Cannabis has a long and complex history, dating back thousands of years. The oldest known written record of cannabis use comes from Emperor Shen Nung of China in 2727 B.C., who documented its medicinal properties. The plant was also known to Ancient Greeks and Romans, and its use spread throughout the Islamic empire, reaching North Africa. Over centuries, cannabis was valued for its therapeutic, recreational, and industrial applications. Although cannabis has been found to have beneficial medicinal effects for patients who have certain medical issues, for decades, concerns have existed regarding a possible connection between the use of cannabis, and effects on brain functions such as cognizance and memory. But for most of the 20th century, medical research on cannabis was extremely limit due to legal, political, and regulatory barriers. In 1937, the U.S. passed the Marijuana Tax Act, which heavily regulated and effectively criminalized cannabis. This discouraged research by making it difficult to legally obtain cannabis for studies. In 1970, the Controlled Substances Act (CSA) classified marijuana as a Schedule I drug, meaning it was considered to have no accepted medical use and a high potential for misuse, a classification it still holds at the federal level. Schedule I status made it nearly impossible for researchers to access cannabis legally, as obtaining government approval required navigating complex and time-consuming bureaucratic processes. Until recently, the only federally approved source of cannabis for research in the U.S. was the University of Mississippi, which grew marijuana under a contract with the National Institute on Drug Abuse (NIDA). This limited supply meant that researchers could not study different strains or potencies commonly available in legal markets today. The "War on Drugs" in the 1980s and 1990s led to anti-cannabis propaganda, further discouraging funding and interest in medical cannabis research. Fear of losing funding or facing professional consequences*made many scientists and institutions hesitant to study cannabis. Most medical research is funded by government agencies, universities, or pharmaceutical companies. Because cannabis was illegal and not patentable, pharmaceutical companies had little financial incentive to invest in cannabis research. Federal funding agencies prioritized research on cannabis harms rather than potential benefits. In 1996, California legalized medical cannabis, leading to increased public interest in studying its effects. In 2014, the U.S. allowed more research access by passing the Farm Bill, which permitted limited hemp-derived cannabinoid studies. In 2021, the DEA announced an expansion of cannabis cultivation licenses, allowing more institutions to grow research-grade cannabis. More recently, state-level legalization has led to more independent studies, but federal restrictions still limit large-scale clinical trials. The combination of legal barriers, lack of access, stigma, and lack of funding prevented serious medical research on cannabis for decades. However, as legalization expands and restrictions loosen, research into cannabis’s medical benefits is finally progressing, providing new insights into its potential therapeutic applications. In the largest study to date, regarding cannabis use and its effects on brain function, researchers at the CU Anschutz Medical Campus used functional MRI imaging to examine over a thousand young adults aged 22 to 36, in order to evaluate how their recent and lifetime cannabis use has affected their neural activity across different cognitive tasks. It's not surprising that this study would focus on negative effects of cannabis, rather than medicinal benefits, since the study appears to have been funded mostly by various government grants. The study was published in JAMA Network Open (Gowin, et al., 2025).1 The study found that: Cannabis use is linked to reduced brain activity during working memory tasks.
The regions of the brain most affected were:
These areas are responsible for decision-making, memory, attention, and emotional regulation. Working memory decline is statistically significant.
Other cognitive tasks were less affected. The study tested seven cognitive functions, including:
Considering recent use versus lifetime use: Both recent cannabis use (detected via urine screening) and heavy lifetime use (>1,000 instances) led to lower brain activation. Long-term use had a more persistent effect, even when adjusting for recent consumption. This suggests that long-term cannabis use may have lasting effects on brain function, rather than just short-term impairment. Abstaining tends to improve cognitive performance. Although quitting cannabis use before performing cognitive tasks may help recover some function, heavy users may experience withdrawal related cognitive impairments when stopping suddenly. The study suggests that longer abstinence periods may be required for full cognitive recovery. Limitations of the study, included several confounding possibilities. Although the study was adjusted for factors like age, sex, race, education, income, alcohol, and nicotine use, no assessment was made for any psychiatric conditions (for example, ADHD, anxiety, or depression). It should be noted that such issues often tend to be a primary reason why some individuals choose to use cannabis, in the first place, and that might, or might not, affect the findings of the study. Also, there was no long-term follow-up to determine if cognitive function normalizes after prolonged abstinence. And cannabis use history in this study was self-reported, which obviously introduces some risk of underreporting, or misclassification. There were no surprises in the findings of this study. The study only confirmed what we all suspected — that heavy cannabis use has negative effects on cognizance and memory. But the same can be said for many prescription drugs manufactured by Big Pharma. So if cannabis is being used to mitigate the symptoms of PTSD or some other health syndrome, the resulting symptoms and side effects of cannabis use may be acceptable. On the other hand, if it's being used strictly for recreational purposes, then the cost in terms of negative mental health attributes is considerable. But then, that's true of virtually all drugs used for recreational purposes. There are other reasons why medical research often focuses on the negative aspects of cannabis use. Compromised cognizance and memory aren't the only problems associated with cannabis use. Another serious problem that many daily cannabis users have to deal with is a condition known as cannabinoid hyperemesis syndrome (CHS). Contrary to cannabis’s well-known ability to ease nausea—especially in cancer patients undergoing chemotherapy—CHS triggers cyclical bouts of severe nausea, uncontrollable vomiting, and excruciating abdominal pain. The only known cure is stopping cannabis use entirely. A study by researchers at George Washington University, and published in the annals of emergency medicine, surveyed 1,052 individuals who reported suffering from CHS (George Washington University, 2025, February 20; Meltzer, et al., 2025).2,3 They found that:
Although CHS appears to present a serious risk for long-term cannabis use, it seems only fair to point out that many high dollar medical drugs have a similar problem — after a few years of use, many so-called "biologicals", for example, provoke the immune system so that it develops an allergic reaction to the drugs, for many patients. Other drugs (corticosteroids come to mind, for example) slowly lose efficacy, so that they eventually provide little to no benefit. Is cannabis useful for MC patients? The jury is still out on that issue, with a few users posting on the MC Discussion and Support Forum that it helps suppress their MC symptoms (especially pain), while others say that it doesn't seem to help. Back in October, 2016, the Microscopic Colitis Foundation published a newsletter that discussed the possibility of using cannabis to treat IBD symptoms. For those who wish to review the article in the newsletter, here's a direct link to that newsletter: https://www.microscopiccolitisfoundation.org/uploads/5/8/3/2/58327395/final_corrected_copy_of_october_1_2016_newaletter_5_for_website.pdf References: 1. Gowin, J. L., Ellingson, J. M., Karoly, H. C., Manza, P., Ross, J. M., Sloan, M. E., . . . Volkow, N. D. (2025). Brain Function Outcomes of Recent and Lifetime Cannabis Use. JAMA Network Open, 8(1), e2457069. Retrieved from https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2829657 2. George Washington University. (2025, February 20). Daily cannabis use linked to public health burden. ScienceDaily, Retrieved from https://www.sciencedaily.com/releases/2025/02/250220122931.htm 3. Meltzer, A. C., Morrison, C., Loganathan, A., Shahamatdar, S., Moon, A., Heidish, R., . . . Cooper, Z. D. (2025). Cannabinoid Hyperemesis Syndrome Is Associated With High Disease Burden: An Internet-Based Survey. Annals of Emergency Medicine, 0(0). Retrieved from https://www.annemergmed.com/article/S0196-0644(25)00018-6/abstract
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Why do so many MC patients relapse within a few weeks to a few months after their initial budesonide treatment is ended? This hasn't been explored by researchers so there's no medical data to support the possibilities listed here, but it's very likely that relapse is caused mostly by one or more of 3 possibilities:
Regarding dose tapering of budesonide: When ending a budesonide treatment, although most clinicians recommend tapering the dose, most of them don't recommend taking the dose reduction tapering far enough to be optimally effective. The experiences shared by many budesonide users who are members of our discussion and support forum, show that longer, more drawn out dose tapering is far less likely to result in a relapse.
When the prescribed treatment tapering ends (one 3 mg capsule per day), most users begin taking a 3 mg capsule every other day, for a week or so, followed by a capsule every 3rd day for a week or so, followed by a capsule every 4th day for a week or so. And many users go on to take a capsule every 5th day, or 6th day, or even longer. And any patients who don't feel secure when tapering at that rate, tend to stay at each dose level longer, for example, at least a couple of weeks before going on to the next level. In addition, anyone who feels that they need something extra to help them remain in remission as they taper off budesonide, taking a daily over-the-counter antihistamine for a couple of weeks after they stop taking budesonide, usually helps to maintain remission when ending a budesonide treatment.
For decades, physicians have puzzled over the contradictory effects of smoking on inflammatory bowel diseases (IBD). Smoking makes Crohn’s disease worse, but appears to protect against ulcerative colitis (UC). Recent research from RIKEN has uncovered a surprising mechanism: smoking alters the gut environment in a way that allows oral bacteria such as Streptococcus mitis to colonize the colon, where they shape the immune response (Miyauchi et al., 2025).1 These findings may help guide the development of safer therapies for colitis and may also shed light on the inflammation associated with microscopic colitis (MC). The study found that: 1. Smoking reshapes the gut microbiome via metabolites. Smoking produces metabolites such as hydroquinone, which allow oral bacteria, particularly Streptococcus mitis, to take hold in the colonic mucosa. This effect was seen in smokers with UC, but not in ex-smokers, suggesting the change depends on ongoing exposure to smoking compounds. 2. Oral bacteria influence immune responses. When S. mitis was introduced into mouse models:
3. Immune modulation is key. In UC, inflammation is largely driven by Th2 immune responses, so activating Th1 cells creates a balancing effect that reduces inflammation. In Crohn’s, which already involves Th1-driven inflammation, the effect piles on more damage. Similar to MC, Crohn’s disease (CD) can affect any part of the gastrointestinal tract, but in practice it shows a fairly typical pattern of distribution. Large cohort studies (including European and North American IBD registries) give us good estimates of how often each region is involved. Statistics show that for Crohn's disease (at diagnosis):
UC is very different, because it:
For UC, statistics show that:
How does MC compare with these? Similar to Crohn's disease, MC can affect (cause the inflammation of) any organ in the gastrointestinal tract. Although you won't find many references to small intestinal involvement for MC in recent research, many credible, older pathology-focused studies reported frequent small intestinal involvement, especially involving the terminally ileum. Most modern reviews incorrectly refer to MC as a disease of the colon. Why is small bowel involvement ignored in most current literature discussing MC? With such biased treatment, it's no wonder gastroenterologists are confused about MC and its treatment. In 2003, for example, Nature published a research study in its Modern Pathology series, showing that 78% of lymphocytic colitis patients and 50% of collagenous colitis cases (versus 9% of controls) had intraepithelial lymphocytosis (lymphocytic infiltration) of their terminal ileum (Padmanabhan, Callas, Li, and Trainer, 2003).2 That article also mentions duodenal and jejunal changes in subsets of MC patients, and summarizes prior literature describing abnormal duodenal and jejunal findings, including villous atrophy and collagen deposition in some MC patients, again pointing to small bowel immune activation in a fraction of MC cases. How might this research relate to MC?
Experiences shared by MC patients on our discussion and support forum suggests that bacteria commonly found in the mouth, and sometimes trapped by dental procedures (such as root canals) can contribute to MC flares if they reach the gut. The studies suggest that immune balance between Th1 and Th2 cells is critical. MC has been linked to abnormal T-cell activity, so understanding whether S. mitis–like bacteria can shift this balance is highly relevant. The bottom line: The discovery that smoking promotes oral bacteria growth in the gut, altering immune pathways in opposite ways for Crohn’s disease and ulcerative colitis, solves a decades-old puzzle in gastroenterology. For MC patients, these findings highlight the importance of the microbiome-immune connection, and point toward new therapies that could harness microbial modulation—without the dangers of smoking. However, in the absence of dedicated research data, definite conclusions regarding MC, cannot be drawn. We know that when medical discoveries revealed the extent of the risks associated with smoking, many people who stopped a long-term smoking habit developed MC (almost surely due to the stress that resulted). But the unanswered question remains — “Does MC more closely resemble Chron's, or UC?” The evidence suggests that it more closely resembles Crohn's, than UC, but without compelling evidence, we can't be sure. And as we all know as MC patients, what works for some, does not work for all. So there is a possibility that this line of research may well lead to treatments that benefit some of us, but worsen symptoms for others. References: 1. Miyauchi, E., Taida, T., Uchiyama, K., Nakanishi, Y., Kato, T., Koido, S., . . . Ohno, H. (2025). Smoking affects gut immune system of patients with inflammatory bowel diseases by modulating metabolomic profiles and mucosal microbiota. Gut, Published Online First Retrieved from https://gut.bmj.com/content/early/2025/08/06/gutjnl-2025-33492 2. Padmanabhan, V., Callas, P. W., Li, S.. C., and Trainer, T, D. (2003). Histopathological Features of the Terminal Ileum in Lymphocytic and Collagenous Colitis: A Study of 32 Cases and Review of Literature. Nature Modern Pathology, 16. pp 115–119. Retrieved from https://www.nature.com/articles/3880725
Official statistics show women being diagnosed with depression at twice the rate of men, creating the impression that depression primarily affects women. However, strong evidence suggests this diagnostic pattern may contribute to a distortion of reality — men may actually experience depression at equal or higher rates than women, with their suffering remaining largely invisible until it culminates in the most tragic outcome — suicide. Suicide statistics tell a different story. The most powerful evidence that men's depression is severely underrecognized comes from suicide mortality data. Despite receiving depression diagnoses at half the rate of women, men die by suicide at three to four times the rate across virtually all age groups, cultures, and countries. This stark disparity suggests that the 2:1 female-to-male depression diagnosis ratio severely underrepresents the true magnitude of depression in men. The extent of this difference can't be explained by method lethality alone. While men do choose more immediately fatal suicide methods, the sheer scale of the gender gap (consistently 3-4 times higher across populations) points to a massive amount of unrecognized depression in men. These statistics suggest that for every woman diagnosed with depression, there may be one or more men experiencing equally severe depression that goes unidentified by current diagnostic approaches. And there's a good possibility that this pattern may indicate that rather than men experiencing depression at "similar rates" to women, they may actually suffer from depression at substantially higher rates. The suicide data serves as a tragic but revealing endpoint that exposes the disconnect between current mental health services and depression in men. The healthcare system's depression diagnostic criteria are biased against men. Current depression screening tools were developed and validated primarily using female symptom presentations, creating systematic bias against recognizing male depression. Standard instruments like the PHQ-9, Beck Depression Inventory, and Hamilton Depression Rating Scale emphasize symptoms such as sadness, tearfulness, guilt, worthlessness, and withdrawal — characteristics that align closely with how women typically express emotional distress. Male-typical depression symptoms are poorly represented in these diagnostic criteria. When men experience depression through irritability, anger, aggression, risk-taking behaviors, substance abuse, or workaholism, these presentations score poorly on traditional screening methods. This diagnostic bias means that men with severe, potentially life-threatening depression may appear "normal" on standard assessments, while women with similar severity levels receive appropriate diagnoses. The consequences of this diagnostic failure extend beyond individual cases to create systematic underrepresentation of male depression in research, treatment development, and healthcare resource allocation. When depression research and treatment protocols are based primarily on female populations, they are almost surely inadequately designed for males who are experiencing the condition. Our culture hides signs of male distress. Gender socialization creates powerful barriers that not only prevent men from seeking help but also make their depression invisible to others. From early childhood, boys learn that expressing vulnerability, sadness, or emotional need contradicts masculine identity. This cultural programming becomes so deeply internalized that many men genuinely cannot recognize their own depression or frame their distress in psychological terms. When depressed men do visit healthcare providers, they typically focus on physical symptoms such as fatigue, pain, sleep problems, and digestive issues, while avoiding discussion of emotional concerns. Expressing psychological or emotional issues as physical symptoms is known as somatization. And somatization can effectively mask severe depression, particularly when providers lack training in recognizing this behavior as potential mood disorder symptoms. The cultural expectation that men should be stoic and self-reliant means that male depression often remains hidden from family members, friends, and colleagues until it reaches crisis levels. Unlike women, who are more likely to discuss emotional struggles with social networks, men typically suffer in isolation, missing opportunities for early identification and intervention. The bottom line:
Scientists from the University of Tartu in Estonia studied over 2,500 Estonian Biobank samples and found that drugs we took years (sometimes many years) ago can still be detected in our gut microbiome today (Aasmets, Taba, Krigul, Andreson, and Org, 2025).1 And it’s not just antibiotics. Antidepressants, beta-blockers, proton-pump inhibitors (PPIs), and benzodiazepines leave distinct microbial fingerprints, some comparable to the impact of broad-spectrum antibiotics. That means a person’s medication history is a hidden confounder that microbiome researchers (and clinicians) have been overlooking in their work. Does that list of medications look familiar? It should, because it includes many of the medications that some of us have blamed for the development of our microscopic colitis (MC). This study considered long-term medication effects. The research team used shotgun sequencing to analyze 2,509 stool samples from the Estonian Biobank Microbiome cohort, linking each sample to years of electronic prescription records. A smaller cohort (328) from the same original 2,509 samples were used as second samples to see what happens when people start or stop specific drugs. Shotgun sequencing involves DNA sequencing by breaking a large DNA molecule into millions of smaller, random fragments, sequencing the fragments independently, and then using computer algorithms to reassemble these fragments into their original order by identifying overlapping sections. By utilizing this process, scientists can determine the complete sequence of long DNA strings, such as an entire genome. Up until now, at least, most human microbiome studies only control for current medications. This study explicitly modeled past use, allowing the team to test for carryover (lingering) and additive (cumulative) drug effects on the microbiome. The study found that: 1. Medication echoes are common and long-lived. Prior use of several drug classes, including antibiotThe study found that:ics, psycholeptics (notably benzodiazepines), antidepressants, PPIs, and beta-blockers, was associated with persistent shifts in microbiome composition years after the last prescription. In media summaries of the work, the authors note that nearly half of the assessed drugs still showed microbiome associations more than a year after use. 2. Benzodiazepines stood out. Surprisingly, benzodiazepines produced alterations on par with broad-spectrum antibiotics, and different drugs within the same class (for example, diazepam compared with alprazolam) showed unequal microbiome disruption. That heterogeneity matters: “which benzo” or “which SSRI” could leave different long-term microbial signatures (Estonian Research Councilm 2025, October 9).2 3. There are additive effects. The more often (or longer) a medication was used in the past, the stronger its detectable microbiome impact — evidence for dose–history relationships, not mere coincidence. 4. Direction of effect (causality) gets support from follow-up samples. In the smaller subset, starting or discontinuing certain meds led to predictable shifts in specific microbes (for example, with PPIs, SSRIs, and several antibiotic classes), strengthening a cause-and-effect interpretation. (It’s not a randomized trial, but the within-person changes are compelling.) How can non-antibiotics drugs do this? This study result joins a growing body of literature showing that many human-targeted (non-antibiotic) drugs have direct antimicrobial activity or change the gut environment (for example, gastric pH, motility, bile acids) in ways that reshape the microbiome. In vitro screens have found that 24% of tested non-antibiotic drugs inhibit gut bacterial strains, and newer studies show such drugs can weaken colonization resistance against pathogens (Maier, et al., 2018).i The Estonian data extend those insights to real-world, long-term human outcomes The bottom line. The Estonian Biobank study makes a clear case: our microbiomes carry long-lasting imprints of medications — antibiotics and many others. For researchers, past prescriptions are a hidden confounder that must be accounted for. For clinicians and patients, the work encourages thoughtful use and periodic re-evaluation of long-term medications, recognizing that the gut ecosystem may remember them long after we do. References 1. Aasmets, O., Taba, N., Krigul, K. L., Andreson, R., and Org, E. 0. (2025). A hidden confounder for microbiome studies: medications used years before sample collection. mSystems 0:e00541-25. Retrieved from https://journals.asm.org/doi/10.1128/msystems.00541-25 2. Estonian Research Council. (2025, October 9). "Common medications may secretly rewire your gut for years." ScienceDaily, <www.sciencedaily.com/releases/2025/10/251008030953.htm>. Retrieved from https://www.sciencedaily.com/releases/2025/10/251008030953.htm 3. Maier, L., Pruteanu, M., Kuhn, M., Zeller, G., Telzerow, A., Anderson, E. E., . . Typas, A. (2018). Extensive impact of non-antibiotic drugs on human gut bacteria. Nature, 555(7698). pp 623–628. Retrieved from https://pubmed.ncbi.nlm.nih.gov/29555994/
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