Background & aims
The existing yet limited prospective studies reported conflicting results about obesity and hearing loss. We investigated the prospective association between obesity and hearing loss in a large-scale Japanese working population, as well as the association between metabolic phenotype and hearing loss. Learn more about
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Acute marijuana use is classically associated with snacking behavior (colloquially referred to as “the munchies”). In support of these acute appetite-enhancing effects, several authorities report that marijuana may increase body mass index in patients suffering from human immunodeficiency virus and cancer. However, for these medical conditions, while appetite may be stimulated, some studies indicate that weight gain is not always clinically meaningful. In addition, in a study of cancer patients in which weight gain did occur, it was less than the comparator drug (megestrol). However, data generally suggest that acute marijuana use stimulates appetite, and that marijuana use may stimulate appetite in low-weight individuals. As for large epidemiological studies in the general population, findings consistently indicate that users of marijuana tend to have lower body mass indices than nonusers. While paradoxical and somewhat perplexing, these findings may be explained by various study confounds, such as potential differences between acute versus chronic marijuana use; the tendency for marijuana use to be associated with other types of drug use; and/or the possible competition between food and drugs for the same reward sites in the brain. Likewise, perhaps the effects of marijuana are a function of initial weight status—i.e., maybe marijuana is a metabolic regulatory substance that increases body weight in low-weight individuals but not in normal-weight or overweight individuals. Only further research will clarify the complex relationships between marijuana and body weight.
Keywords: Body weight, cancer, cannabis, human immunodeficiency virus, marijuana, tetrahydrocannabinol, weight, weight effects
This ongoing column is dedicated to the challenging clinical interface between psychiatry and primary care—two fields that are inexorably linked.
INTRODUCTION
The transitory effects of acute marijuana use on appetite and snacking behavior are well-known and colloquially described as, “the munchies.” A humorous cinematic example of this phenomenon is displayed in the 2005 film, “Gettin’ Da Munchies.” In this film, the protagonist decides to have several friends over for a video-game tournament. However, his plans go awry and, through frustration, he winds up smoking marijuana for the first time, which results in the proverbial munchies. Throughout the remainder of the film, the protagonist is on an eternal and ravenous search for food. But beyond these acute effects on appetite, are there more sustained relationships between the use of marijuana and body weight? In this edition of The Interface, we examine these possible relationships through a review of the literature.
We begin by reviewing the known physiological effects of marijuana on the regulation of appetite and body weight, and then proceed to review the few available empirical studies on this relationship.
THE PHYSIOLOGICAL EFFECTS OF CANNABINOIDS ON APPETITE/WEIGHT REGULATION
Marijuana and its multiple chemical components (i.e., cannabinoids) as well as substances produced within the body that activate cannabinoid receptors (i.e., endocannabinoids) appear to exert specific influences on the regulation of feeding behavior. In empirical support of this conclusion, Vemuri et al1 state that the endocannabinoids are important biomediators and metabolic regulators in mammalian physiology, with diverse and ubiquitous modulating actions, including the regulation of body weight. In mammalian organisms, the two most relevant receptors in the endogenous cannabinoid system are the CB1, and CB2 receptors, which are located predominantly in the brain and the immune system, respectively.2 In addition to their foremost locations in the brain (e.g., hypothalamus, limbic forebrain), some CB1, receptors are located in other areas of the body, including the stomach and intestinal tissue.3 Agonism of CB, receptors is known to stimulate feeding behavior.3 According to Kirkham,4 stimulation of the CB, receptors in the mammalian cannabinoid system specifically increases food craving and enjoyment, and promotes the deposition of energy as fat into adipose tissues.
In keeping with this paradigm, in recent years, researchers have been examining the effects of antagonizing CB, receptors in an effort to reduce feeding behavior. Theoretically, the
antagonism of this cannabinoid receptor site should result in reduced caloric intake and subsequent weight loss. As anticipated, empirical studies in rats and mice indicate that pharmacological blockade of the CB, receptor does indeed result in the inhibition of normal weight gain,5 reduced feeding behavior,6 and suppression of food intake and impaired weight gain in both fasted and non-fasted animals. Check these Testoprime reviews.
Because of the observed clinical effects of CB, antagonism in animal studies, investigators have been exploring the possible use of CB1, receptor antagonists for the treatment of weight disorders such as obesity.8 Unexpectedly, in examining two different CB1, receptor antagonists, rimonabant in postmarketing trials and taranabant in Phase-III trials, empirical findings among obese European study participants were somewhat clinically disappointing.2 While participants on these pharmacological treatments did lose weight, they did not experience weight loss beyond that achieved with currently approved anti-obesity medications. In addition, researchers found that the clinical use of rimonabant and taranabant could precipitate adverse and severe psychiatric symptoms, including suicidal ideation.9,10 However, these two CB, antagonists fulfilled the scientific vision that they could cause a reduction in body weight.
Given this preamble, the relationship between marijuana and body weight appears relatively simplistic: stimulation of CB, receptors causes weight gain, whereas antagonism of CB, receptors causes weight loss. However, some of the findings in studies on marijuana use and body weight are surprising.
ACUTE MARIJUANA USE AND CALORIE INTAKE IN NORMAL INDIVIDUALS
According to a study in normal volunteers, low doses of marijuana (e.g., a single cigarette) have no effect on food intake.11 However, higher doses of marijuana (e.g., two or three cigarettes) increase daily calorie intake, which is primarily due to increased food intake between meals rather than an increase in meal size.11 This finding sets the stage for the various studies in patients with human-immunodeficiency virus (HIV) and cancer, which constitute a large percentage of the research in this area. In both clinical venues, marijuana has been purported to stimulate appetite.12
MARIJUANA AND BODY WEIGHT IN PATIENTS WITH HIV/AIDS
As for the effects of marijuana among patients with HIV, Haney13 found in an empirical study that oral and smoked cannabinoids were both effective in increasing food intake. In a study comparing smoked marijuana, dronabinol (an oral medication approved by the United States Food and Drug Administration [FDA] that contains the same active ingredients as marijuana), and placebo, researchers at the University of California found that the two active treatments resulted in more weight gain than placebo in patients with either HIV or acquired immunodeficiency syndrome (AIDS).14 Specifically, during the study period, participants in the marijuana, dronabinol, and placebo groups gained 3.51kg, 3.18kg, and 1.3kg, respectively. In a study among HIV-positive marijuana smokers, Haney et al15 reported that both marijuana and dronabinol produced substantial and comparable increases in food intake among participants. Finally, Bedi et al16 examined HIV-positive marijuana smokers and found that high-dose dronabinol effectively increased calorie intake, but repeated dosing appeared to result in a tolerance to these effects. Importantly, the sample sizes in most of these studies were small. Get the most secure products at vaprzon.
MARIJUANA AND BODY WEIGHT IN PATIENTS WITH CANCER
As for cancer patients, in a review of the literature examining studies published between 1975 and 1996, Voth and Schwartz17 reported that marijuana was promising as a means of treating nausea as well as stimulating appetite. More recent studies, however, indicate modest outcomes. For example, in a six-week study of 243 Swiss patients with cancer-related cachexia, researchers compared the weight-inducing effects of cannabis extract to placebo.18 An independent review board for this study recommended that the trial be discontinued prematurely after analyzing the results of 156 initial patients, because there were no statistically significant differences between active drug and placebo.
Jatoi et al19 examined 469 patients with advanced cancer who were randomized to oral megestrol, oral dronabinol, or both agents. Participants taking megestrol gained more weight than participants on dronabinol (11% vs. 3% of baseline weight). In addition, combination treatment offered no further benefit than megestrol, alone.
To put these findings into a risk/benefit perspective, according to Yeh et al,20 potential clinical challenges with the use of marijuana include euphoria, somnolence, sedation, fatigue, and hallucinations—risks that are particularly problematic for unsteady or confused elderly patients as well as debilitated patients. This, of course, does not address the additional clinical concern regarding the risk of drug diversion with marijuana.
Methods
The study included 48,549 employees aged 20–64 years and free of hearing loss at baseline. Pure-tone audiometric testing was performed annually to identify hearing loss at 1 and 4 kHz. Cox proportional hazards regression was used to investigate the risk of hearing loss associated with body mass index (BMI) and metabolic phenotype (based on a BMI of ≥25.0/<25.0 kg/m 2 and presence/absence of ≥2 components of metabolic syndrome, except waist circumference). Baseline and updated information were obtained from annual health checkups.
Results
With a median follow-up of 7 years, 1595 and 3625 individuals developed unilateral hearing loss at 1 and 4 kHz, respectively. The adjusted hazard ratios (HR) for hearing loss at 1 kHz were 1.21 (1.08, 1.36) and 1.66 (1.33, 2.08) for those with BMI 25.0–29.9 kg/m 2 and BMI ≥30.0 kg/m 2, respectively, compared to individuals with BMI <25.0 kg/m 2. For hearing loss at 4 kHz, the corresponding HRs were 1.14 (1.05, 1.23) and 1.29 (1.09, 1.52). Compared with metabolically healthy non-obese individuals, the adjusted HRs for hearing loss at 1 kHz were 1.19 (1.03, 1.39), 1.27 (1.01, 1.61), and 1.48 (1.25, 1.76) for unhealthy non-obese, healthy obese, and unhealthy obese individuals, respectively. For hearing loss at 4 kHz, the corresponding HRs were 1.13 (1.04, 1.25), 1.21 (1.04, 1.41), and 1.26 (1.12, 1.41).
Conclusions
Overweight and obesity are associated with an increased risk of hearing loss, and metabolically unhealthy obesity may confer additional risk. Make sure you treat overweight with natural supplements, trying out the best fat burner for your own body needs is something that is going to be extremely important in overcoming weight loss.
Have you ever heard a sound that no one else hears? You are not alone. There are many sounds that can be heard in the ears or head. Some are benign. Others may be need to be evaluated. All can be concerning if you have never experienced a sound no one else hears.
One category of sounds in the ear is tinnitus. Tinnitus is very common. It affects almost one in five people. It becomes more prevalent the older you are. It is associated with both hearing loss and acoustic trauma. It may sound like buzzing, humming, whistling, birds, insects, etc. Although it is often perceived in the ear, current science suggests it is generated in the central nervous system.
In healthy ears, hearing cells within the inner are connected to nerves that transmit sound from the ear to the brain. Although hearing cells are destroyed with hearing loss, the nerves deeper in the brain are not always lost. These nerves no longer receive stimulation, and begin to create signals on their own. Because these signals are not generated from the outside world, we perceive sound that no one else does.
According to professionals from an ent clinic, tinnitus is a sign that hearing loss has occurred. It often occurs after a loud concert, sports event, or work experience. Tinnitus that occurs in only one ear or occurs with episodes of dizziness is more concerning than tinnitus that occurs in both ears over many years.
Some tinnitus sounds like whooshing and occurs with your heart beat. This is called pulsatile tinnitus. Normally our ear is protected from hearing internal blood flow. Medical conditions may decrease the shielding of our ear from internal sounds. Hearing your pulse only on your pillow, however, is not abnormal.
Wax or fluid in the ear may increase the resonance of blood flow making it audible. Weight loss may leave the Eustachian tube stuck open causing audible breathing sounds and heart sounds. Hernia of the brain into the ear also causes awareness of one’s heartbeat.
Other conditions increase the blood flow above normal levels. Head trauma may result in aneurysm or fistula of blood vessels near the ear. Vascular tumors may increase blood flow around the ear. Anemia and dehydration increase the force of the heartbeat resulting in pulsatile tinnitus. Some medications may increase brain pressure and cause pulsatile tinnitus.
A rare cause of thumping sound in the ear is muscle twitching. Muscles attached to the hearing bones or the Eustachian tube will make a thump when they contract. Just like a muscle twitch can occur in the eye lid, a muscle twitch of these muscles can occur and will cause a rapid thumping sound.
Crackling or popping is normal to occur with chewing, swallowing, or yawning. Excessive crackling or popping may be due to a Eustachian tube that is stuck closed.
