Tea tree oil is touted as having anti-fungal properties. So what happens when it's put to the test against a variety of fungal infections? Watch the video to find out. Our entire understanding of the cause of dandruff shifted with this landmark article published in 1984. Instead of relying on secondary sources, reviews, editorial opinion pieces, he looked at the primary literature, the original studies, and was amazed to find out how overwhelming was the evidence of the true cause and how it had been ignored because it was so well buried under the mountain of error since some expert in the 1800s put forth some bogus theory. We now know that dandruff is triggered by a fungus that lives and feeds on the human scalp, the two major implications being, first, how alarming it is that some bogus theory can remain in the medical literature unchallenged for a century, despite evidence to the contrary, and second, hey, if it's a fungus, what about trying tea tree oil, which contains components that have anti-fungal activity against a range of fungi? That was based on studies like this, though, where tea tree oil in a Petri dish can fight off pathogenic skin fungi, but you don't know if it works for dandruff, until you put it to the test. 126 men and women randomized the daily use of a 5% tea tree oil shampoo or placebo for a month. The placebo worked a little bit, decreasing dandruff severity by about 10%, but the tea tree oil shampoo worked better, about a 40% drop. Looks like more than 40% from the graph, but that's because they misleadingly started the Y-axis at negative 60. This is a classic deception featured in chapter 5 of the 1954 classic How to Lie with Statistics. The graph should really look like this, which makes the effect less impressive, but it was still statistically significant. Only one patient in the tea tree oil group actually achieved a complete response, the one in the placebo group did as well. Thus it seems that the tea tree oil shampoo would require ongoing application for control of dandruff. Speaking of fungus, what about tea tree oil in the treatment of athlete's foot? That may actually be our most common fungal skin infection, affecting up to 1 in 10. So about 100 patients randomized into one of three groups. A 10% tea tree oil cream, tynactin, an antifungal drug, or a placebo cream. A month later, the fungus was wiped out in 85% of the drug group, but only about a quarter of the placebo in tea tree oil groups. This is somewhat surprising, since tea tree oil can kill off the fungus in a tea tree dish, but apparently not on toes. That reminds me of some of the oral health data on tea tree oil. I can wipe out some oral pathogens in a tea tree dish, but have people swish a tea tree oil solution around their mouth. And here's the dental plaque buildup after four days of no brushing, swishing with a placebo. Here's swishing with a medicated chlorhexidine mouthwash, which helps keep the plaque a bit at bay. But the tea tree oil mouth rinse has no effect, so if tea tree oil doesn't influence the amount of plaque, presumably it wouldn't help with gingivitis, the gum inflammation that's caused by plaque buildup. But no, here's the twist. True, no reduction in plaque with a 2.5% tea tree oil gel, yet significant reduction in gingivitis scores. Since decreased gum inflammation occurred without a decrease in plaque, it appeared to just be helping more from an anti-inflammatory, rather than anti-microbial mechanism. Might the same thing be happening here? Yeah, from a mycological cure standpoint, a fungus cure standpoint, tea tree oil didn't really do any better than placebo. But though the drug wiped out the fungus in 85% of cases, in some of those cases, the patient actually didn't notice an improvement in symptoms, or they actually felt worse after the drug, probably a reflection of tinnactin's irritant side effects. If instead of mycological cure, you looked at symptom improvement, tea tree oil works as well as the drug. So this may be the basis for the popular use of tea tree oil in the treatment of athlete's foot. But people should realize it's just symptomatic relief, and they're not necessarily eliminating the underlying clause. Of course, maybe they didn't use a strong enough concentration, and indeed, if you go with not a 10% cream, but up to 25 or 50%, you can get mycological cure rates above that of placebo, but still not as good as the drug. And in those high concentrations, some of the patients applying tea tree oil developed moderate to severe dermatitis. They broke out in a rash. But hey, if you have a patient that doesn't want to use the medicated creams, then a 25% tea tree oil application has a decent chance of knocking it out without being too risky, but the standard over-the-counter antifungal creams may work better. Onchomycosis is a fungal infection of our nails, usually toe nails, but sometimes fingernails, characterized by nail discoloration to form the detachment, thickening, crumbling, ridging. Here's an example of what it can look like. Reported prevalence is estimated to be about 125 people, though it's more common in older individuals, 1 in 5, over 16, and like half of 70-year-olds. Unfortunately, it's really hard to treat because the fungus can hide deep inside the nail, protected from the blood supply on one side, or anything you want to put on topically on the other. So recurrence after treatment is common due to residual fungus, even if you're able to beat it back. Many of the oral systemic treatments can be toxic, and many topical applications require long treatment courses, which may limit patient compliance, especially in patients who want to use nail polish or something to cover it up. So, given all the problems with a lot of prescription antifungals, there has been renewed interest in natural remedies. Well, if tea-troyal can affect athlete's foot and dendro fungus, what about nail fungus? Well, there was this study of a combination of the antifungal drug in Lothriman cream with tea-troyal that seemed pretty effective compared to nothing, but what about compared to each other? Well, there was one head-to-head study comparing tea-troyal with a common antifungal drug, a double-blind, randomized, controlled trial, twice-daily application of either the drug or pure tea-troyal on the nail for six months. Debringment was performed every few months where some of the fungal mass is debulked, scraped, ground off, and after six months, the drug only wiped the fungus out completely in about one in 10 cases, but looked better with partial full resolution of the appearance in the majority of patients, either from the doctor's assessment or the patient's. And the tea-troyal did just as well. The two preparations were comparable in efficacy of cure clinical assessment and subjective improvement, even though cost was comparable. So for patients desiring a natural treatment for athlete's foot or nail fungus, topical tea-troyals are a reasonable alternative to prescription or over-the-counter antifungals. Speaking of natural treatments, how about a truly natural treatment? You know, one potential reason for the poor long-term benefits of any therapy for nail fungus is that it may only be treating a manifestation of underlying disease, such as generalized immune suppression or peripheral micro or macrovascular disease. Maybe fungal nail infections are just a manifestation of poor peripheral blood circulation that would normally allow your body's natural defenses to keep the fungus from taking root in the first place. Evidently, there was a non-English language study of 400 patients that looked at the relationship between blood circulation of the skin and development of fungal disease. That was the title, and found a greater than 50% reduction in blood flow in patients with athlete's foot and nail fungus, compared with patients without these disorders. So if fungal nail infections are just a symptom of an underlying process, then treatment named it a eradication of a pathogen may be unrealistic. No wonder it just grows right back. A more appropriate goal then may be to just give up and live with it. But wait, if it's a circulation problem, why not instead improve the circulation? We've known since the 1950s that you can effectively switch peripheral artery circulation on and off like a light switch within days by switching people between a low-fat plant-based diet and a more conventional diet that contributed to the problem in the first place.


This paper examined the relationship between plasma concentrations of DMT and its effects on the brain. It found that DMT suppressed alpha power, increased beta power, and increased Lempel Ziv complexity. Additionally, it showed that there was significant between subject variability in the EC50e, concentration needed to reach half of the maximum response for each effect. This suggests that the effects of DMT are highly dependent on individual differences in the subject's physiological state. This article was authored by Emma Ekernaz, Christopher Timmerman, Robin Carhart-Harris, and others.


In this lecture, I want to discuss acute colonitis. I want to mention a few highlights. We'll talk about the pathogenesis, how acute colonitis develops, the organisms involved under microbiology, what the clinical pictures, what you should look out for when you see patients, the special investigations that you can do, either laboratory-wise or on the imaging side. I want to talk about the management of this very dangerous condition, and we'll look at some specific types of colonitis, the parasitic infections, AIDS cholangiopathy, and then lastly, the current pyogenic colonitis. Let's start. The highlights. What is colonitis? It's a potentially life-threatening obstruction and infection of the biliary tree. Lots of alternate terms. Some people talk about ascending colonitis. Some talk about suprative colonitis. It's all about the infection and growth of organisms in an obstructed biliary tree. What do we look out for? It's Charcot's triad. What is that? It is these three symptoms and signs that write up a quadrant pain, a patient with fever who actually has chills, that refers to the bacteremia that we have here, and of course, jaundice. Those three combined is called Charcot's triad. Now, 80% of cases of ascending colonitis is from coladocular thiesis. That means gallstones in the biliary tree. The rest, the patients that we see have either benign or malignant biliary strictures, can develop as a complication of pancreatitis and also of biliary parasites. We'll look at that. What is the priority in the management of these patients? It's fluid and electrolyte resuscitation, broad spectrum antibiotic cover, correction of your coagulopathy because most of these patients will go for some form of procedure, and the mainstay of therapy is biliary drainage. Got to drain that pressurized infected biliary tree. Good, let's start with acute ascending colonitis. Going to mention the pathogenesis, the causes, the microbiology, the clinical features, the investigations, and the management. So, I've said it before, it's a partial or complete obstruction of the biliary tree, which then overwhelms the normal defense mechanisms. Human beings don't develop colonitis. You have an intact swinger of ODI that keeps organisms out of the biliary tree. You have an entregrate flow of bile that washes the system out. Bile salts help in the prevention of infection. Immunoglobulin A produced by the cell walls in the liver. You have the cupra cells, which take part in normal defense of the biliary tree. So, these get overwhelmed because of various circumstances. You get multiplication of organisms. The pressure inside the biliary tree increases. Very good blood supply. Those organisms get into the bloodstream. You have a bacteremia, and the patient goes into septic shock. Various thoughts is where these organisms actually come from. They might be from the duodenum itself, from the portal venous system, some which suggests peridactylamphatics, secretions from the liver itself, and infected gallbladder. There's a variety of ways for organisms to get into this obstructed biliary tree. Irrespective of where they come from, with the raised intraluminal pressure, it does lead to systemic bacterial seeding, and as I mentioned, it leads to bacteremia, septicemia, septic shock. Again, just with the causes, as I said, 80% plus are gallstones, secondary stones. Those that mean gallstones that come from the gallbladder. Primary stones, stones that develop inside the biliary tree themselves. You can also mention some complicated forms of stone complications, such as myritzy syndrome, we can also put there. Then we see bile duct structures lowered down. You get benign malignant ones, benign post-operative. A patient might have had an injury during a colostectomy. Acutin and chronic pancreatitis can lead to damage and stricture formation of the distal common bile duct. Primary sclerosis and colonitis, where there's fibrosis in the biliary tree. Autoimmune colonitis. Colloidal cysts, biliary atresias. And on the malignant side, colandrocarcinoma, pancreatic cancers in the head of the pancreas, and pillary and duodenal cancers, gallbladder cancers, and even a large volume of metastatic lymph nodes in the portohypitus. All those malignancies can cause and will cause obstruction of the biliary tree. Instrumentation further down the line. Any patient who's had cannulization of their biliary tree via ERCP, placement with a stent, obstruction of that stent, any exogenous material that goes into a procedure done on that biliary tree can cause colonitis. Infections, parasitic, well described in certain parts of the world. On the other side, we do get the AIDS colongeopathy. I'll talk about that. The oriental or recurrent pygenic colonitis causes and various fungal infections, so a myriad of causes. Most commonly, though, you are going to see stones and malignancies. 80% of people will have organisms on a blood culture. It's very important to do a blood culture before starting draw-spectrum antibiotics as the patient is admitted and diagnosed. Most of these organisms are enteric in nature, so we're talking about negatives. Once a patient has had instrumentation, for instance an ERCP or the vet surgery, most of these infections become polymicrobial and you can see all sorts of negatives, even getting positive and anaerobes, importantly the anaerobes. So what are we talking about? Ecoli, clip cellar, enterobacter species, also some enterococci, and as I said, patients with instrumentation, got a look at the anaerobes, bacteroids and clostridia. In Asia, we really have to think about parasites and secondary bacterial infection, not so common in the rest of the world. Immunocompromised patients, specifically Africa, South America, areas such as this, where we see hepatitis C, and HIV with cryptosporidium or cytomagallivirus, or even Candida infections. So a wide variety of organisms to consider when deciding on antimicrobial therapy. So, what does the patient present with? I've mentioned shock-caught striad. Now, only 20-50% of people will actually have that very nicely defined picture. There's also Reynolds pentad, pentad referring to five, and that's just the addition to shock-caught striad of hypertension in an altered mental state. Now, there's nothing special about this Reynolds pentad. What is described here is a patient who's in septic shock. The process has gone on too far, might have taken time for the patient to present, or there was an initial misdiagnosis in hospital, time has passed, the patient will eventually develop septic shock, and that is what Reynolds pentad refers to. Jaundice also, not everyone with colonitis has jaundice. Seen in 60-70% of cases, certainly in the majority, but don't be fooled that if there's no jaundice, this cannot be colonitis. It is still possible to be colongetic without jaundice. A vast majority of patients will be there. What am I trying to say is heaven-high index of suspicion. Especially in the elderly, they're not going to have all the symptoms and signs. Those with a known anatomic abnormalities, they've had a lab collie before, they've known to have an injury, they've had instrumentation before. If they present with pain and fever, whether without jaundice, always a high index of suspicion and it might be colongitis, and it might be worth your while to institute antibacterial therapy and get your investigations done and your management. What are you going to see on the blood test that you do?  With that, you're going to see either normal white cell count with a bit of a left shift that's earlier, later on, full on leukocytosis and most commonly, a neutrophilia. If you do an ERCP, it will be raised, it might be raised from a variety of causes, but certainly a raised CRP that keeps on rising is very suspicious. On your liver function test, you are going to see a colostatic picture. What is that? You're going to see a conjugated hyperbillirubinemia. As I mentioned, not everyone's jaundice, not everyone is going to have a raised bilirubin levels, but certainly it would be in the vast majority of cases. Together with that, your ductal enzymes will be up. Those are alkaline phosphatase and KemeGT. Not uncommon though to see the cellular enzymes raised as well, ALT and AST. You have to do blood cultures before starting antibiotics, but don't let the taking of the blood cultures delay the start of the broad spectrum antibiotics, but it helps you to de-escalate, helps you to know what organism you're dealing with a couple of days down the line. Imaging is important. The patient might have the clinical picture, we've instituted our management and I'll talk about that, but we have to confirm the diagnosis in some other form. Now the choice of imaging really depends on the availability and the patient's condition. Now trans-abdominal ultrasound would be the first investigation most facilities would have available. It's easy, it's non-invasive and it's very good to show biliary dilatation. Of course further down the tree it might get a bit difficult hidden behind the gas in the duodenum. Endoscopic ultrasound as opposed to trans-abdominal is a newer modality, not available commonly in many centers and expertise for it does not exist everywhere, but it has become part of the working algorithm of many advanced units dealing with colonitis. FNA aspirate can be taken and a variety of procedures can actually be performed with endoscopic ultrasound. It really gives you excellent sensitivity for common bile duct stones all variety of ductal malignancies can be diagnosed you can get tissue from an endoscopic ultrasound as I said and it really can also be less invasive than an ERCP. We move on to CT scan now CT scan is going to be excellent to show you other causes other than stones not all stones are seen on a CT scan but certainly malignancies and pancreatitis is cause of colonitis can be seen remembered is like the trans-abdominal ultrasound purely diagnostic there is a radiation risk and there is the risk of giving contrast to these patients who might have a borderline renal function due to the septic state so just be careful the MRCP beautiful to do, nice delineation of anatomy very sensitive for detecting the bile duct stones and other causes of obstruction again purely diagnostic expensive limited availability long waiting lists in many places and of course patients with large metal implants can have an MRCP then we get to the ERCP that is the gold standard and it's preferred for the severely ill patients you've got to decompress the bile ducts as soon as possible and most common way to do it is via an ERCP now PTC one should also in here as part of the imaging that is where we're going to get access to the bile ducts not as ERCP which is endoscopically via the stomach and duodenum but transcutaneously where excess is gained through the liver itself management well we're going to use we have to diagnose, we know now about the laboratory investigations we know about the special investigations the diagnosis confirming the diagnosis concerned we do go for this updated Tokyo guidelines you see there A, B and C that's systemic inflammation cholestasis and imaging on the systemic inflammation called A temperature more than 38 degrees celsius or Chols, white cell count less than 4 more than 10 under cholestasis a raised total bilirubin or alkaline phosphatase gamma G, T, A, S, T, L, T more than one and a half times normal values and under C imaging biliridilitation from whatever imaging technique you use or on the actual imaging techniques the cause seen are the structure stones of stents now if you have at least one on all three of A, B, C that's a definite diagnosis of acute colonitis if you have one in A so they either have a temperature in Chols or raised over a low white cell count and then one from B or C just one certainly don't always need that raised bilirubin it is very suspicious of colongitis and that is the updated Tokyo guidelines for diagnosis so what do you have to do? you really have to distinguish initially between mild which might be self limiting and then the severe disease that is life threatening if you do nothing about it the mortality rate is extremely high so what I mean by this mild self limiting if we think about stones it is quite possible that a stone can pass spontaneously don't rely on that happening though a case that you see that is now mild will not be mild again tomorrow you have got to keep your eye on that patient Sydney they don't have to be rushed off for any RCP but you might be well fine the next morning the temperature is down the bilirubins are improving the pain is gone and it might very well be that that stone has passed more commonly though you have to interfere you have to do something about it that stone does not pass spontaneously and the situation will deteriorate so what do we do? we initiate fluid resuscitation and electrolyte correction some of these patients do have electrolyte abnormalities and it forms part of your fluid resuscitation so you commence antibiotic cover broad spectrum talk about that and you do it after taking cultures to not delay giving antibiotics though just to get the cultures a mild setup system that should be easy to do you have got to also diagnose and correct the coagulopathy many of these patients most of these patients are going to go for ERCP and you want to know that they don't have coagulopathy which they might very well have you obstructing the bilir system and that is in the liver at least is where you make your clotting factors so antibiotics your choice is really irrespective of biopinitration if such high pressures that makes penetration poor even of well excreted or hepatically excreted antibiotics it really is not that important or biopinitration is really not that important so if a patient comes community-acquired, acine colngitis whithl stone or malignancy broad spectrum penicillins most notably we do use a moxicillin with clebulinic acid or even ciprofloxacin as far as the quinolins goes might be good first choices remember I said you have to think of anaerobes in the elderly those with altered anatomy or those who have had prior instrumentation and for those that is advisable just to add metroninazole if this is hospital-acquired and the patient is severely ill in septic shock you might want to go one step up start very broad spectrum with carbapenems or 4th generation and we usually stop when improving after the drainage there is no such thing as a course of antibiotics and really if they have mild self-limiting and not responding cases you might only use antibiotics for 3 days if they are very severe and they've had their drainage you might want to stop after about 5 to 7 days you want to see that the patient has responded well that there is no more signs of sepsis and you can just continue the antibiotics of course as you've seen results are out you can de-escalate specifically in the severely ill that have gone to an intensive care unit that you have started on the very broad spectrum carbapenems or 4th generation kephalosporins you want to de-escalate and that is why it's so important to get your blood cultures I've said it many times now biliary drainage is the most important aspect of the management and it can occur naturally don't depend on that most commonly so what are the interventions possible endoscopic ERCP percutaneous transepatic a PTC some of the centers have this EUS and they have built it into their management algorithms and their various techniques that I will just quickly mention if nothing else is available none of this patient is extremely ill do not forget good old fashioned open surgery common bile duct exploration decompress that leave in a T-tube and we can always think about definitive therapy later if the stone cannot be extracted under that first setting stones easy to extract extracted during that time of patients too unstable can't get to the stone too difficult to put in a T-tube and get out of course that has got to be proximal to the obstruction no use putting a T-tube distal to that good and in most places of the world at least there is access to perhaps not at the facility but you are able to transfer the patient in a stable condition to a center that allows for this facility so get a patient to a center with ERCP expertise the severely ill within the first 24 hours really 24 might be too long it's really the outside limit get them to ERPs facilities and they are able to transfer the patient in a stable condition to a center the outside limit get them to ERPs facility they need cannulation of their validity and drainage of the duct and if possible removal of obstruction if a stone is the course of course if they moderately ill really within you know there is always these missions on a Saturday or Sunday within 48 hours at least you want that drainage to be done after it's cannulized the biliris system is cannulized it is decompressed first and that aspirate is then sent for MCNS there is a variety of things to do and it is at the choice of the endoscopist they might do stone extraction right then then with or without a syntorotomy now syntorotomy allows for larger and easiest larger stones to be extracted easier stone extraction it does allow the recurrence of colonitis but there is this risk of bleeding perforation and you increase the risk of pancreatitis it's a decision to be made it might not be possible to extract the stone or the cause of the obstruction you might have to leave a drain or a temporizing stent it might even be the prudent thing to do if the patient is so severely ill that there really isn't time for anything more complicated than just one drainage is at the discretion of the endoscopist so what is the role of the PTC then percutaneous transipatic so excess is going to be gotten to the biliri tree through the skin through the liver advanced deeper and deeper until one of the larger biliri ducts are cannulated salting a technique over that guide wire through the needle or guide wire so it's more accessible many centers won't have ERCP but they will at least have radiology that can help with the PTC can be done under local anesthesia can be done in a very unstable patient that cannot go for general anesthetic cannot be transported to the endoscopy unit patient might just be trans-stable there's no I think RCT is really to show which one is better set up for an ERCP it's much more definitive as far as the stone extraction is concerned and getting biopsies at least if it's malignant many more things to be done by ERCP and that is preferred there's high morbidity and mortality to the PTC we see a lot of pain bioperitonitis, hemorrhage, hemabilia definitely increased length of stay so we really do reserve it for the unstable patients and the patients that have a high lesion, a high-level lesion for instance with colonic carcinoma with colonitis that still need decompression because of that worsening colonitis so really just for those patients in a very very unstable with colonitis we consider PTC so the ultrasound guided biliary drainage very specific to advanced centers and the algorithms it's usually used when there's ERCP failure there's the two techniques of getting biliary drainage the so-called rendezvous technique and the coladoho diodinostomy technique done over dilatation over a guide wire so know about these know that it's available but as I mentioned really in advanced units then the vast majority of cases are from secondary gallstones that means gallstones from the gallbladder are taken to do a colostectomy after the patient has recovered fully to prevent further stones going down the cystic duct into the common bile duct I want to mention parasitic infections seen in tropical countries it's diagnosed by microscopy of the stool bile or duodenal aspirate we see the parasites serologies really have secondary value you might get positive serology because the patient does have the parasites that have joined us is not because of parasitic infection of the biliary tree so it doesn't always help and you're going to get a lot of negative serology false negatives and false positives it is made managed medically medication and then reinvestigation of the patient and only in cases where your medical management against the parasites whether without antibiotics fail that you would consider an ERCP more importantly sitting around these parts it's the AIDS cholangiopathy it is a form of sclerosing cholangitis in other words there's fibrosis in the biliary tree as well and it results from infection by specific opportunistic organisms mostly cryptosporidium and cytomegalovirus patients present with right upper quadrant pain, fever and chills and nausea so they look like cholangitis except that most of them are not jaundiced you do the liver functions though in this picture with normal or neonormally Rubens CT4 counts are usually quite low less than a hundred we'll do an ultrasound under these sort of circumstances and see the duct dilatation you can do a CT scan and give you a better delineation of the intrapartic ducts at least ERCP will show a symptom assigned at least of AIDS cholangiopathy so pictures that are seen are the sclerosing cholangitis with papillary stenosis the sclerosing cholangitis alone it's the fibrosis in the biliary tree the papillary stenosis alone all those with the long extrapartic structures without intrapartic structures different pictures that are seen in ERCP antimicrobials are usually ineffective in these patients if they have papillary stenosis syngtorotomy will be of help if these stitches are higher up you can consider balloon dilatation or placing of stents if it's higher up it might be problematic might have to do it by PTC now the institution of HEART really returns to patients immune function in countries where there's a good program treating these patients we really see less and less of the AIDS cholangiopathy lastly the current pyogenic cholangitis it's a primary also known as primary pediclethysis the current pyogenic cholangitis oriental is intrapartic stones and the recurrent attacks of cholangitis there is an association with pedicelic infections what we usually see is pigment in stones with calcium bilirubinate and the hallmark of this is repeated attacks repeated attacks and the treatment will basically be as we've discussed before other than the fact that the fibrosis might develop and well as you see at the bottom they might eventually develop secondary cirrhosis in 10% and after 10% might even develop cholangio carcinoma so either your PTC is still going to drain the system as I said now the stitches do cause the problems and it might even be so bad that we need segmental resections of the liver so that is it for acute cholangitis most importantly if you resuscitate the patient start blood spectrum antibiotics after getting blood cultures and get your imaging you are going to see the obstructive pattern on your liver functions remember the Tokyo guidelines for the diagnosis on ultrasound which most of us will start with you will see the dilatation you might have a CT scan as well which will give you a bit of definition and show the other causes as I said the patient needs drainage after the drainage the patient needs eventually when they are better a cirrhosis stick to me thanks


Today, I have the pleasure of being on the floor of PDAC 2019 to get an update from Tom Meredith of West Red Lake Gold. How are you today? Good. Thanks, Tracy. So Tom, PDAC, Gold, the Australians are buzzing about their gold bull market right now. What's happening in Canada and when should we start following suit in North America? I believe it's really a function of the interest rate market, better known as the bond market. And when central banks stop raising rates and actually start putting rates down, then that'll draw money into gold because the bond market, which is the biggest capital pool out there, considers gold to be a triple A zero coupon bond. And when interest rates go down, bonds go up, which means gold will go up, and that will draw money into the sector. Okay. Any anticipation on when interest rates are going to drop? Watch the Fed. And there, ideally, they want to try and put them up another rate hike. Time will tell whether they'll be able to do that or whether they'll have to throw on the towel and start dropping rates. We'll know better later this year. So the inevitable conclusion would be it's time now then to buy gold stocks. It's time to be watching them closely because the time's coming fairly soon, I think. And of course, those of you out investor intel, we've been trying to draw in the cannabis investors out there and explain to them that they should widen and diversify and move into gold. Can you tell me a little bit more about why they should select West Red Lake Gold versus many of your competitors? Well, we trade based on the value of ounces in the ground. So right now our market value is about $10 an ounce in the ground and a strong market north of $100 an ounce in the ground. So you'll see a significant appreciation in our share price when capital flows into the sector. And of course, in the news flow, West Red Lake, of course, has got amazing management. You have regular milestones are being met. Your last drilling results were impressive. Can you talk to us about the highlights of those? Well, we started drilling a new zone. Our main zone has three former producing mines on it. One of them, the areas has a million ounce resource of seven and a half grams. You started drilling in a new zone and we think the NT zone, we think that has some potential to create another decent sized gold deposit. And of course, you have a major like gold core that's a partner. There are 40% partner in the project and they're looking for additional gold resources to feed their Red Lake milling complex. So what should we anticipate as shareholders in the next quarter or two? Well, we'll be just continuing to do our drilling and looking forward to the market getting better. All right. Well, that sounds wonderful. Thank you so much, Tom, for joining us today. Thank you, Tracy.