlled trial, researchers in China assessed effects of 1 year of vitamin D3 supplementation (400 IU/day) on cognition and lipid levels in 181 patients who met criteria for MCI (mean age, 67; 45% men).Treatment groups did not differ on history of diabetes or hypertension, mental status scores, and vitamin D levels. At the 12-month assessment, the vitamin-D group significantly improved from baseline and had better scores than the placebo group on multiple measures in the Chinese version of the Wechsler Adult Intelligence Scale–Revised (full-scale IQ, verbal IQ, performance IQ, and multiple subtests). The vitamin-D group also had higher 25-D and 1,25-D levels. Levels of total cholesterol, triglycerides, HDL, and LDL decreased in the vitamin-D group but increased in the placebo group. Total cholesterol concentration in the vitamin-D group was inversely associated with full IQ.

Bidirectional Associations Between
Self-Reported Gaming Disorder and
Adult Attention Deficit Hyperactivity
Disorder: Evidence From a Sample of
Young Swiss Men.

Simon Marmet 1*, Joseph Studer 1, Véronique S. Grazioli 1 and Gerhard Gmel 1,2,3,4

1 Alcohol Treatment Centre, Lausanne University Hospital/CHUV, Lausanne, Switzerland, 2 Addiction Switzerland, Lausanne,
Switzerland, 3 Centre for Addiction and Mental Health, Toronto, ON, Canada, 4 Department of Health and Social Sciences,
University of the West of England, Frenchay, Bristol, United Kingdom
Background: Gaming disorder (GD) has been shown to co-occur with attention deficit
hyperactivity disorder (ADHD), yet few studies to date have investigated their longitudinal
associations.
Method: The sample included 5,067 young Swiss men (mean age was 20 years at
wave 1 and 25 years at wave 3). Measures were the Game Addiction Scale and the Adult
ADHD Self-Report Scale (6-item screener). Longitudinal associations were tested using
autoregressive cross-lagged models for binary measures of GD and ADHD, as well as
continuous measures for GD score and ADHD subscales of inattention and hyperactivity.
Results: ADHD at age 20 increased the risk for GD at age 25 (probit = 0.066
[0.023, 0.109]; p = 0.003). GD at age 20 also increased the risk for ADHD at wave
3 (probit = 0.058 [0.013, 0.102]; p = 0.011). Only the ADHD inattention subscale
showed a bidirectional longitudinal relationship with the GD score (standardized Beta
from inattention at age 20 to GD score at age 25: 0.090 [0.056, 0.124]; p < 0.001; from
GD score at age 20 to inattention at age 25: 0.044 [0.016, 0.071]; p = 0.002), whereas
associations between the hyperactivity subscale and GD were not significant.
Discussion: GD had bidirectional longitudinal associations with ADHD, in that ADHD
increased the risk for GD and GD increased the risk for ADHD, and they may reinforce
each other. These associations may be linked more to the inattention ADHD component
than to the hyperactivity ADHD component. Individuals with ADHD or GD should be
screened for the other disorder, and preventive measures for GD should be evaluated in
individuals with ADHD.

Abstract

Objective To determine the independent and additive effects of aerobic exercise (AE) and the Dietary Approaches to Stop Hypertension (DASH) diet on executive functioning in adults with cognitive impairments with no dementia (CIND) and risk factors for cardiovascular disease (CVD).

Methods A 2-by-2 factorial (exercise/no exercise and DASH diet/no DASH diet) randomized clinical trial was conducted in 160 sedentary men and women (age >55 years) with CIND and CVD risk factors. Participants were randomly assigned to 6 months of AE, DASH diet nutritional counseling, a combination of both AE and DASH, or health education (HE). The primary endpoint was a prespecified composite measure of executive function; secondary outcomes included measures of language/verbal fluency, memory, and ratings on the modified Clinical Dementia Rating Scale.

Results Participants who engaged in AE (d = 0.32, p = 0.046) but not those who consumed the DASH diet (d = 0.30, p = 0.059) demonstrated significant improvements in the executive function domain. The largest improvements were observed for participants randomized to the combined AE and DASH diet group (d = 0.40, p = 0.012) compared to those receiving HE. Greater aerobic fitness (b = 2.3, p = 0.049), reduced CVD risk (b = 2.6, p = 0.042), and reduced sodium intake (b = 0.18, p = 0.024) were associated with improvements in executive function. There were no significant improvements in the memory or language/verbal fluency domains.

Conclusions These preliminary findings show that AE promotes improved executive functioning in adults at risk for cognitive decline.

Sources:

James A. Blumenthal, Patrick J. Smith, Stephanie Mabe, Alan Hinderliter, Pao-Hwa Lin, Lawrence Liao, Kathleen A. Welsh-Bohmer, Jeffrey N. Browndyke, William E. Kraus, P. Murali Doraiswamy, James R. Burke, Andrew SherwoodFirst published December 19, 2018,  DOI: https://doi.org/10.1212/WNL.0000000000006784 FULL PDF CITATION PERMISSIONS COMMENTDownloads0 Add to Cart ($39)

• Article
• Info

Abstract

Objective To determine the independent and additive effects of aerobic exercise (AE) and the Dietary Approaches to Stop Hypertension (DASH) diet on executive functioning in adults with cognitive impairments with no dementia (CIND) and risk factors for cardiovascular disease (CVD).

Methods A 2-by-2 factorial (exercise/no exercise and DASH diet/no DASH diet) randomized clinical trial was conducted in 160 sedentary men and women (age >55 years) with CIND and CVD risk factors. Participants were randomly assigned to 6 months of AE, DASH diet nutritional counseling, a combination of both AE and DASH, or health education (HE). The primary endpoint was a prespecified composite measure of executive function; secondary outcomes included measures of language/verbal fluency, memory, and ratings on the modified Clinical Dementia Rating Scale.

Results Participants who engaged in AE (d = 0.32, p = 0.046) but not those who consumed the DASH diet (d = 0.30, p = 0.059) demonstrated significant improvements in the executive function domain. The largest improvements were observed for participants randomized to the combined AE and DASH diet group (d = 0.40, p = 0.012) compared to those receiving HE. Greater aerobic fitness (b = 2.3, p = 0.049), reduced CVD risk (b = 2.6, p = 0.042), and reduced sodium intake (b = 0.18, p = 0.024) were associated with improvements in executive function. There were no significant improvements in the memory or language/verbal fluency domains.

Conclusions These preliminary findings show that AE promotes improved executive functioning in adults at risk for cognitive decline.

Donald Rauh M.D., Ph.D., FAPA
Diplomate of the American Board of Psychiatry & Neurology 
Board Certified in General Psychiatry and in  Child & Adolescent Psychiatry

DrDARauh@me.com
RauhPsychiatry.com

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• CME DISCLOSUREVicki Brower, CME Writer, MedPage Today; Robert Jasmer, MD, Associate Clinical Professor of Medicine, University of California, San Francisco, Reviewer; and Dorothy Caputo, MA, BSN, RN, Nurse Planner have disclosed that they have no relevant financial relationships or conflicts of interest with commercial interests related directly or indirectly to this educational activity. The staff of Projects In Knowledge®, Inc. and the staff of MedPage Today have no relevant financial relationships or conflicts of interest with commercial interests related directly or indirectly to this educational activity.

Target Audience and Goal Statement:

Internists, family medicine specialists, neurologists, and cardiologists

The goal of the study was to determine whether older adults with mild cognitive impairment but no dementia and cardiovascular risk factors can improve executive functioning, memory, and verbal fluency by adding moderate, regular aerobic exercise, and/or the the Dietary Approaches to Stop Hypertension (DASH) diet.

Questions Addressed:

What are the independent and additive effects of aerobic exercise (AE) and the DASH diet on executive functioning (primary endpoint), and on measures of language/verbal fluency and memory (secondary endpoint) in adults at risk for cardiovascular disease and who have mild cognitive impairment?

Study Synopsis and Perspective:

In a randomized clinical trial of exercise and diet in 160 sedentary adults with mild cognitive impairment but no dementia (CIND) and cardiovascular risk factors, regular aerobic exercise three times a week for 6 months resulted in significant improvements in executive function, but not in memory or language/verbal fluency domains, James Blumenthal, PhD, of Duke University Medical Center in Durham, N.C., and colleagues for the ENLIGHTEN trial reported.

The researchers employed a 2-by-2 factorial design (exercise/no exercise and DASH/no DASH) to compare the independent effects of exercise and diet on a range of cognitive abilities. At baseline, participants had subjective memory complaints, objective evidence of cognitive impairment, and at least one additional cardiovascular disease risk factor besides being sedentary. They had a mean age of 65.4, and 66% were female.

The team randomly assigned 160 inactive men and women to 6 months of either exercise alone (n=41), DASH diet alone (n=41), combined exercise and DASH diet (n=40), or a no-exercise, no-diet control group that received weekly phone calls about health-related topics (n=38). Effect sizes were measured with the Cohen’s d to indicate the difference between means.

Participants in the exercise group worked out under supervision three times a week for 35 minutes at 70% to 85% of their initial peak heart rate reserve for 3 months, then continued exercising at that rate at home, documenting activity in weekly exercise logs. DASH diet group members received education about the DASH diet and frequent feedback about adherence from a nutritionist.

At the end of 6 months, individuals who engaged regularly in aerobic exercise (beta coefficient 4.2, 95% CI 0.2-8.2, d=0.32, P=0.046), not those only in the DASH group (beta coefficient 3.7, 95% CI −0.2 to 7.7, d=0.30, P=0.059), demonstrated significant improvements in the executive function domain. There were no significant improvements in the memory or language/verbal fluency domains, however.

The largest improvements in executive functioning occurred for participants in the combined exercise and DASH diet group (d=0.40, P=0.012) compared with controls. To illustrate the potential clinical significance of this, the authors estimated that participants had average scores for select subtests of executive function consistent with 93-year-old people at baseline — 28 years older than their chronological age. After 6 months, people who exercised and followed the DASH diet had average executive function scores corresponding to 84-year-olds, a 9-year improvement. In contrast, executive function scores for control group participants worsened by a half year (which actually was the duration of the study).

Follow up examination of specific CVD risk factors showed that participants on the DASH diet had reductions in total cholesterol, reduced weight and LDL lipoprotein, and a reduction in the number of hypertensive medications taken. There were no significant differences in systolic blood pressure. Individuals in the exercise and exercise + DASH diet showed greater improvements in insulin compared with those who did not exercise.

Regarding neurocognitive function, while researchers saw no significant changes in executive function for those on the DASH diet, those in the aerobic arm of the trial saw significant improvement in executive function. Reduced sodium intake was also associated with improved executive function, changes in potassium, magnesium, and calcium were not related to executive function.

“Individuals with CIND — cognitive impairment, no dementia — are at risk for developing dementia over time,” Blumenthal said. “Currently there are no known treatments to prevent the progression of this disorder, so findings from this study are very important by suggesting that regular exercise can improve cognitive function and potentially delay the onset of dementia in these individuals.”

Although study researchers conducted APOe4 genotyping, they did not comment on genotype status and outcomes for individuals, although they did control for APOE genotype as well as education and CVD medication burden, and long-term use of anti-inflammatory medications. Participants were evenly divided between whites and minorities.

Source Reference: Neurology Dec. 19, 2018; DOI:10.1212/WNL.0000000000006784

Study Highlights: Explanation of Findings

In the ENLIGHTEN trial, 6 months of regular aerobic exercise led to improved executive functioning in adults at risk for cognitive decline, researchers reported. And while the DASH diet boosted the executive functioning benefits of exercise, it did not show any cognitive function benefit by itself, the study authors wrote in Neurology.

Blumenthal and colleagues observed that this trial may be the first randomized study to investigate the independent and combined effects of a diet and aerobic exercise on neurocognitive function in older adults at elevated risk for progressive decline in cognitive functioning. Results of previous meta-analyses of randomized trials have been inconsistent, they noted.

“An interesting finding is that the DASH diet alone did not provide any benefit for cognitive function, even though the DASH diet did improve cardiovascular health,” observed Teresa Liu-Ambrose, PhD, PT, of the University of British Columbia in Vancouver, who was not involved with the study. “However, it should be noted that aerobic exercise not only improves cardiovascular health, but also induces the release of growth factors that are beneficial for neuronal health.”

While participants who engaged in both aerobic exercise and DASH demonstrated the most improvement in executive functions, the difference in the magnitude of benefit — of exercise alone vs exercise plus DASH — was 25%, Liu-Ambrose told MedPage Today. “As adoption and adherence to health habits is often a challenge for individuals, one may consider adopting one habit first, i.e., exercise, and then slowly incorporating the second habit, i.e., diet,” she said. In the combined exercise and DASH group, greater aerobic fitness, reduced cardiovascular disease (CVD) risk, and reduced sodium intake were associated with executive function improvements.

Researchers pointed out that “because there is considerable overlap in risk factors for CVD and dementia, strategies designed to reduce CVD risk may also be effective in improving neurocognition and reducing the risk of developing dementia.”

“These findings raise the possibility that adopting a healthy lifestyle of diet and exercise can not only reduce the risk of heart disease, but also reduce the risk of developing dementia later in life,” he added. “Future studies, with larger samples followed over more extended time periods are needed, along with studies that examine the mechanisms by which these lifestyle modifications improve cognitive functioning,” he told MedPage Today.

The ENLIGHTEN trial may have been underpowered to detect differences between aerobic exercise and DASH diet alone, Blumenthal and co-authors noted; because of this potential limitation, they provided limited evidence of the relative benefits of these two interventions. The study also was only 6 months long and longer-term effects of exercise and diet on cognitive outcomes are unknown. No one dropped out of the study and trial results may not apply to less motivated groups, they added.

Judy George wrote the original story for MedPage Today

Source:

by Vicki Brower, CME Writer, MedPage Today December 23, 2018 

Home » Library » Understanding & Coping with the Christmas Blues

Understanding & Coping with the Christmas Blues

By Darlene Lancer, JD, MFT

The stress of the holidays triggers sadness and depression for many people. This time of year is especially difficult because there’s an expectation of feeling merry and generous. People compare their emotions to what they assume others are experiencing or what they’re supposed to feel. Then they think that they alone fall short. They judge themselves and feel like an outsider.

There’re a host of things that add to stress and difficult emotions during the holidays.

• Finances. Not enough money or the fear of not having enough to buy gifts leads to sadness and guilt. The stress of financial hardship during this economic downturn is often compounded by shame. When you can’t afford to celebrate, it can feel devastating.
• Stress. For example, there is the stress of shopping and planning family dinners when you’re already overworked and tired.
• Loneliness. A whopping 43 percent of Americans are single, and 27 percent of Americans live alone. When others are with their families, it can be very painful for those who are alone. Seventeen percent of singles are over 65, when health, age, and mobility can make it more difficult to enjoy yourself.
• Grief. Missing a deceased loved one. Seniors have more reasons to grieve.
• Estrangement. When you’re not speaking to a relative, family get-togethers can usher in feelings of sadness, guilt, resentment, or inner conflict about whether to communicate.
• Divorce. If you’re newly divorced, the holidays may remind you of happier times and accentuate your grief. It’s especially difficult for adult children of divorce who have to balance seeing two sets of parents. The stress is multiplied for married children who have three or even four sets of parents to visit.
• Pleasing. Trying to please all of your relatives – deciding what to get, whom to see, and what to do – can make you feel guilty, which leads to depression.
• SAD. Many people experience the blues during gloomy weather due to decreased sunlight, called Seasonal Affective Disorder (SAD).

Much of the planning, shopping, and cooking is done by women, so they carry the greater burden in preparing for family gatherings. Women are at greater risk for depression than men. They’re twice as likely to experience depression. After heart disease, depression is the most debilitating illness for women, while it’s tenth for men.

Some measures you can take to cope with the holiday blues include:

• Make plans in advance, so you know how and with whom your holidays will be spent. Uncertainty and putting off decision-making add enormous stress.
• Shop early and allow time to wrap and mail packages to avoid the shopping crunch.
• Ask for help from your family and children. Women tend to think they have to do everything, when a team effort can be more fun.
• Don’t buy things you can’t afford. Shame prevents people from being open about gift-giving when they can’t afford it. Instead of struggling to buy a gift, let your loved ones know how much you care and would like to, but can’t afford it. That intimate moment will relieve your stress and nourish you both.
• Don’t allow perfectionism to wear you down. Remember it’s being together and goodwill that matters.
• Make time to rest and rejuvenate even amidst the pressure of getting things done. This will give you more energy.
• Spend time alone to reflect and grieve, if necessary. Pushing down feelings leads to depression. Let yourself feel. Then do something nice for yourself and socialize.
• Don’t isolate. Reach out to others who also may be lonely. If you don’t have someone to be with, volunteer to help those in need. It can be very uplifting and gratifying.

The signs of depression are feelings of sadness, worthlessness or guilt, crying, loss of interest in usual activities, fatigue, difficulty concentrating, irritability, social withdrawal, and changes in sleep, weight, or appetite. If these symptoms are severe or continue for a few weeks, more than the holidays may be the cause. Seek professional help.

SOURCE: https://psychcentral.com/lib/understanding-coping-with-the-christmas-blues/

Effects of Long-Term Use of Prescription Methylphenidate on Myocardial Performance in Children with Attention-Deficit/Hyperactivity Disorder: A Tissue Doppler Imaging Study.

Source:

Roundup Chemical in Your Cereal:

Oats are the basis of many favorite children’s snacks,
including Cheerios and other baby finger-food cereals.
Because of their small size and still-developing bodies,
babies and young children are more vulnerable to
environmental harms than adults are.

Organic products had lower levels of glyphosate; and almost
two-thirds of the samples made with organically grown oats
didn’t have any detectable glyphosate at all. That’s not too
surprising since glyphosate is banned from use in organic
farming. Still, some organic products — 5 samples in total —
did have some glyphosate.

Even organic oats can be contaminated if they sit next to
fields where glyphosate is sprayed, or if they’re processed
on the same equipment as conventionally grown oats.
What’s the Risk?

So how much should a parent worry about what they’re
feeding their kids?

Experts are divided on this point. In 2015, the respected
International Agency for Research on Cancer declared that
glyphosate was “probably carcinogenic to humans.” There
are efforts under way in Europe to ban the chemical. More
than 1 million people signed a petition calling on the
European Union to prohibit its use, and Germany announced
plans to stop its use there by 2021.
Yet in 2017, the EPA said the chemical was “not likely” to
cause cancer in people.

“This is where it gets tricky. This isn’t straightforward,” says
Michael Davoren, PhD, who studies molecular toxicology at
UCLA. He was not involved in the Environmental Working
Group’s tests.
Olga Naidenko,
PhD, the
Environmental
Working Group’s
senior science

What Does Organic Mean?
What USDA standards does a food have to
pass in order to earn the word organic on its
label?

Advisors for children’s environmental health, says glyphosate
shouldn’t be in food, especially the foods we feed to young
children.

“We believe that toxic pesticides, especially ones that may
be linked to cancer, really don’t belong in the diet,” she says.
But even Naidenko and her co-author, toxicologist Alexis
Temkin, PhD, say the odds of getting cancer from eating
glyphosate-contaminated oats are really low.

Based on their own calculations, they say a single serving of
most of the foods they tested, eaten each day for a lifetime,
would cause just one additional case of cancer in every
million people.

“That’s such a low increased risk to speculate about,”
Davoren says. “When you’re dealing with something like
that, a 1-in-a-million increased risk of cancer, I would say that
isn’t a significant level to be particularly concerned about.”
He says the risk definitely wouldn’t outweigh the health
benefits of eating oats, which are high in fiber and low in fat.
In a statement, Monsanto, a company that makes Roundup
and other glyphosate-based products, said “the EWG’s claim
about cancer is false. Glyphosate does not cause cancer.
Glyphosate has a more than 40-year history of safe use.
Over those four decades, researchers have conducted more
than 800 scientific studies and reviews that prove glyphosate
is safe for use.”

Does that mean glyphosate is safe? You could say the jury is
still out on that, but actually, one jury is in back in, and they
didn’t think so.
Last week, jurors in California found Monsanto liable for
causing cancer in a 46-year-old groundskeeper, Dewayne
Johnson. Johnson was awarded $250 million in punitive
damages after the jury said the company failed to warn the
public about its products’ health risks. Johnson’s case is only
the first to come to trial. The company faces thousands of
similar challenges across the U.S.
Versatile, Popular Weedkiller

Glyphosate doesn’t merely kill weeds. It also helps get crops
Roundup Chemical in Your Cereal.

Glyphosate doesn’t merely kill weeds. It also helps get crops
ready for harvest. Farmers spray it on oats and other grains
so they can move into the field to harvest them sooner. It
also helps to promote even drying so they can harvest more
of their grain at the same time.

For years, the chemical, which was first used in the U.S. in
1974, was considered to be virtually nontoxic to people and
other animals. That’s because it works by blocking an
enzyme that’s only made by plants. Since people don’t make
the enzyme, the chemical was thought to be basically inert in
the body.

But some studies in cells in petri dishes and animals have
found that glyphosate and the weedkillers that use it may be
able to damage DNA.

Internal company emails presented as evidence in Dewayne
Johnson’s trial show Monsanto knew it was “very vulnerable
in this area” and that the company hired outside scientists in
an effort to discredit this science.

Exactly how the weedkiller might be causing this damage
isn’t clear.
Davoren says new studies are pointing to a possible
explanation. Though animals don’t contain the enzyme that’s
blocked by glyphosate, bacteria do.
In fact, in addition to marketing the chemical as a weedkiller,
Monsanto patented glyphosate as an antibiotic in 2010.
Davoren says that because glyphosate is so popular — it’s
the most commonly used weedkiller in the U.S., with more
than 250 million pounds used each day — it’s really hard to
avoid.

“We’re learning more and more about the complexity and the
importance of the human microbiome,” says Davoren. The
microbiome refers to the genes of trillions of bacteria that live
in and on our bodies. Our bodies contain about 100 times
more bacterial DNA than human DNA. “What’s going on in
your microbiome can end up affecting your cancer risk.”
Davoren says the science is still early, but it seems like
glyphosate may be most harmful to “good” bacteria — the
kind that dampen inflammation in the body.
“You’re potentially adding one more subtle environmental
factor that could tip the scales from a healthy microbiome to
Roundup Chemical in Your Cereal.

factor that could tip the scales from a healthy microbiome to
an unhealthy microbiome,” he says, though this is still just a
theory. Much more research is needed before this can be
accepted as fact.

Source: https://www.webmd.com/food-recipes/news/20180815/roundup-chemical-in-your-cereal-what-to-know?

“©2016, WebMD, LLC. All rights reserved”

In arecent blog entry, I wrote about how some of the young people I treat in my practice are using cannabis as a means of avoiding the anxiety-provoking stressors of becoming an adult and how that avoidance is contributing to a delay in maturation.

The good news is that most young people who experiment with cannabis in adolescence will not develop psychosis. But a small percent, especially with genetic loading, can develop psychotic symptoms at a younger age with exposure to cannabis.

In this entry, I want to explore a far more serious question: Does cannabis increase the chances of developing psychosis?

The answer is not a simple one. Cannabis appears to interact with neurodevelopmental processes in a way that in some people can contribute to the genesis of psychotic illnesses such as schizophrenia. However, fortunately for most people, this will not be the case. Global epidemiology studies attribute only a tiny amount of the risk of developing schizophrenia to the use of cannabis. (6) But even if this percentage is small, even as low as 1% of users, the increasing prevalence of cannabis use among young people, coupled with the appearance of relative safety (an image of safety that has been promoted by the cannabis industry, just as the safety of tobacco was once purported by the likes of R.J. Reynolds) and growing societal acceptance of cannabis means that more young people will be exposed to cannabis and this potential attendant harm. Even if this risk is relatively small, the level of disability and suffering associated with schizophrenia behooves us to work towards preventing any cases that we can.

Schizophrenia is a complex illness, likely resultant from disrupted neurotransmission, both on the cellular and network level. It typically emerges in late adolescence and early adulthood, before the age of 25. This is also the time when many people experiment with substance use, and cannabis is the most widely used substance among young people after alcohol and tobacco. In one study, 7.3% of people 12 and older reported using cannabis in the previous month compared with 52.1% who reported alcohol use and 26.7% who reported tobacco use. (1)

We clinicians have all seen the tragedy of young patients who, just as they are getting ready to launch into the world, began to develop the disabling symptoms of schizophrenia. Some of them have also been using cannabis. The question often arises from family members and patients: Did the cannabis cause the illness?

The simple answer in clinical practice is “we will never know,” because of course, there is no ability to have a “control” patient who is not exposed to cannabis to see if the illness would not develop in its absence. Additionally, patients with schizophrenia and their families can better direct their efforts towards helping their loved one heal and manage their illness, rather than feeling regrets about past choices.

However, as clinicians, it is important for us to educate our young patients about the risks of psychosis associated with early, heavy cannabis use. Epidemiologic data indicates that young people who are daily users of cannabis before the age of 15 have a greater risk of developing schizophrenia than their peers who either abstain from cannabis or wait until adulthood to begin using the drug. This risk is further increased by the use of cannabis that is high in THC (9-delta tetrahydrocannabinol), the psychoactive ingredient in cannabis, as many contemporary strains are grown for high levels of this compound. (2) This relationship between psychosis and cannabis use appears to be dose dependent, which further underscores the harm reduction message that while no use is best, any reduction or forestalling of use is better. (3)

Curiously, subjects with prodromal schizophrenia have been found to have elevated endocannabinoid activity. Anandamide, the endogenous ligand for the cannabinoid-1 receptor, has been found to be elevated up to eight times normal in the CSF of patients with emerging schizophrenia. This may represent an attempt by the brain to restore homeostasis to a brain that has become overactive with dopamine. Anandamide may be trying to “put the brakes on” the emerging excessive dopamine activity seen in emergent schizophrenia. Unfortunately, exposing a brain that is already struggling with dopamine homeostasis to the perturbing activity of THC may further worsen the psychotic symptoms. (7)

Why might cannabis use both increase the risk of psychosis? It may be partially explained by genetics. The gene that codes for COMT (catechol-O-methyltransferase) has some regulation of dopamine degradation at the synapse. Schizophrenia is associated with an excess of dopamine activity, particularly at the mesolimbic tract of the brain. (4) Carriers of the Val158Val polymorphism for the COMT gene were more likely to develop psychotic symptoms  at a younger age after exposure to cannabis than peers who carried the Met158Met polymorphism. (5) As genetic testing becomes cheaper, might it make sense to screen young people prior to the age at which drug use is typically initiated for this polymorphism and warn those who are Val/Val carriers that they are at a higher risk for developing a psychotic illness with cannabis exposure?

So what do we tell our young patients? One – by first acknowledging that we have damaged our credibility with a historic message that “all drugs are bad for all people all the time,” young users may be more willing to hear a more nuanced message. Two – there are real risks for young people who use cannabis daily. If they haven’t tried the drug, try to explain the benefits of waiting. Each year that passes before drug initiation lessens the risk of developing psychosis. If they have used the drug, and are unwilling to stop, adopt a position of harm reduction: any reduction of use is better than more use. Discuss changing the relationship with the drug to use less of it and to use it less frequently.

References

1. Results from the 2012 National Survey on Drug Use and Health: Summary of National Findings. Substance Abuse and Mental Health Services Administration.

2. Di Forti M, Sallis H, Allegri, F, et al. Daily use, especially of high-potency cannabis, drives the earlier onset of psychosis in cannabis users. Schizophr Bull. 2014;40(6):1509-17.

3. Andreasson S, et al. Lancet. 1987;2(8574):1483-1486. Fergusson DM, et al. Addiction. 2005;100(3):354-366. Henquet C, et al. BMJ. 2005;330(7481):11. Moore TH, et al. Lancet. 2007;370(9584):319-328. Schubart CD, et al. Acta Psychiatr Scand. 2011;123(5):368-375.

4. Stahl, S  (2013) Stahl’s Essential Psychopharmacology. Cambridge Press

5. Estrada G, et al. Acta Psychiatr Scand. 2011;123(6):485-492. Verdejo-Garcia A, et al. Neuropsychopharmacology. 2013;38(8):1598-1606.

6. Degenhardt L, Ferrari A, Calabria B, et al. The global epidemiology and contribution of cannabis use and dependence to the global burden of disease: results from the GBD 2010 study. PLoS One. 2013;8(10):e76635. doi:10.1371/journal.pone.0076635. 

7. Leweke FM. Curr Pharm Des. 2012;18(32):5188-5193. Meltzer HY, et al. Am J Psychiatry. 2004;161(6):975-984. Leweke FM, et al. Transl Psychiatry. 2012;2:e94. Guffrida A, et al. Neuropsychopharmacology. 2004;29(11):2108-2114.

Andrew Penn was trained as an adult nurse practitioner and psychiatric clinical nurse specialist at the University of California, San Francisco. He is board certified as an adult nurse practitioner and psychiatric nurse practitioner by the American Nurses Credentialing Center. Currently, he serves as an Assistant Clinical Professor at the University of California-San Francisco School of Nursing. Mr. Penn is a psychiatric nurse practitioner with Kaiser Permanente in Redwood City, CA, where he provides psychopharmacological treatment for adult patients and specializes in the treatment of affective disorders and PTSD. He is a former board member of the American Psychiatric Nurses Association, California Chapter, and has presented nationally on improving medication adherence, emerging drugs of abuse, treatment-resistant depression, diagnosis and treatment of bipolar disorder, and the art and science of psychopharmacologic practice.