Many people who struggle with weight loss may find the answer in CBD oil. This product is miraculous for those who have tried several diet plans and still wounded up heavier. CBD oil helps increase metabolism, increasing the body’s ability to burn fat, and decreasing the overall body weight naturally. Losing weight, even with CBD products, is not going to happen overnight. However, these products can help the body shed excess weight and get to a healthy weight, which is easier to maintain. The benefits of using CBD to lose weight are just starting to be recognized. However, the people who have already tried it are quite pleased overall with the results.
Where Does CBD Oil Come From?
CBD oil comes out when hemp plants get pressed. It is often referred to as hemp oil. They are the same product. These are not marijuana plants as those contain higher levels of tetrahydrocannabinol or THC. THC is what gives the high psychoactive effect and leaves users with a “high” feeling. CBD, or cannabidiol, is the other main chemical in these plants that offers the relaxed, pain-relieving effects that many people associate with marijuana, without the “high”.
CBD is known for its health properties, including:
- Relieving nausea
- Stopping or slowing seizures
- Relieving anxiety
- Reducing inflammation
- Alleviating psychotic feelings or episodes
- topping or slowing down tumor growth.
It is also the focus of many clinical trials that aim to reduce the amount of fat someone has on his or her body. Some of the other ongoing clinical trials to find out about how CBD can improve overall health include:
- Seeing how CBD can help decrease the tremors for Parkinson’s patients
- Looking at how CBD helps those who struggle with anxiety and depression
- Comparing how strong the cardiac muscle is after exposure to CBD, which is being used to determine if it can help fight heart disease
- Using CBD to fight some of the effects of drug or alcohol withdrawal
- Easing the pain of those with chronic arthritis or an MS diagnosis, plus seeing if the CBD improves the immune system with one of these ailments
- Treating glaucoma by easing pressure within the eye itself
- Looking at how CBD reduces violent urges in people who struggle with schizophrenia
- Seeing how people sleep after taking CBD in any of its forms
People who have been using products containing CBD for quite some time experienced positive results. It is now time for science to catch up to what people have begun discovering on their own.
How Does CBD Oil Affect Weight Loss?
When people give CBD oil a try, they almost instantly notice that they feel better overall, without necessarily being able to pinpoint what feels different. The effects of CBD can be felt all over, from the mind to how well the body functions. These effects allow the chemicals of the body to function more precisely as well. CBD travels through the endocannabinoid system, allowing it to recognize the chemicals of the brain more effectively. As it moves, the CB1 receptors that are naturally occurring in the body begin to open up, which allows the receptors in the brain to read the chemicals moving around them more effectively. Normally, a person would feel the effects of the relaxation or relief from chronic pain as the CBD moves along this system. However, there is more that is happening around the body as well.
According to a study for molecular and cellular biochemistry, CBD’s effects on immature fat cells are also started during the traveling process. The goal of this study was to look into how CBD could potentially treat and even prevent obesity. The results that were found were unexpected and included:
- The proteins and genes that break down and oxidize fat got stimulated.
- The quantity and the level of activity within the mitochondria were increased. This helped to increase how effectively the body burned calories.
- Fewer proteins that generate fat cells were active.
When combined, these effects led to what is called fat browning. This is when white fat cells, or scientifically called adipose tissue, from inside the body is changed over to brown fat. Once the body notices brown fat, it begins to burn that fat for energy instead of holding it as it does with white fat. The white fat, which is beige in color, is more tolerant to glucose, which allows the person to be more resistant to medical conditions like diabetes.
The study was also able to determine that using too much CBD had opposite side effects. It led to increased storage of fat in the midsection of the body, glucose being absorbed into the cells, and insulin resistance within the different muscle tissues. This could lead to overeating and weight gain, an increase in total body fat, and other health issues like high blood pressure and uncontrolled blood sugar levels.
Other studies were done with rats showing the effects of exposure to CBD. During one of these animal studies, the rats were exposed to cannabinol (CBN) and CBD. Those exposed to CBN gained more weight and ate more than before they were exposed. Those exposed to only CBD ate less and lost weight during the study. This was also due to the change from white to beige fat.
What Body Systems Does CBD Help With?
CBD is known for helping with many systems all around the body. The relaxing and improved function of the body can help with issues, such as:
- Suppressing appetite
- Giving people the ability to feel more motivated
- Controlling or stopping the pain
- Improving overall mood
- Reducing how much pain is felt
- Increasing metabolism
- Decreasing overall inflammation
- Helping regulate the temperature of the body
- Regulating the pressure inside the eye (easing the symptoms of glaucoma)
- Better control over the muscles of the body
- Helping people sleep better
- Increased energy
- Improving memory
- Better balance
- Responding to stress more effectively
CBD is also known to improve the overall function of gut microbes. These microbes are responsible for regulating how much fat the body keeps, how long the body feels full after eating and regulating levels of blood sugar in the body. With full-spectrum CBD products, these functions increase, and a decrease in weight can happen more naturally.
CBD Also Provides a Sideline Benefit to Those Seeking a Way to Lose Weight
CBD can also help with improving mood. Anxiety and depression often control how much a person turns to food. CBD has mood stabilization as one of the effects most people experience, which prevents the highs and lows that people often go through when they struggle with mood disorders.
People who struggle with depression turn to food often as a way to feel better since food helps enhance one’s mood, at least temporarily. With the addition of CBD in any form, the person struggling with depression does not need to turn to food to feel better as often. This can help with the efforts to lose weight, and it can also start helping improve a person’s ability to see him or herself in a more positive light. Many who struggle with depression also have low self-esteem. Losing weight is one of the ways that a person may begin to feel better. This, in turn, boosts someone’s confidence level, which repeats the positive effects.
For someone struggling with anxiety, feeling a bit more in control over any aspect of life is often helpful. This simple addition to life can give someone with anxiety the ability to face various situations. By not feeling so anxious, a person may also feel more comfortable going out and getting some exercise. This can help a person reach his or her weight goals and give them a better sense of self.
How Does CBD Oil Reduce Appetite?
Most people struggle with the idea that CBD oil can effect changes, like reducing the appetite of users. After all, cannabis users constantly struggle with the munchies. However, that is a result of THC, not CBD. CBD allows the body to receive the proper signals that brain chemicals release. It does not force the brain to do anything other than function at a higher level naturally. This means the body can recognize when it is hungry and when it is full on its own. Furthermore, there is much anecdotal evidence that supports the theories that weight loss stems from a decreased appetite.
CBD has also been shown to help avoid metabolic disorders that typically accompany obesity. These can include problems with cholesterol, blood pressure, and diabetes. Since there are too many CB receptors in the body of obese people, the body does not always read the signals that are moving around it the right way. With the introduction of CBD, the body then begins to read what it needs and send the right responses more effectively. One study alone reduced the cholesterol of the participants by an average of 25 percent by lowering triglycerides, or fats in the blood. This was done by decreasing bad cholesterol levels and increasing the good cholesterol levels of the participants.
Ways of Improving the Chances of Achieving Weight Loss With CBD
CBD is only one thing that can be done to increase the chances of a successful weight loss. Changing habits can also help with those efforts. Plus, the earlier habits change, the more likely they are to stick around once the desired loss has been achieved. This means that people are more likely to keep the weight off. Here are some habits that need to change to get the weight down in a way that can be sustained.
- Eat a healthy diet: The more varied a person’s diet is, the better, so long as the basis for that diet is healthy food. This should be full of produce, mostly vegetables, and lean meats. Fats should be limited, as should sweets. That way, the body has the best chance to pull the nutrients it needs and dispose of what it does not need after eating.
- Alleviate sugar: Sugar is not good for the body, and it teaches the body to hold on to fat. It increases the risks of obesity and the likeliness of diabetes. Avoid any food or beverage that has sugar whenever possible. Read all labels, as sugar is often seen in foods that have a healthy label.
- Make sure to drink water: Water is vital to anyone who has weight loss goals. Water consumed before meals allows the body to feel full sooner, but also digest food easier. It can trigger the metabolism for a few hours, which can help burn more calories than CBD on its own.
- Carbs in moderation: Carbs are necessary. However, they do not need to be consumed heavily. When carbs are eaten, they should include whole-grain carbs so that the person eating them also gets the fiber they provide. Refined carbs, such as those that come from white bread and different types of pasta, increase blood sugar, leaving the person feeling hungrier than when they started.
- Increase fiber intake: When people eat more fiber, it helps them with their weight loss goals. This is because it fills the body quicker and stays with the body longer. This leaves the person feeling full longer, meaning he or she consumes fewer calories. It has also been shown to help regulate levels of blood sugar more effectively than other foods, allowing the body to feel better overall when fiber is consumed.
- Exercise regularly: The hardest part about exercise is to make sure it includes all different parts of the body. Each part of the body needs time, so the schedule should be changed up. Some days the focus should be on cardio, while on other days, the focus can be strength training. The days when strength training is the focus should also include variations, such as working the upper body sometimes while other times, the focus is on the lower body.
- Include black coffee: By starting the day with black coffee, the metabolism boost of caffeine can last the rest of the day. It is the problematic foods like the added sugar that negate what benefits black coffee could provide.
- Snack on healthy foods: Eliminate all snacks that would fall into the unhealthy category. By having only healthy snacks as an option, the temptation to stray from the best possible food is gone.
- Sleep: In all health-related goals, sleep needs to be factored in. For those seeking a way to reduce their weight, sleep is a key. Getting too little sleep, or not enough good quality sleep, can increase the chances of obesity by almost 100 percent in children, and by about half in adults.
- Build muscle: The more muscle a person has, the more calories get burned while doing nothing at all. The muscles need calories to stay strong, and this is true 24 hours per day. So while people sleep, eat, exercise, and work, those muscles are still burning calories.
- Stick with real foods: If a food item has ingredients that cannot easily be pronounced, then the food should not be eaten. Those foods are often unnecessary as part of a human diet. Plus, those foods are usually put in there to preserve the food. Opt for real foods that are raw or lightly cooked, ideally, whole foods which are easy to cook and easy for the body to digest.
How Can CBD Be Taken?
The point of taking CBD is to experience the effects as quickly as possible. The effect is for it to help start burning fat, increase metabolism, reduce anxiety, or improve the mood of someone. People have many options when it comes to taking CBD, and the option will determine how quickly the effects will be felt. For those who want to start taking CBD oil, there are several ways of taking it whatever product a person chooses and the desired results. Here are some of the most popular:
- Take a tincture: A tincture is a drop that a user would place under his or her tongue to begin being absorbed before swallowing. Most users wait between 30 and 60 seconds before swallowing the CBD to give it the best chance of working.
- Ingestion: There are many ways of ingesting CBD, from adding drops of CBD oil to foods and beverages to consuming edibles regularly. Some lollipops and gummies that contain CBD provide the same effects. They can be taken as often as necessary since they normally wear off after about 4 hours for most people.
- Inhaling: One of the fastest ways to get CBD into the body is through inhalation. It can be vaped or smoked. However, a user would need to invest in some type of vape pen or similar apparatus to get the CBD aerosolized enough to inhale it.
- Topical methods: There are many ways that CBD can also be spread on the skin. It can be done through a lotion, balm, many types of ointments, and even dabbers that allow the user to put the CBD directly on the area that hurts. There are also suppositories that could be used, but those must be placed against a mucous membrane of the body in order to work properly.
How long each option will take to work depends on what method was used to ingest it. Some methods hit the system almost instantly, like vaping. The same is true with tinctures. However, other methods, like ingesting, take a little longer. CBD must go through the liver before it gets disbursed to the rest of the body, slowing its delivery. However, it is also important to note that the dose also is part of what determines how long the effects will last. The quicker an option hits the body’s system, the sooner it normally wears off. Higher doses last longer than lower doses, and those with higher functioning livers will metabolize the CBD faster than those who have livers with lower function.
Does CBD Cause Any Unexpected Side Effects?
There are occasional effects that people feel when they take CBD, but those effects usually come as a result of taking a dose that was higher than what was necessary. Most of the effects can be reduced or negated by taking a lower dose. Here are some effects people may notice upon first taking CBD:
- Occasional diarrhea comes with higher doses than the body can handle or is used to. Lowering the dosage normally gets rid of this effect.
- Some people notice they feel tired when first taking CBD, but this is because of the relaxing effect. It normally lasts for a couple of hours before fading.
- Some people experienced dizziness when first taking CBD because of its inherent ability to reduce blood pressure. Taking care when standing until this passes is usually all that is necessary.
- Rarely people feel hungrier when taking CBD, but this is usually only with poor-quality products that have some of the effects of marijuana left in them. Getting good-quality CBD should get rid of this feeling.
- People taking CBD often notes having dry mouth. This can be easily combated by drinking more water, which helps with the desire to lose weight.
What Risks Need to Be Considered Before Using CBD for Weight Loss?
There are some inherent risks to adding CBD to a person’s life. One of them is the lack of regulation. The FDA does not regulate CBD oil or other products as effectively as it could at this point because there has only been one product that has been approved for use by humans in a medication form. While high-quality CBD is safe for almost everyone, only the best quality products must be used. Using lower-quality products could introduce psychoactive chemicals into the body, which would not produce the desired results.
Another risk is not knowing what specific dose is required for weight loss. People who regularly use cannabis would likely need to take more since their bodies are used to the chemicals already being there. However, it all depends on the desired effects and the starting point of the individual. The best method for figuring out what dose to take is to start small and then increase gradually until the desired effect is achieved.
CBD oil helps with many different aspects of functionality within the body; it is hard to consider people not benefiting from it. However, the full effects when it comes to losing weight are still being studied through many research settings. As more benefits of this product are understood, people will be able to start using it to get even more benefits than they are already getting. CBD alone is not going to be the perfect way for anyone to lose weight. However, it can be part of a full-spectrum effort on how to tackle weight loss goals and keep that weight off. From its anti-inflammatory effects to how it can curb appetites, CBD could be a wonder product that has the potential to change the future of how people take care of themselves.
Main Risks and Target Organs
Acute central nervous system stimulation, cardiotoxicity causing tachycardia, arrhythmias, hypertension and cardiovascular collapse. High risk of dependency and abuse.
Summary of Clinical Effects
Cardiovascular – Palpitation, chest pain, tachycardia, arrhythmias and hypertension are common; cardiovascular collapse can occur in severe poisoning. Myocardial ischaemia, infarction and ventricular dysfunction are described.
Central Nervous System (CNS) – Stimulation of CNS, tremor, restlessness, agitation, insomnia, increased motor activity, headache, convulsions, coma and hyperreflexia are described.
Stroke and cerebral vasculitis have been observed. Gastrointestinal – Vomiting, diarrhoea and cramps may occur. Acute transient ischaemic colitis has occurred with chronic methamphetamine abuse.
Genitourinary – Increased bladder sphincter tone may cause dysuria, hesitancy and acute urinary retention. Renal failure can occur secondary to dehydration or rhabdomyolysis. Renal ischaemia may be noted.
Dermatologic – Skin is usually pale and diaphoretic, but mucous membranes appear dry.
Endocrine – Transient hyperthyroxinaemia may be noted.
Metabolism – Increased metabolic and muscular activity may result in hyperventilation and hyperthermia. Weight loss is common with chronic use.
Fluid/Electrolyte – Hypo- and hyperkalaemia have been reported. Dehydration is common.
Musculoskeletal – Fasciculations and rigidity may be noted. Rhabdomyolysis is an important consequence of severe amphetamine poisoning.
Psychiatric – Agitation, confusion, mood elevation, increased wakefulness, talkativeness, irritability and panic attacks are typical. Chronic abuse can cause delusions and paranoia.
A withdrawal syndrome occurs after abrupt cessation following chronic use.
The diagnosis of acute amphetamine poisoning is made on the history of exposure or abuse, and the characteristic features of CNS and cardiovascular stimulation. The presence of amphetamines in urine or blood can support the diagnosis but is not helpful in management. Whilst some patients show signs of toxicity at blood concentrations of 20 µg/L, chronic abusers of amphetamine have been known to have blood concentration of up to 3000 µg/L.
First Aid Measures and Management Principles
Management of amphetamine and its complications is essentially supportive. The initial priority is stabilisation of the airway, breathing and circulation. Monitoring of pulse, blood pressure, oxygenation, core temperature and cardiac rhythm should instituted. Supplemental oxygen should be administered. Specific supportive care measures that may be necessary include: maintenance of hydration, control of seizures, relief of agitation, control of hyperthermia, control of hypertension, management of rhabdomyolysis. Decontamination with oral activated charcoal is appropriate if the patient is conscious. There are no suitable methods of enhancing elimination of amphetamine and no specific antidotes.
Contraindications include anorexia, insomnia, psychopathic personality disorders, suicidal tendencies, Gilles de la Tourette syndrome and other disorders, hyperthyroidism, narrow angle glaucoma, diabetes mellitis and cardiovascular diseases such as angina, hypertension and arrythmias (Dollery, 1991; Reynolds, 1996). Amphetamine interacts with several other drugs (see 7.6).
Routes of Exposure
Oral – Readily absorbed from the gastro-intestinal tract and buccal mucosa. It Is resistant to metabolism by monoamine oxidase.
Inhalation – Amphetamine is rapidly absorbed by inhalation and is abused by this route (Brust, 1993).
Parenteral – Frequent route of entry in abuse situations.
Kinetics of Amphetamine
Absorption by route of exposure – Amphetamine is rapidly absorbed after oral ingestion. Peak plasma levels occur within 1 to 3 hours, varying with the degree of physical activity and the amount of food in the stomach. Absorption is usually complete by 4 to 6 hours. Sustained release preparations are available as resin-bound, rather than soluble, salts. These compounds display reduced peak blood levels compared with standard amphetamine preparations, but the total amount absorbed and time to peak levels remain similar (Dollery, 1991).
Distribution by route of exposure – Amphetamines are concentrated in the kidney, lungs, cerebrospinal fluid and brain. They are highly lipid soluble and readily cross the blood-brain barrier. Protein binding and volume of distribution varies widely, but the average volume of distribution is 5 L/kg body weight (Dollery, 1991).
Biological Half-Life by Route of Exposure
Under normal conditions, about 30% of amphetamine is excreted unchanged in the urine but this excretion is highly variable and is dependent on urinary pH. When the urinary pH is acidic (pH 5.5 to 6.0), elimination is predominantly by urinary excretion with approximately 60% of a dose of amphetamine being excreted unchanged by the kidney within 48 hours. When the urinary pH is alkaline (pH 7.5 to 8.0), elimination is predominantly by deamination (less than 7% excreted unchanged in the urine); the half-life ranging from 16 to 31 hours (Ellenhorn, 1997).
The major metabolic pathway for amphetamine involves deamination by cytochrome P450 to para-hydroxyamphetamine and phenylacetone; this latter compound is subsequently oxidised to benzoic acid and excreted as glucuronide or glycine (hippuric acid) conjugate. Smaller amounts of amphetamine are converted to norephedrine by oxidation. Hydroxylation produces an active metabolite, O-hyroxynorephedrine, which acts as a false neurotransmitter and may account for some drug effect, especially in chronic users (Dollery, 1991).”
Elimination and excretion
Normally 5 to 30% of a therapeutic dose of amphetamine is excreted unchanged in the urine by 24 hours, but the actual amount of urinary excretion and metabolism is highly pH dependent (Dollery, 1991).
Amphetamine appears to exert most or all of its effect in the CNS by causing release of biogenic amines, especially norepinephrine and dopamine, from storage sites in nerve terminals. It may also slow down catecholamine metabolism by inhibiting monoamine oxidase (Hardman et al., 1997).” (edited)
The use of amphetamine for medical indications does not pose a significant risk to the fetus for congenital anomalies (Briggs, 1990). Amphetamines generally do not appear to be human teratogens. Mild withdrawal symptoms may be observed in the newborn, but the few studies of infant follow-up have not shown long-term sequelae, although more studies of this nature are needed. Illicit maternal use or abuse of amphetamine presents a significant risk to the foetus and newborn, including intrauterine growth retardation, premature delivery and the potential for increased maternal, fetal and neonatal morbidity.
These poor outcomes are probably multifactorial in origin, involving multiple drug use, life-styles and poor maternal health. However, cerebral injuries occurring in newborns exposed in utero appear to be directly related to the vasoconstrictive properties of amphetamines. Ericksson et al. (1989) followed 65 children whose mothers were addicted to amphetamine during pregnancy, at least during the first trimester. Intelligence, psychological function, growth, and physical health were all within the normal range at eight years, but those children exposed throughout pregnancy tended to be more aggressive.”
Interactions with Other Drugs
Acetazolamide – administration may increase serum concentration of amphetamine.
Alcohol – may increase serum concentration of amphetamine.
Ascorbic acid -lowering urinary pH, may enhance amphetamine excretion
Furazolidone – amphetamines may induce a hypertensive response in patients taking furazolidone.
Guanethidine – amphetamine inhibits the antihypertensive response to guanethidine.
Haloperidol – limited evidence indicates that haloperidol may inhibit the effects of amphetamine but the clinical importance of this interaction is not established.
Lithium carbonate – isolated case reports indicate that lithium may inhibit the effects of amphetamine.
Monoamine oxidase inhibitor – severe hypertensive reactions have followed the administration of amphetamines to patients taking monoamine oxidase inhibitors.
Noradrenaline – amphetamine abuse may enhance the pressor response to noradrenaline.
Phenothiazines – amphetamine may inhibit the antipsychotic effect of phenothiazines, and phenothiazines may inhibit the anorectic effect of amphetamines.
Sodium bicarbonate – large doses of sodium bicarbonateinhibit the elimination of amphetamine, thus increasing the amphetamine effect.
Tobacco smoking – amphetamine appears to induce dose-related increases in cigarette smoking.
Tricyclic antidepressants – theoretically increases the effect of amphetamine, but clinical evidence is lacking. (Stockley, 1994; Dollery, 1991)
Overall Interpretation of All Toxicological Analyses and Toxicological Investigations
Sample collection: Creatinine, urea, and electrolyte measurement are important to establish whether renal impairment or hyperkalaemia is present. Measurements of serum creatine kinase, aspartate transaminase and myoglobin can help to establish if there is rhabdomyolysis, and myoglobin can be detected in urine.
Liver function tests are relevant, since hepatitis can occur. A full blood count and coagulation studies can be helpful, with measurement of fibrinogen and of fibrin degradation products, in establishing a diagnosis of disseminated intravascular coagulation.
Temperature, blood pressure, and pulse rate should be monitored frequently. A temperature above 40°C, and marked hypertension and tachycardia are seen in severe poisoning. An electrocardiogram can be useful in detecting myocardial ischaemia or arrhythmia. Electrocardiographic monitoring can be helpful in patients with arrhythmia.
Urine or serum analysis for amphetamine can help to confirm exposure, but cannot be used to establish poisoning, because of difference in individual tolerance to amphetamines.
Acute Poisoning Through Ingestion
Effects are most marked on the central nervous system, cardiovascular system, and muscles. The triad of hyperactivity, hyperpyrexia, and hypertension is characteristic of acute amphetamine overdosage. Agitation, confusion, headache, delirium, and hallucination, can be followed by coma, intracranial haemorrhage, stroke, and death. Chest pain, palpitation, hypertension, tachycardia, atrial and ventricular arrhythmia, and myocardial infarction can occur.
Muscle contraction, bruxism (jaw-grinding), trismus (jaw clenching), fasciculation, rhabdomyolysis, are seen leading to renal failure; and flushing, sweating, and hyperpyrexia can all occur. Hyperpyrexia can cause disseminated intravascular coagulation. (Brust, 1993; Derlet et al., 1989)
Acute Poisoning ThroughInhalation
The clinical effects are similar to those after ingestion, but occur more rapidly (Brust, 1993).
Acute Poisoning Through Parenteral exposure
Intravenous injection is a common mode of administration of amphetamine by abusers. The euphoria produced is more intense, leading to a “rush” or “flash” which is compared to sexual orgasm (Brust, 1993). Other clinical effects are similar to those observed after ingestion, but occur more rapidly.
Acute Poisoning Through Ingestion
Tolerance to the euphoric effects and CNS stimulation induced by amphetamine develops rapidly, leading abusers to use larger and larger amounts to attain and sustain the desired affect. Habitual use or chronic abuse usually results in toxic psychosis classically characterised by paranoia, delusions and hallucinations, which are usually visual, tactile or olfactory in nature, in contrast to the typical auditory hallucinations of schizophrenia.
The individual may act on the delusions, resulting in bizarre violent behaviour, hostility and aggression, sometimes leading to suicidal or homicidal actions. Dyskinesia, compulsive behaviour and impaired performance are common in chronic abusers. The chronic abuser presents as a restless, garrulous, tremulous individual who is suspicious and anxious.
Course, Prognosis, and Cause of Death
Symptoms and signs give a clinical guide to the severity of intoxication as follows (Espelin and Done, 1968):
Mild toxicity – restlessness, irritability, insomnia, tremor, hyperreflexia, sweating, dilated pupils, flushing;
Moderate toxicity – hyperactivity, confusion, hypertension, tachypnoea, tachycardia, mild fever, sweating;
Severe toxicity – delirium, mania, self-injury, marked hypertension, tachycardia, arrhythmia, hyperpyrexia, convulsion, coma, circulatory collapse.
Death can be due to intracranial haemorrhage, acute heart failure or arrhythmia, hyperpyrexia, rhabdomyolysis and consequent hyperkalaemia or renal failure, and to violence related to the psychiatric effects (Kalant & Kalant, 1975).
Systematic Description of Clinical Effects
Cardiovascular symptoms of acute poisoning include palpitation and chest pain. Tachycardia and hypertension are common. One third of patients reported by Derlet et al. (1989) had a blood pressure greater than 140/90 mmHg, and nearly two-thirds had a pulse rate above 100 beats per minute. Severe poisoning can cause acute myocardial ischaemia, myocardial infarction (Carson et al., 1987; Packe et al., 1990), and left ventricular failure (Kalant & Kalant, 1975). These probably result from vasospasm, perhaps at sites of existing atherosclerosis. In at least one case, thrombus was demonstrated initially (Bashour, 1994).
Chronic oral amphetamine abuse can cause a chronic cardiomyopathy; an acute cardiomyopathy has also been described (Call et al., 1982). Hypertensive stroke is a well-recognised complication of amphetamine poisoning (see 9.4.3). Intra-arterial injection of amphetamine can cause severe burning pain, vasospasm, and gangrene (Birkhahn & Heifetz, 1973).
Pulmonary fibrosis, right ventricular hypertrophy and pulmonary hypertension are frequently found at post-mortem examination. Pulmonary function tests usually are normal except for the carbon monoxide diffusing capacity. Respiratory complications are sometimes caused by fillers or adulterants used in injections by chronic users. These can cause multiple microemboli to the lung, which can lead to restrictive lung disease. Pneumomediastinum has been reported after amphetamine inhalation (Brust, 1993).
For the central nervous system (CNS), main symptoms include agitation, confusion, delirium, hallucinations, dizziness, dyskinesia, hyperactivity, muscle fasciculation and rigidity, rigors, tics, tremors, seizures and coma. Both occlusive and haemorrhagic strokes have been reported after abuse of amphetamines. Twenty-one of 73 drug-using young persons with stroke had taken amphetamine (Kaku & Lowenstein, 1990), of whom six had documented intracerebral haemorrhage and two had subarachnoid haemorrhage. Patients with underlying arteriovenous malformations may be at particular risk (Selmi et al., 1995).
Stroke can occur after oral, intravenous, or nasal administration. Severe headache beginning within minutes of ingestion of amphetamine is usually the first symptom. In more than half the cases, hypertension which is sometimes extreme, accompanies other symptoms. A Cerebral vasculitis has also been observed (Brust, 1993). Dystonia and dyskinesia can occur, even with therapeutic dosages (Mattson & Calverley, 1968). Psychiatric effects, particularly euphoria and excitement, are the motives for abuse. Paranoia and a psychiatric syndrome indistinguishable from schizophrenia are sequelae of chronic use ( Hall et al., 1988; Flaum & Schultz, 1996; Johnson & Milner, 1966).
In the autonomic nervous system, stimulation of alpha-adrenergic receptors produces mydriasis, increased metabolic rate, diaphoresis, increased sphincter tone, peripheral vasoconstriction and decreased gastrointestinal motility can occur. Stimulation of ß-adrenergic receptors produces increased heart rate and contractility, increased automaticity and dilatation of bronchioles.
For skeletal and smooth muscle, myalgia, muscle tenderness, muscle contractions, and rhabdomyolysis, leading to fever, circulatory collapse, and myoglobinuric renal failure, can occur with amphetamines can occur. (Kendrick et al., 1977).
Common gastrointestinal symptoms include nausea, vomiting, diarrhoea, and abdominal cramps. Anorexia may be severe. Epigastric pain and haematemesis have been described after intravenous amphetamine use. A case of ischaemic colitis with normal mesenteric arteriography in a patient taking dexamphetamine has been described (Beyer et al., 1991). Hepatitis and fatal acute hepatic necrosis have been described (Kalant & Kalant, 1975). Renal failure, secondary to dehydration or rhabdomyolysis may be observed.
Increased bladder sphincter tone may cause dysuria, hesitancy and acute urinary retention. This effect may be a direct result of peripheral alpha-agonist activity.Spontaneous rupture of the bladder has been described in a young woman who took alcohol and an amphetamine-containing diet tablet (Schwartz, 1981).
Transient hyperthyroxinaemia may result from heavy amphetamine use (Morley et al., 1980). Skin is usually pale and diaphoretic, but mucous membranes appear dry. Chronic users may display skin lesion, abscesses, ulcers, cellulitis or necrotising angiitis due to physical insult to skin, or dermatologic signs of dietary deficiencies, e.g. cheilosis, purpura. Mydriasis may be noted on the eye, ear, nose, and throat. Diffuse hair loss may be noted. Chronic users may display signs of dietary deficiencies. Disseminated intravascular coagulation is an important consequence of severe poisoning ( Kendrick et al., 1980). Idiopathic thrombocytopenic purpura may occur. For fluid and electrolyte disturbance, increased metabolic and muscular activity may result in dehydration.
Special Risks on Pregnancy
Eriksson et al. (1989) followed 65 children whose mother were addicted to amphetamine during pregnancy, at least during the first trimester. Intelligence, psychological function, growth, and physical health were all within the normal range at eight years, but those exposed throughout pregnancy tended to be more aggressive. A case report describes a normal female infant born to mother who took up to 180 mg/day of dexamphetamine for narcolepsy throughout pregnancy (Briggs et al., 1975).
Special Risks on Breast-feeding
Amphetamine is passed into breast milk and measurable amounts can be detected in breast-fed infant’s urine. Therefore lactating mothers are advised not to take or use amphetamine.
Amphetamine Withdrawal Syndrome
Abrupt discontinuance following chronic use is characterised by apathy, depression, lethargy, anxiety and sleep disturbances. Myalgias, abdominal pain, voracious appetite and a profound depression with suicidal tendencies may complicate the immediate post-withdrawal period and peak in 2 to 3 days. To relieve these symptoms, the user will often return to use more amphetamine, often at increasing doses due to the tolerance which is readily established. Thus a cycle of use-withdrawal-use is established (Kramer et al., 1967; Hart & Wallace, 1975). Physical effects are not life threatening but can lead to a stuporose state (Tuma, 1993); the associated depression can lead to suicide. It may take up to eight weeks for suppressed REM (rapid eye movement ) sleep to return to normal (Brust 1993).
When the intravenous dosage is increased too rapidly the individual develops a peculiar condition referred to as “overamped”: in which he or she is conscious but unable to speak or move. Elevated blood pressure, temperature and pulse as well as chest distress occurs in this setting. Death from overdose in tolerant individuals is infrequent.
General supportive measures should be used. These should include stabilisation of the airway, breathing, and circulation; relief of agitation, adequate hydration, and control of core temperature. Convulsions, hyperthermia, and rhabdomyolysis may require specific treatment. Activated charcoal may be helpful for decontamination after oral ingestion. Ipecacuanha is contra-indicated because of its stimulant properties. There are no effective methods of enhancing elimination and no antidote. Agitation and convulsion can be treated with diazepam. If agitation is severe, then chlorpromazine may have specific advantages over other major tranquillisers ( Espelin & Done, 1968; Klawans, 1968). Parenteral dosages of 0.5 to 2 milligrams per kilogram have been used in Infants ( Espelin & Done, 1968). Severe hyperthermia (core temperature greater than 40°C) requires forced cooling by fans, tepid sponging or other means, and may also require the administration of diazepam or dantrolene or both agents in order to eliminate muscle activity.
Rhabdomyolysis associated with muscle overactivity can cause hyperkalaemia or renal failure, and should be treated conventionally. Dialysis may be needed if renal failure supervenes. Acute severe hypertension (diastolic blood pressure greater than 100 mmHg) can be controlled by infusion of sodium nitroprusside by continuous intravenous infusion at an initial rate of 3 mcg/kg/min, titrated to achieve the desired response. Patients who are addicted to amphetamines may develop withdrawal syndrome described in 9.5.
Life Supportive Procedures and Symptomatic/Specific Treatment
Treatment is supportive. Administration of supplemental oxygen, establishment of intravenous access and monitoring of vital signs including core temperature, and cardiac rhythm are recommended. The following may be necessary according to clinical indication: maintenance adequate airway and ventilation, rehydration with intravenous fluids, control of seizures, control of agitation with benzodiazepines, control of severe hypertension (diastolic blood pressure greater than 110 mmHg), control of hyperthermia, treatment of hyperkalaemia, and cardiac intensive care for ischaemia or arrhythmia. No regime of oral decontamination has been demonstrated to improve outcome. Ipecacuanha is contra-indicated. Oral activated charcoal may be helpful following oral overdosage. Forced acid diuresis has been abandoned as a decontamination procedure. Neither haemodialysis nor charcoal haemoperfusion is likely to be of benefit. There is no antidote to amphetamine poisoning in adults or children.
There are differences between dexamphetamine and related compounds such as 3,4-methylenedeoxymetamphetamine (“ecstacy”); for example, hyperthermia appears to be more of a problem with the latter, and this may be because of the association between use and frenetic physical activity (“rave” dancing) (Henry et al., 1992). In the past, energetic gastric decontamination procedures were suggested (Espelin & Done, 1968). There is no evidence that such procedures improve outcome in amphetamine poisoning, and they are potentially hazardous. Oral activated charcoal is probably the safest option for decontamination, but is only likely to bind drug in the stomach if a substantial oral dose of amphetamine has been taken, and the charcoal is given within an hour or two of ingestion. If should only administered to patients in whom swallowing and gag reflexes are intact. In drug smugglers who have swallowed supposedly inert packages of amphetamines (“stuffers” or “packers”), and who develop symptoms because of leakage from the packages, then repeated doses of oral activated charcoal with a cathartic are likely to be worthwhile.
Forced acid diuresis has now been abandoned as an elimination treatment, because it is intrinsically difficult and potentially dangerous. Treatment of agitation in amphetamine poisoning is required when a patient is a danger to himself or herself, or to others. Because poisoning is associated with sympathetic overactivity, and chlorpromazine has alpha-adrenoreceptor antagonist actions, chlorpromazine has been recommended as the sedative treatment of choice (see 10.1). There is no study to demonstrate that chlorpromazine is in fact superior to benzodiazepine.
Ingestion of 2.2g (28mg/kg) in a 21 year old man resulted in severe toxicity (Ginsberg et.al., 1970).
An 18 month old male infant ingested an unknown amount of amphetamine, subsequently detected in the urine. He had a history of restlessness and vomiting for 10 hours and was admitted to hospital with mild fever (38°C), pulse rate of 140 per minute and a respiratory rate of 34 per minute. He looked acutely unwell, hyperactive and combative and had normal pupils with a bi-lateral light reflex. Some irregular flushing was found over the skin of the trunk. He was given diazepam 10mg intravenously, 10% chloral hydrate 10ml rectally and haloperidol 20mg intravenously. After a sleep of 20 hours normal activity resumed and the patient was clinically well and discharged (Soong et.al., 1991).
A 20-month-old male infant was admitted to hospital with a history of being too restless, hyperactive and agitated to be manageable for several hours, and had not responded to 10mg diazepam given intravenously in a local medical clinic. He had dilated pupils, doll’s eyes and normal discs. Generalised hypperreflexia and a mild clonus were noted, but no focal neurological abnormalities could be found. Hisvital signs were – blood pressure 130/90 mmHg, pulse rate 150/min, respiratory rate 46/min and normal temperature. The clinical status remained unchanged for a further 18 hours and the patient then calmed down to sleep for 20 hours. Subsequently the parents found amphetamine powder spread near the infant’s bed (Soong, et.al., 1991). When prescribing amphetamines, due regard must be given to its potential for misuse and addiction.
- Bashour TT (1994) Acute myocardial infarction resulting from amphetamine abuse: a spasm-thrombus interplay? Am Heart J, 128: 1237-1239.
- Beyer K., Bickel JT & Butt JH (1991) Ischemic colitis associated with dextroamphetamine use. J Clin Gastroenterol, 13: 198-201.
- Birkhahn HJ & Heifetz M (1973) Accidental intra-arterial injection of amphetamine: an unusual hazard of drug addiction. Brit. J Anaesthesia, 45: 761-763.
- Briggs GG, Samson JH & Crawford DJ (1975) Lack of abnormalities in a newborn exposed to amphetamine during gestation. Am J DisChild, 129: 249-250.
- Briggs G, Freeman J & Yaffe S (1990) Drugs in pregnancy and lactation: a reference guide to fetal and neonatal risk, ed 3.
- Baltimore, Williams & Wilkins. Brust JCM (1993) Neurological aspects of substance abuse.
- Stoneham, Butterworth-Heineman. Budavari S ed. (1996) The Merck Index: an encyclopedia of chemical, drugs, and biological, 12th ed. Rahway, New Jersey, Merck and Co., Inc. Call TD, Hartneck J, Dickinson WW, Hartman CW & Bartel AG (1982) Acute cardiomyopathy secondary to amphetamine abuse. Ann Int Med, 97: 559-560.
- Carson P, Oldroyd K & Phadkle K (1987) Myocardial infarction due to amphetamine. Brit Med J, 294: 1525-1526.
- Derlet RW, Price P, Horowitz BZ & Lord RV (1989) Amphetamine toxicity: experience with 127 cases. J Emerg Med, 7: 157-161.
- Dollery CT (1991) Therapeutic drugs. Edinburgh Churchill, Livingstone.
- Ellenhorn, M.J. (1997) Ellenhorn’s Medical Toxicology, 2nd edition. Baltimore, Williams and Wilkins.
- Eriksson M, Billing L, Steneroth G & Zetterstrom R (1989) Health and development of 8-year-old children whose mothers abused amphetamine during pregnancy. Acta Paediatrica Scandinavica, 78: 944-949.
- Espelin DE, Done AK (1968) Amphetamine poisoning. Effectiveness of chlorpromazine. New Eng J Med, 278:1361-1365.
- Flaum M & Schultz SK (1996) When does amphetamine-induced psychosis become schizophrenia? Am J Psych, 153: 812-815.
- Ginsberg MD Hertzman M & Schmidt-Nowara WW (1970) Amphetamine intoxication with coagulopathy, hyperthermia and reversible renal failure. A syndrome resembling heatstroke. Ann Intern Med, 73: 81-85.
- Hall RCW, Popkin MK, Beresford TP & Hall AK (1988) Amphetamine psychosis: clinical presentation and differential diagnosis. Psychiatric Med, 6: 73-79.
- Hardman JG, Limbird LE, Molinoff PB, Ruddon RW & Goodman Gilman A (1996) Goodman & Gilman’s the pharmacological basis of therapeutics, 9th ed. New York, McGraw Hill.
- Hart JB & Wallace J (1975) The adverse effects of amphetamines. Clin Toxicol, 8: 179-190.
- Henry JA, Jeffreys KS & Dawling S (1992) Toxicity and deaths from 3,4-methylenedeoxymetamphetamine (“ecstasy”). Lancet, 340: 384-387.
- Johnson J & Milner G (1966) Psychiatric complications of amphetamine abuse. Acta Psychiatrica Scandinavica, 42: 252-263.
- Kalant H & Kalant OJ (1975) Death in amphetamine users: causes and rates. Canad Med Assoc J, 112: 299-304.
- Kaku DA & Lowenstein DH (1990) Emergence of recreational drug abuse as a major risk factor for stroke in young adults. Ann Int Med, 113: 821-827.
- Kendrick WC, Hull AR & Knochel JP (1977) Rhabdomyolysis and shock after intravenous amphetamine administration. Ann Int Med, 86: 381-387.
- Klawans HL (1968) Chlorpromazine vs. amphetamine. New Engl J Med, 279:329.
- Kramer JC, Fischman VS & Littlefield DC (1967) Amphetamine abuse. Pattern and effects of high doses taken intravenously. JAMA, 201: 305-304.
- Mattson RH & Calverly JR (1968) Dextroamphetamine-sulphate-induced dyskinesias. JAMA, 204: 400-402.
- Morley JE, Schafer RB, Elson MK, Slag MF, Raleigh MJ, Brammer GL, Yuwiler A & Herschman JM (1980) Amphetamine-induced hyperthyroxinemia. Ann Int Med, 93: 707-709.
- Packe GE, Garton MJ & Jenning K (1990) Acute myocardial infarction caused by intravenous amphetamine abuse. Brit Med J, 64: 23-24.
- Reynolds JEF (1996) Martindale; The extra pharmacopoeia, 31st ed. London, Pharmaceutical Press.
- Schwartz DT (1981) Idiopathic rupture of the bladder. J Urol, 125: 602.
- Selmi F, Davies KG, Sharma RR & Neal JW (1995) Intracerebral haemorrhage due to amphetamine abuse; report of two cases with underlying arteriovenous malformation. Brit J Neruosurg, 9: 93-96.
- Soong WJ, Hwang BT, Tsai WJ & Deng JF (1991) [Amphetamine poisoning in infants: report of 2 cases]. Chung-Hua-I-Hsueh-Tsa-Chih, 48: 228-231.
- Stockley IH (1994) Drug interactions, 3rd ed. Oxford, Blackwell Science.
- Tuma TA (1993) Depressive stupor following amphetamine withdrawal. Brit J Hosp Med, 49: 361-363.