Ketamine bladder syndrome

Ketamine bladder syndrome

 Is there anything a ketamine user can do to avoid ketamine bladder syndrome? Is there a way to keep bladder as healthy as possible besides obviously limiting and spacing out usage?

Originally posted in SR 2.0 . Reviewed 20/4/22

Ketamine bladder syndrome is a rare but serious condition that can result from long-term, heavy use of ketamine. Symptoms of the condition include frequent urination, pain during urination, blood in urine, and urgency. The exact cause of the condition is not fully understood, but it is thought to involve the toxic effects of ketamine and its metabolites on bladder and urinary tract tissues, leading to inflammation, fibrosis, and scarring.

Toxic effects of ketamine on bladder cells result in oxidative stress and cell death. Chronic exposure to ketamine can cause inflammation, fibrosis, and reduced blood flow to the bladder. If ketamine use is stopped early enough, the condition may be reversible. But in severe cases, surgical intervention, such as bladder removal, may be necessary. Treatment may involve pain relief, bladder retraining, and medications to reduce inflammation and urinary symptoms.

Ketamine has a high potential for abuse and addiction.So, individuals who use ketamine regularly and at high doses are at increased risk of developing ketamine bladder syndrome and other serious health problems.

There are only a few cases of ketamine bladder in non-intensive users of ketamine. Most of them are dependent people using several grams a day. So, limiting and spacing out usage seems to be a very useful strategy.

There are other measures, although their efficacy is theoretical and not based in evidences. Drinking enough water while on K and a day after could help to keep bladder cleaner.

So,it is possible that a simple urine test could detect early symptoms (microscopic blood and other alterations). Probably, very frequent users should take a simple urine test to rule out problems, and go to the doctor if urinary symptoms are present..

It seems likely that ketamine derivatives as methoxetamine involve similar risks

 

Diabetes and drugs: harm reduction

I hace Type 1 Diabetes. I am interested in diabetes and drugs: harm reduction strategies, tips…Also, I want to kow which drugs are more and less harmful.

Originally posted in SR 2.0 . Reviewed 20/2/22

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In this post we will focus on Type 1 Diabetes Mellitus (DM1), the most common type of diabetes mellitus in youth and young adults. 2021, It is estimated that there were about 8 million individuals worldwide with type 1 diabetes: of these 1,5 million (18%) are less than 20 years, 5,4 million (64%) are 20–59 years, and 1·6 million (19%) are 60 years or older.

DM1, also known as juvenile diabetes, is a chronic autoimmune disease. This occurs when the body’s immune system mistakenly attacks and destroys the insulin-producing cells of the pancreas. This causes a lack of insulin production and can lead to high blood glucose (sugar) levels.

  • Some common symptoms of DM1 s include:
  • Increased thirst and frequent urination
    Increased hunger
    Fatigue and weakness
    Blurred vision
    Unintentional weight loss
    Irritability or mood swings
    Slow healing sores or frequent infections

Treatment for DM1 usually involves insulin injections or an insulin pump. It is important for people with DM1 to  monitor blood glucose levels and adjust insulin dose.

In addition, people with DM1 should follow a healthy eating plan, engage in regular physical activity. Also, monitor blood pressure and cholesterol levels. So, they can reduce the risk of cardiovascular, neurological or kidney complications .

1-Diabetes Mellitus and drugs

 

DM1 affects mostly young people. This segment of the population has the highest frequencies of recreational drug use.

Young people with DM1 have the same motivations and concerns as those without the disease. It is clear that not using drugs is the best way to avoid problems. But it is also clear that a significant proportion of them will use them. Indeed, there are studies that indicate this:

There are specific risk reduction measures for people with diabetes who use drugs.

2.-General measures:

 

In the first months after diagnosis, disease management is often particularly complicated. Some training is necessary to learn to manage the timing of blood sugar measurements.  To recognise hypoglycaemia or hyperglycaemia can be difficult. Also to measure insulin doses or calculate the meal before or after exercise. All this becomes simpler over time. Before considering the use of any drug, it is important to know how to manage diabetes.

Monitor blood glucose levels frequently: It is important for individuals with DM1  to monitor blood glucose levels frequently. This should be don both during drug use and in the hours following use. This can help them identify and treat hypoglycemia or hyperglycemia  as quickly as possible

Carry fast-acting sources of glucose: Individuals with DM1 who use recreational drugs should carry fast-acting sources of glucose with them always. For example,  glucose tablets, candy, or juice. These can be used to quickly treat hypoglycemia.

Stay hydrated: Some recreational drugs can cause dehydration, which can exacerbate the symptoms of hyperglycemia. DM1 drug users should drink plenty of water and avoid alcohol, that causes dehydration.

Never take drugs alone. Make sure that someone with you knows your situation. A friend who knows how to measure your blood sugar. And also to inject the right amount of insulin or fast-acting sources of glucose.

3.- Specific substances:

 

Alcohol:

Alcohol consumption can have an impact on blood glucose levels, which can be particularly concerning for individuals with Type 1 diabetes who rely on insulin therapy to manage their blood glucose levels. However, in moderation, alcohol can be safely consumed by many individuals with diabetes.

When it comes to choosing which alcoholic beverages to consume, it’s important to consider the carbohydrate and sugar content of the drink. Drinks that are high in carbohydrates and sugar can cause a rapid increase in blood glucose levels, which can be particularly problematic for individuals with diabetes.

Here are some examples of alcoholic beverages that are generally considered to be less harmful for individuals with Type 1 diabetes:

Light beer: Light beer contains fewer carbohydrates and calories than regular beer, which makes it a better choice for individuals with diabetes.

Red or white wine: Red or white wine can be a good option as they typically contain fewer carbohydrates than beer and some mixed drinks.

Spirits: Spirits such as vodka, gin, or whiskey are lower in carbohydrates than beer or wine, and can be mixed with sugar-free mixers such as diet soda or Coke Zero.

On the other hand, there are other drinks particularlly risky:

Regular beer: Regular beer typically contains a higher amount of carbohydrates than other alcoholic beverages, which can cause a rapid increase in blood glucose levels. may pack 35–44 grams of carbs per 7-ounce (225-mL) serving

Sweet wines: Sweet wines such as dessert wines, port wines, and some sparkling wines contain higher amounts of sugar and carbohydrates than other wines, which can cause a rapid increase in blood glucose levels.

Mixed drinks: Mixed drinks, such as margaritas, daiquiris, and other cocktails, may pack 35–44 grams of carbs per 7-ounce (225-mL) serving. The same goes for cream liqueurs such as Bailey’s and Kahlua. These provide around 13 grams of carbs, of which 12 grams are from sugar, for every 2 ounces (60 grams) of beverage.

 

Tobacco:

Probably, tobacco is the most harmful drug for a diabetic.Smoking tobacco is a major risk factor for cardiovascular disease, and individuals with diabetes are already at an increased risk of developing this condition. Smoking can further increase the risk of cardiovascular disease in individuals with diabetes, potentially leading to heart attacks, stroke, and other complications.

Tobacco can enhance insulin resistance and reduce the effectiveness of diabetes medications.

Smoking can impair wound healing, which can be particularly problematic for individuals with diabetes who are already at an increased risk of developing foot ulcers and other wounds.

E-cigs probably pose less risk than smoked, conventional tobacco.

Cannabis:

The consequences of cannabis use in diabetic patients are not very clear. Some studies suggest that the risks are similar to those of tobacco although they are probably biased by the fact that many of the participants also smoke tobacco.
On the other hand, it has been suggested that some cannabinoids may have a beneficial effect on blood glucose control, although there are also not enough good studies.

It is important to remember that cannabis increases appetite, which may have consequences in DM1.

The use of vaporisers instead of combustion (with or without tobacco) is also particularly advisable.

 

Stimulants (cocaine, amphetamine, methamphetamine):

There is no direct effect between stimulant use and blood sugar levels. But it is important to be aware of what you are doing while using them. Intense physical exercise (sex, dancing) can have an impact on carbohydrate expenditure and facilitate hypoglycaemia.It’s important to take regular breaks and rest to avoid exhaustion, which can affect blood glucose levels.

On the other hand, it is important to consider that stimulants can also reduce appetite. It’s important to have healthy snacks available, such as fruit, juices and low-carbohydrate foods, to maintain blood glucose levels.

 

Psychedelics and psychedelic-like (MDMA):

The previous considerations on stimulants (in terms of exercise and appetite) apply.

In addition, some psychedelics alter the perception of time. It may be important to set an alarm clock to remember to monitor glucose.

Psychedelics, MDMA and ketamine alter the perception of one’s own body. In the usual state of consciousness diabetics can recognise a rise or fall in blood sugar by their bodily sensations. These substances can alter these perceptions, making it difficult to recognise them.

 

Ketamine as antidepressant

How can I use ketamine as antidepressant?

Originally posted in SR 2.0 27/10/2013. Reviewed 20/2/22

Ketamine is a drug that works as a non-competitive antagonist at glutamate N-methyl-D-aspartate (NMDA) receptors. Its main use is  dissociative anesthesia. It was found to have antidepressant properties in 2000. Then,  subsequent studies have shown it to be effective in treating treatment-resistant depression (TRD) with a rapid clinical effect within several hours.

However, its antidepressant properties are transient. It lasts around  1 week following a single infusion and 18-19 days following repeated infusions. Ketamine has also been reported to have anti-suicidal and anti-anhedonic actions

Ketamine has been found to have a rapid antidepressant effect in several studies, with multiple meta-analyses concluding that it is effective for major depressive episodes in both unipolar and bipolar depression. While some studies suggest the effect can last up to 7 days, others suggest it may be shorter in bipolar depression. And other modalities of ketamine administration such as intranasal and oral routes have been studied. But their efficacy is less clear.

Intranasal esketamine has been approved by the FDA for major depression that has failed treatment with two or more antidepressants, with studies showing significant improvement in depression at 4 weeks compared to placebo. Ongoing trials are being conducted to track safety outcomes up to 5 years and explore the efficacy of R-ketamine.

Recent studies show that ketamine has strong antidepressant properties. Typical dosage is 0.5 mg/kg intravenous in infussion in 30-40 minutes; oral route seems also effective at that dosage (0.5 mg/kg). The effect is fast and strong but not lasting in time, it disappears in hours or days and further dosages do not reply this effect.

With actual knowledge, Ketamine may prove useful in a select group of patients but current medical knowledge looks to other treatments as the first line against depression
http://www.ncbi.nlm.nih.gov/pubmed/23661785

http://www.ncbi.nlm.nih.gov/pubmed/23805864

http://www.ncbi.nlm.nih.gov/pubmed/23825857

http://www.ncbi.nlm.nih.gov/pubmed/23893490

 

5-MeO-DMT risks

Which are 5-MeO-DMT risks?

I am very interested in exploring entheogens. But I am concerned about 5-MeO-DMT risks.  I am apprehensive about whether there are any dangers . I have never read about deaths or serious complications.

But the many trip reports mention breathing irregularities, having to remember to breath, people turning a bit blue in the face, extremely elevated heart rate or blood pressure, feeling like an elephant in sitting on you…

I read the LD50 is very high though, far higher than the active dose. So my question, are these physical effects all in peoples’ heads? Is 5-MEO-DMT just as safe as N-N-DMT or are there any real dangers involved?

Originally posted in SR 2.0 . Reviewed 20/2/22

Effects and risks of 5-MeO-DMT have been studied during decades. In fact, 5-MeO-DMT is a common constituent of many different plants and has been used traditionally in psychoactives snuffs. Examples are  Yopo (Anadenanthera colubrina seeds), Epena from Virola spp, and some ayahuasca-type brews. Risks are basically psychological. As many other classical psychedelics, physical toxicity is  very low. 5-MeO-DMT can cause intense and overwhelming psychedelic experiences, which may lead to anxiety, panic attacks, and paranoia.

Short term (1-10 minute) non-responsiveness or unconsciousness can appear with smoked doses over 8-10 mg or insufflated doses over 15-20 mg. So sitting down and have a person that can take care of you are extremely important. The drug can cause physical symptoms such as increased heart rate, elevated blood pressure, dizziness, and nausea.

I think breathing problems are probably related to psychological stress. There are no cases in science of organic toxicity associated to 5-MeO-DMT

It is importantto avoid using 5-MeO-DMT in combination with other substances. Specially those that affect serotonin levels in the brain, such as antidepressants, SSRIs, and MAOIs.

This is because combining 5-MeO-DMT with these substances (particularly MAOIs) could potentially result in serotonin syndrome. This is a a potentially life-threatening condition characterized by high levels of serotonin in the body. Additionally, the use of stimulants such as amphetamines and cocaine may increase the risk of adverse effects associated with 5-MeO-DMT. This includes hypertension and tachycardia.

 

MDMA, amphetamines and breast-feeding

Should MDMA and amphetamines be avoided during lactation? Is it strictly forbidden or risks are acceptable?

Originally posted in SR 2.0 31/10/2013. Reviewed 20/2/22

The relation between MDMA and lactation is not clear. As far as I know, there are no published studies on this particular issue. Available data on amphetamine show that «In dosages prescribed for medical indications, some evidence indicates that amphetamine might not affect nursing infants adversely.». On the other hand, data from methamphetamine show that meth is secreted to breast milk and it should be avoided.

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~LJwPas:1

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~LJwPas:2

In my opinion, it is basic to avoid use that can be harmful to third persons. A person can asume risks for himself but not for others, even less a baby. So there would be three options:

1) Wait to finish lactation and then use MDMA or amphs

2) Interrupt natural lactation (use artificial milk) and use MDMA or amphs

3) Collect enough milk for 3-4 days (using a breast-pump), keep it in the fridge and use it during the following days to MDMA or amphetamines use.

 

Dextroamphetamine and neurotoxicity

Dextroamphetamine and neurotoxicity

What makes you believe that dextroamphetamine is not neurotoxic at therapeutic dosages?

Originally posted in SR 2.0 25/10/2013. Reviewed 20/2/22

Dosages of dextroamphetamine that produce neurotoxicity are much higher than those used in human therapeutics. In animal experiments dosages are between 20-60 mg/kg injected. That would be 1.2-3.6 gr of injected d-amphetamine for humans. In animals, these dosages produce neurotoxicity but also death caused by hyperthermia of most specimens. And these effects do not appear in humans.

http://www.sciencedirect.com/science/article/pii/S0006899398008464

http://www.nature.com/npp/journal/v30/n11/full/1300771a.html

In science, proofs must be shown in positive. So, there are no data to suppose that d-amphetamine is neurotoxic at therapeutic dosages. Human dosages are 1000 times lower than neurotoxic dosages. There are no data also long time d-amphetamine exposure causes neurotoxic damage, and there is long time, intensive experience with amphetamine in humans for over a century.