Talk about, it's actually both the difficult and the most interesting subject to speak about because the changes that we've had in the myeloma world over the last few years and in fact over the 25 years that I've been working in myeloma have been extraordinary. I don't think that there is another disease in which we have had more clinical insights and more drug development than in multiple myeloma. I don't know that we have kept up biologically. We've managed to sort of empirically turn out a lot of new drugs, but I don't know how much that has translated into changes. So the point of this slide isn't to say look at all of these drugs and for everybody to remember them and apply them to their practice or to themselves, but the point is that we've had a whole bunch of drugs that have been approved recently. We have a whole bunch of drugs that are being studied that have been approved in other diseases and we have an enormous list and this is nowhere close to a complete list of drugs that are currently in clinical trials and I have several of my research nurses and I have several of my research data coordinators here and they will attest to the misery that this success has brought upon their personal lives but it has been extraordinary what we've been able to bring to the lives of our patients. So the subject that we get the most questions about when patients come to us, when I get phone calls from physicians and from patients and their family members is about immunotherapy. Now immunotherapy is a sort of difficult definition what is immunotherapy? Well we've been working with thalidomide, linalidomide, and pomalidomide for a number of years. There are other derivatives of thalidomide that are coming on. We call those immunomodulatory drugs. I don't have them up here on that list. We still don't really understand how those drugs work but they certainly change the immunologic milieu significantly so the reality of it is that we've been doing immunotherapy in multiple myeloma for a very long time. You heard David Viesel not particularly eloquently but speak about stem cell transplant in multiple myeloma and Josh was speaking, and if you think that David wasn't eloquent, Josh was even less eloquent speaking in the other room. Yeah, but about autologous stem cell transplant in multiple myeloma. Well the reality of it is the real big successes with autologous transplant multiple myeloma are not chemotherapy successes, they're immunologic successes. And the reason that those patients do as well as they do for as long as they do is because there is some resetting of the immunologic environment that allows the immune system to either re-equilibrate with the disease and keep it at bay when it had failed previously and the proof of that is that we have patients who don't achieve complete remissions after their stem cell transplants. Yet their disease remains stable for sometimes decades. So that is immunotherapy. But the questions now are about the drugs and the strategies that are coming along. So we have monoclonal antibodies. We have a whole series of monoclonal antibodies. We've had two monoclonal antibodies approved recently and what's a monoclonal antibody? Well, the oncologists and the other professionals in the room know exactly what monoclonal antibodies are. Somebody jammed something into a mouse, let the mouse make antibodies and now we've humanized them and we're using them in human beings.  They interact with the target on the surface of the cell and actually induce apoptosis in the cell. I think more typically these monoclonal antibodies bind to the surface of the cell and attract the cells that are capable of killing things that are coated with antibodies. We have other monoclonal antibodies, checkpoint inhibitors, that have become the hottest thing in oncology in general that are being applied to multiple myeloma and they interfere with pathways that are meant to dampen our immune system. So we have monoclonal antibodies that work via all kinds of mechanisms. They fix complement, they attract cells that are capable of punching holes in the surface of cancer cells and K cells, things like that and they attract cells that are capable of phagocytizing tumor cells and those might be the most interesting ones because those cells then present antigens from the killed cell to our immune system and may propagate that immunologic response beyond just the antibody itself. So those are exciting. Then we have active ones and Ed Statenauer is speaking next door right now about CAR T cells. We have had an enormous series of questions from patients about CAR T cells because there was an article about a patient who was dying from myeloma who got CAR T cell therapy actually by Ed and achieved a complete remission. Now unfortunately that success in that one patient wasn't, didn't last forever and the overwhelming majority of patients who got that therapy don't respond as well as that sort of index case that we're talking about but CAR T cells are very interesting therapies. We can remove your T cells, engineer a receptor for a target on the cancer cell of interest and have that engineered receptor put into the T cell and let it activate the T cell, get it to proliferate and kill tumor cells via that the person who first developed that strategy was a guy named Zellig Escher who actually just developed it as a tool in the laboratory. Carl June sort of moved that into the clinical realm and it is a particularly exciting strategy. Vaccines, there was a very large vaccine study going on in the United States in which tumor cells are fused with dendritic cells, one of the most competent types of cells in terms of presenting antigens to our immune system and those dendritic cell tumor cell fusions are then given back to the patient in the hope of stimulating an immune response in the patient and there are other strategies as well including all kinds of targets. So I talk to you now about the checkpoint inhibitors. So checkpoint inhibitors have been approved, they were first developed in melanoma, sounds sort of like myeloma, but not half of our patients always talk about their melanoma but we are talking about myeloma. These drugs have not been nearly as successful in myeloma, but it turns out that when we combine them with image, with lenalidomide, with pommalidomide, we can take patients who are refractory to the pommalidomide or lenalidomide and who have no response to the checkpoint inhibitors. So we're going to talk to you now about myeloma and how to respond to the checkpoint inhibitor, pembrolizumib or nevolumimab and when we combine them we get excellent responses and some of these responses are quite sustained. Now what we don't know is if there is a population of patients in which we actually get over the hump in which we will educate the immune system to sort of propagate that response indefinitely and those are things that we're going to lose. We're going to not lose but use. Noah Baran is piloting a study here in which we're trying to leverage that in patients who are post-transplant. So some very exciting kinds of things. Denosumab, you guys use it in the treatment of hypercalcemia, it is a drug that has not been approved in myeloma, certainly has a potential for benefit and we will see other drugs in those categories used as well. So we started to talk about this. So we have CAR T cells that look at a number of different targets. So again, CAR T cells, most of what they do although there are some variations in this is that a T cell requires two signals in order to become activated and proliferate and in normal circumstance, the native T cell will engage those two targets on the surface of a cancer cell, it will start to proliferate and it will kill targets that have those paired antigens. What the current CAR T cell strategy does now is they combine both of those activating signals into a single receptor. But they engineer the receptor by attaching a monoclonal antibody to it. So you have a monoclonal antibody against whatever in our institution here against BCMA, a fairly ubiquitous target on B cells but particularly plasma cells and you form a chimeric protein. So those two activating signals that are normally in two separate receptors into one protein and on the end of that protein you have the antigen binding characteristic of the monoclonal antibody.  So we know that it works, we know that we can kill these cells, we don't know that we can cure myeloma with this kind of strategy but we're just starting to do it, the cell doses that we are using right now are still relatively low, the dangers are relatively high but this is certainly something that is going on. We can, yeah. So the bite antibodies in by all? So there are no bite antibodies that are actually in clinical trials yet. There are bite antibodies that are coming along and have slides that we'll talk about that. So mills, there's a whole science, one of my friends at Hopkins is particularly interested in this. We can remove tumor cells from, we can remove T cells from tumor. We can expand those T cells that are specific for the cancer. Part of the reason that these cells fail is because the cancers are very, very smart. They can teach those cells to not proliferate and not respond but when we grow them and can engineer their environment, sometimes we are capable of putting them back into the patient and having them kill tumor cells. So far, this stuff hasn't been particularly successful but most of the reason that this is not successful is because we don't really understand where all the checkpoints fall. We have drugs that we call checkpoint inhibitors but the reality of it is that we are just starting to understand the environment in which these cells work most efficiently. So we will eventually be able to do that. Bob Corngold and his group here has particular expertise in expanding T cells. We can now start to identify what are the targets that those T cells attack and instead of using monoclonal antibodies that have many problems in terms of engineering car T cells, we may be able to cut out the intact T cell receptor and put them into our T cells. So engineer T cells with activating molecules that are meant to be in T cells. And so this is a very complicated biology. So this has been done to some level with New York Esau One. Unfortunately, it turns out that New York Esau One is also found on myocardial sites. So in treating patients with some of these strategies, there are potentially very large pitfalls like the T cells actually attacking the myocardium in addition to attacking the tumor cells. So all kinds of things. And then there's lots of things that we can do in the post transplant environment. Engineered DLI is something that is being tried. We have been collaborating with a company from Italy that actually allows us to turn the T cells off.  But in doing so, they can also kill the patients because of uncontrolled graft versus host disease. Well, we have the ability to now engineer the cells that we give back so that when they are doing more than we would like them to do, we can actually ask them to commit suicide. So there's all kinds of interesting strategies there. I talked to you about the dendritic cell fusion vaccines, interesting stuff, many, many targets that are being used. One of the things that was very, very exciting about a year and a half ago was a report of a patient at the Mayo Clinic who got a very, very high dose of the measles vaccine. It turns out that the measles virus specifically infects activated plasma cells, proliferative plasma cells, and that they gave an enormous dose of the engineered virus that is used to vaccinate patients against the measles, and that it specifically infects the plasma cell and actually can kill the plasma cell. Now, they had a success in one patient, that patient relapsed quite quickly. But just to extrapolate from another area in which this kind of work is being done, so glioblastomas, a cancer that we have much to achieve in the future is infectable by the polio virus. So you can take an engineered polio virus and you can kill glioblastomas with that.  Now, admittedly, this is a very, very minor population that achieves that level of response, but we are just starting to do that in multiple myeloma. And there's a whole bunch of companies out there that are not just working with the measles virus, but are looking at other viruses that are tropic to specific kinds of cancers or engineering those viruses to make them tropic to particular kinds of cancers. And as we learn more about immunotherapy, these two fields are going to come together. So we're going to be infecting our patients with the measles virus. We are then going to be turning on and off their immune response to those measles virus infected cancer cells. And we're going to see this kind of stuff evolve, I hope fairly quickly over the next decade. So all kinds of things like that. So to go through each of these things one after another, I don't know that that's really the point of this. I think the main point is to say that we have a lot of interesting things. The PVX, I don't know what that is, so the PVX for 1.0, why this is more interesting in smoldering myeloma? I think people feel that a lot of these therapies are going to be more effective in people who have more intact immune responses. I have some sort of philosophical objection to saying we should be taking all myeloma patients and treating them, all smoldering myeloma patients and treating them. We still don't know who are the ones who are going to progress to active myeloma and those who are not, we're still not sure that those strategies can't have a negative impact on either the likelihood of progressing or in terms of selecting for resistance when we in fact have therapies that are better therapies. So unless we are very damn sure that we can identify those who will need treatment and that the treatments that we are giving them aren't going to hamstring us in terms of treating with more established and more effective therapies later on, I find it a little bit difficult to do that. I will readily admit that I am probably in the minority in feeling that way, but I think that that kind of strategy needs to be thought out very, very carefully. So monoclonal antibodies in phase two. So, implicitly, and darsilex are the two that are approved. We have a whole series of monoclonal antibodies that are very interesting. I can't tell you which ones. I think are going to be the best ones. There are a number of monoclonal antibodies with different targets, and there are now monoclonal antibodies that have been engineered to include toxins so we can target the cells using the monoclonal antibodies. We have had great success, although not without toxicity in using an engineered monoclonal antibody here. In patients in whose disease has responded to nothing else, we have had very, very durable responses, not without a lot of complaints because the drugs are not as benign and trivial as the more traditional. I guess traditional is hard to use in drugs that we've only been using for a short number of years, but these engineered monoclonal antibodies are certainly very exciting. We have a couple of other ones that are coming online. Hopefully they'll be less toxic and more effective, but I think that this is certainly a very exciting way to go, and we have lots of other drugs that can sort of leverage these as well. All of these drugs, and Matt and I don't particularly get along well, but Matt represents cell gene, and all of these drugs work better when we use them with lenalidomide, when we use them with pomalidomide. Now, why that is, I certainly am not sure, but it's quite remarkable that these drugs that have some efficacy become dramatically more efficacious when we add an imid, and we have really no idea why that should be the case. So it is a very exciting world just empirically that even though we don't understand the biology, it's as we mix and match these drugs to find out how effective they are. Just Darzel X, which became commercially available just in the last year, has a response rate of about 30%, and in the real world probably less than that, but when we use it in combination with lenalidomide, the response rates double, and these are in patients who are completely refractory to lenalidomide. So why that is and what it is that makes it possible for that to happen is stuff that we have to understand. Why should a patient in whom lenalidomide does not work when we use it in combination with an imid, in combination with a monoclonal antibody? It's just sitting there on the surface of the cell.  What is it about the imid that makes the cancer cell more sensitive to being killed by the monoclonal antibody? Or perhaps more importantly, what is it that the imid does to activate the immune effector cells to kill those things? And if we understand that, we're going to have an enormous amount of work to do in terms of applying those insights into the management of our patients. As I talked about, we have an enormous number of clinical trials that are going on in patients with smoldering myeloma. We, as a group, argue all the time about what we should be doing and is there a risk of doing harm. And, you know, there's a lot to be done. And if we could identify those patients in whom we know we're going to go on and actually develop symptomatic myeloma and apply therapies that are potentially curative, that might be a very exciting step. I find it difficult to take a smoldering myeloma patient and say it's time to treat them and then not try to cure them. And a lot of the clinical trials, I don't think have cure as their objective but have management as their objective. So it's a little bit difficult of a world. But the point of this slide is to show you how much work is going on. So the Compass study. So this meeting is sponsored by the Multi-Myeloma Research Foundation. And I'm not saying this because the Multi-Myeloma Research Foundation is here. I think this is the single most important study going on in the myeloma world, certainly in the United States. We have a representative of HOVON here who is the Dutch myeloma research consortium that has done very, very similar kinds of work. In the United States, we have never really done this. But this is a clinical trial in which we have sort of genetically mapped all of a thousand patients. And we are going to see what happens to these patients as they've been treated. So we've had a lot of clinical trials in which large numbers of patients have been treated in the same fashion. And then we've been able to identify what genetic variables there are that predict for better or worse outcomes in response to that particular therapy. Now this trial allows us to do a lot of things. It allows us to see what mutations occur as patients are failed by a particular therapy. It allows us to see other pathways that are relevant in other kinds of therapies. But it also allows us to see whether for a patient with a particular genetic background, is there a therapy that is better for that patient? None of the other clinical trials have actually attempted to do that. Peter has brought us a genomic, a gene expression profile platform that I think is going to catch on. They're starting a large clinical trial here in the United States that may allow us to answer some of those questions as well. But for right now, this Compass study is doing things that no other study has done before. We're fortunate here to be participating in that study. There is a new successor to that Compass study. The Compass study does this, but the successor trial does as well. One of the big things in oncology, you've all heard of foundation medicine and things like that, that are trying to identify particular genetic signatures that are associated with better or worse response to particular kinds of therapies.  But 1,600 open reading frames that are sequenced, both by next-gen sequencing and by RNA sequencing to identify potential actionable mutations, meaning therapies that can be directed at patients with particular mutations. So sort of the classic one in myeloma has been a BRAF mutation. There are drugs that are used in other malignancies, melanoma in particular, that target that BRAF pathway and about four or five percent of newly diagnosed myeloma patients have a BRAF mutation. Are those BRAF specific drugs going to work in those myeloma patients? But I think perhaps more importantly, we're going to stop having myeloma doctors and lymphoma doctors and melanoma doctors. We're going to have pathway doctors. We are no longer going to be talking about that you have a cancer that arose from your plasma cells or pre-plasma cells. And we treat plasma cell malignancies in this way. We are going to be saying across all malignancies that you have changes that affect this particular pathway. And so it is going to be the pathway that we treat, and not the malignancy, not the cell type that we're talking about. I'm sorry, this part captures the mutation, I showed you the mutation, but it doesn't have died between yet. But the reason that the MMRF is doing this is to help us in the management of our... But ultimately what we're going to see is these huge, all-encompassing trials. And if we know what mutations our patients have, we're going to be able to direct patients towards clinical trials that are perhaps more applicable to their particular genetic makeup. And again, the place where we fail in doing this kind of stuff is that much of the time the reason we respond or not respond has nothing to do with the cancer itself, but sort of the background of the patient, the immunologic milieu, or the microenvironment. I hate to talk about the microenvironment because the group that brought us that term and I don't see eye-to-eye on things, but there are many host variables that we need to identify. So monoclonal antibodies, we have lots of targets with lots of antibodies being developed. We're fortunate enough to be able to participate in these. We're seeing lots of combinations with monoclonal antibodies and with new drugs. We have done a lot of stuff with histone deacetylase inhibitors here and there are some new histone deacetylase inhibitors that are being looked at, but the point is we have effective drugs. Now we have to figure out what is the most effective way to treat them. We have a ton of clinical trials here at the John Thorough Cancer Center. I'm just showing you sort of the algorithm that we use to pick clinical trials for patients. So it is incredibly complicated because we have been fortunate enough to have a lot of drugs thrown at us that we now have to figure out how to use and which ones are going to be effective. So the point isn't to memorize the JTCC algorithm, but to understand that it's difficult now to choose drugs. I talked about CAR T-cell. So the CAR T-cell study that we are doing here is sponsored by a company named Bluebird. It looks at BCMA as the primary target. I'm not going to detail how this is done. We actually have another cellular therapy trial that is opening here using an engineered NK cell rather than an engineered T cell to attack the cancer cells. So that is a very exciting thing as well. Iced tuximab is a competitor, I guess, at some level of daratumab, of dorsalex. So it is an interesting body. It is an interesting monoclonal antibody that seems to be slightly more active in terms of killing cells in tissue. I need to hurry up. Sorry. So it's another monoclonal antibody targeting CD38. So this is just some of the data. The point is that it is another monoclonal antibody with significant activity in patients who have been heavily pretreated that is now just going into clinical trials in combination. This is just, again, some more of the data. And I don't know how much the particulars of a clinical trial and the responses are of interest to the audience. I think the point is that these things work. Pembrolizumib is a drug that probably most of you know from melanoma and now from a number of other malignancies. It is a checkpoint inhibitor or monoclonal antibody against PD1. And I'm not going to go through all the details. I actually was the PI on a single agent PD1 trial. There is no activity of PD1. We had a couple of patients that had stable disease, but there were no objective responses to PD1 blockade in multiple myeloma. We are now using it in a clinical trial in combination with lanolinimide. And that trial is now expanding to include carfilizumib, pembrolizumib combination. So that may be a particularly interesting combination as well. Certainly something that we are very excited about. And does this slide say anything about the response rates? Yeah. So the point is overall response rate of 50%, but I think that this is the interesting thing so that in patients who are lanolinimide refractory, we are seeing about a third of the patients respond to the combination of pembrolizumib and lanolinimide. So I think that the idea of immune manipulations working is going to be exciting. So we have another monoclonal antibody this time against anti-PDL1 that is being used. And actually both Peter and myself are investigators on this trial. So using this in combination with pembrolizumib in a number of different combinations, and I'm not going to go through the biology of checkpoint inhibition. Let it be said that our immune systems weren't designed to protect us from cancer. We were supposed to be dead well before we got cancer. Our immune systems are there to protect us against infections. And one of the main evolutionary issues is to turn off the immune system once the infection has died down. And unfortunately cancers use that dampening of the immune system to their advantage in terms of teaching immune effector cells to ignore them. And these new molecules, these checkpoint inhibitors, of which there are now many, try to circumvent that part of our biology. So the trial that we are doing here has a number of arms. We are already seeing responses in patients in whom the background therapy we would not expect to be effective. So we know that PD-1 blockade is effective. Now we are learning that PD-L1 blockade is effective. We have another target that we are looking at that is particularly exciting. So there are many proteins that are trafficked in and out of the nucleus, and there are pores that specifically mediate that transport in and out of the nucleus. And there is a small company up in Newton, Massachusetts that has developed a series of molecules that can block that transport of proteins in and out of the nucleus. And the theory was that by blocking this we could capture tumor suppressor proteins in the nucleus, and that would then take very unstable cancer cells and tell them to commit suicide. And it looks like, I'm not sure that that mechanism is actually how the molecule works. It may very well be, but it actually does kill myeloma cells. And so there is now a clinical trial going on with these. There is actually now a newer derivative that is just starting clinical trials, and we have clinical trials here with both the parent compound and now the derivative that we're both, that we're excited about both of these. So Andre asked about bifunctional antibodies that you may have started to use when toximab for the treatment of leukemia. So there are antibody, there are bispecific antibodies and there's many different ways to make bispecific antibodies. So there are clinical trials that are in the midst of starting up with bifunctional antibodies that are specific to BCMA. And I'm just going to show you some data that in comparing in animal models CAR T cells versus bifunctional antibodies, they're indistinguishable. So it's actually easier to see in the next slide. So in terms of the ability to... the controls versus CAR T cells versus a bifunctional antibody, so we may have a much, much less expensive, much more off-the-shelf way of achieving exactly what CAR T cells can achieve using these bifunctional antibodies. And these are just using fluorescent tumor cells. You can see that the bifunctional antibody yields the same kind of protection as the CAR T cell does versus the controls. So these bifunctional antibodies are very, very exciting molecules in general in oncology and perhaps going to be seen to be effective in myeloma in the near future. So I think one of the points that we always have to talk about is in the United States, we're incredibly bad at getting myeloma patients to participate in clinical trials. I think I've seen clinical trials published by Peter that where more than 90% of the eligible patients in the Netherlands participated in clinical trials. In the United States, just for participating in clinical trials at all in myeloma, which is one of the better diseases, we get numbers that are in the single digits. And the myeloma community is a particularly well-organized community with lots of advocacy. So the point is that we need to start taking some of our cues from the Europeans and how they do clinical trials and find ways to get our patients to participate. So when any of you guys sees patients that you think would benefit from the participation in clinical trials, find them. It doesn't necessarily need to be here. But we need to figure out ways to answer the questions and solve the problems that we have much more quickly than we do because we have so many tools now and we just are not learning fast enough how to use those tools. So, yeah. I mean, I think that that's the key question. And we have a little bit of data about we were on a conference call yesterday about that son of compass trial in which one of the investigators was talking about one of his patients that had become refractory to proteasome inhibition but had a mutation that suggested that the clone that was operating at that moment was likely to be a proteasome inhibitor sensitive. So they used the combination of a drug that wasn't approved in myeloma because of other mutations that they saw in combination with a proteasome inhibitor to good effect. Now, whether that answers your question, probably not. But the point is myeloma is genomically incredibly complex and there are not many themes. I have treated, I think at this point, four or five patients with BRAF, with MEK inhibitors. I have not seen a response rate. I have not seen a responder yet, although others of my colleagues have based on identifying BRAF mutations in my patients. So the answer is mostly no, but hopefully yes. Yeah. Can you comment? Obviously that's what I feel when you try to look at these actionable items, but we can have a lot of actionable items that are passengers and not drivers in the disease and what's the threshold of this infection of this because it's not just a tumor verb and given the fact that technology to detect them is so sensitive you can find a mutation in just for a second. Yeah. I mean, so we know that there are many clones that exist in myeloma patient from diagnosis and they don't all have the same mutation. So the question that you're asking is a very complex one, but I think even beyond that, if I had a patient who had a BRAF mutation, I wouldn't treat them with MEK inhibitor. I would treat them with carfilzament. I would treat them with Bordesimid because those are drugs that work. And even though we haven't... you know, this is the problem in myeloma is that we still don't know what are the driver mutations despite all of what we have done and it doesn't appear that they are the same driver mutations in all or even most patients. There is literally no theme and hence we direct our therapy more towards the biology of plasma cells than we do towards the specific mutations that the patient has. I think what the future is going to bring us is the combination of the two. It's therapies that are directed towards the biology of plasma cells in which we then superimpose the therapy that is specific for the pathway that is perturbed in that particular myeloma patient. And right now we haven't gotten there and we don't have the choice. Number one, we don't have the drugs that target those pathways. That will happen. And we don't have the choice. It's too complex. We don't even have that information in most patients. But sometimes we think of those mutations as being what could be really the next radical change is probably going to be more in between what's going to help us select among the sequence of treatment and that's a very difficult question because we have too many drugs. But I think the place that we're going to go is to take these very, very effective therapies we have that are plasma cell directed therapies. They're not myeloma directed therapies. The reason that we have the successes that we have is because we take advantage of the biology of plasma cells and we still don't have any drugs that attack the pathways that are the perturbed pathways in the individual patient. So we will start to learn that. It turns out to be way more complicated in myeloma than in virtually any other cancer that I know that we deal with. But that's going to be how we end up curing that. Curing patients routinely is by combining the pathway-specific therapies with the plasma cell biology-specific therapies. What's the most significant factor that you look in practice to predict from a small to ring myeloma that you're going to have? Do we have something that is reliable? No, I mean because it's a host phenomenon. So she's not in the room but people have heard me that she's going to actually speak today. She may have spoken already. So we have a patient who we take care of who was in her early 30s when she was diagnosed and she had smoldering myeloma but fairly high burden smoldering myeloma that sat there perfectly fine and she was married, she hadn't had a child and when she realized that it was three or four years into her treatment and that she hadn't progressed she said, well, I've always wanted to have a child. I'm going to have a child. So she's the only patient I know who has gotten pregnant on my time. I had nothing to do with the pregnancy. But she decided to get pregnant and as soon as she got pregnant her myeloma exploded. I mean, I introduced her to Peter before. And she went from an M spike of like 0.5 to 2.5 during the pregnancy. And as soon as she gave birth and she was no longer immunosuppressed the myeloma took a right hand turn. So progressed, gave birth, stopped where it was, didn't go back to where it was but the point is that what turned her from a smoldering myeloma into an active myeloma and then back to a smoldering myeloma again was a host thing. It wasn't a cancer thing. So I think the difference between the overwhelming majority of patients who have smoldering myeloma and those who ultimately evolve into symptomatic myeloma has relatively little to do with the cancer but much more to do with the host. I mean, obviously it's a combination of both of those things. Similarly in young women we see a lot of the myeloma while they become pregnant. Yeah. Well, we see, switch to why I tell everybody who works for me not to get pregnant because it's so, I mean, from an oncologic perspective it's a dangerous environment besides the fact that they then take time off and they do.


Busy equals broke and productive equals paid everybody's so freaking busy out here.


Hi guys, what is up? Welcome to my channel. So for today's video, we are going to be doing a very late November favorite. But if you wanted to see the items that I've been loving for the past month, then just keep watching. So I took a little bit of an unannounced hiatus from social media. I just really needed a break and I needed to recalibrate. So I am back on track. I'm so excited to be filming these videos for you guys. And I don't know, I just couldn't live with myself if I didn't get up a monthly favorites, even though it's like the middle of December already, which by the way, Christmas is coming so quickly. So I don't have a ton of items, but I have some really good ones that I wanted to talk about with you guys. The first item is something that I discovered in the very, very beginning of November. I feel like I've had it for much longer, but I've really been loving the Hood of Beauty Mercury Retrograde palette. I just think it's one of those beautiful palettes that's out on the market right now. It's so different. I love the looks you can create with this palette. The textures in here truly are unique and I just think it's an overall great quality palette. Now these colors maybe aren't necessarily something that I found that I reach for every day, but it's just so pretty and it makes me happy. It sparks joy in me. So though I probably haven't used this as much as I would like, I just have been loving it. I love owning it. I love playing with it. I love looking at it. You know you are a true makeup addict when you just sit in your room alone at night and swatch the products and I just feel so happy swatching this. So I've been loving this. The next items are from a review I did pretty recently a couple of weeks ago. I reviewed the new ColourPop Coconut Collection and there are two items in here that really stood out to me that I just love. As you can see I've been loving these like brown topy tones so this collection really did it for me. So we have the ColourPop Going Coconuts palette. Now I recommend you go check out my video where I review this whole collection so you can see everything. But this has to be one of the most beautiful palettes ColourPop has ever come out with. The most perfect tones, the most perfect travel palette. I just I'm so obsessed with this and I feel like everybody who has this is also obsessed with it. The quality is so good. The colors are so good and it just it's been these tones are my whole vibe and I love this and it's just so amazing that this is so affordable and the quality is so good. You know it's not Natasha Denona quality or anything but for what it is the ColourPop formula is definitely comparable to high-end eyeshadow formulas. It's really mind-blowing how they managed to do that but definitely have been loving this palette this month. Also from that collection should be no surprise it is the Call Me On My Shell Phone Super Shock Shadow Trio. So in here you get three of the Super Shock formula which I am in love with. The color in particular that I think I love the most is the darkest color. This is Deep Dive. I wore this all over my eyelid on Thanksgiving. I posted photos and a lot of you guys were like what are you wearing on your eyes? It was this and those photos didn't even do this justice. This was 20 times more beautiful in person when the light would hit it. You would see the little glimmers reflecting and then we have Peek-A-Boo which is a little bit more of a satin-y shade. Still really pretty. Don't like it as much as Deep Dive but still like it. And then we have a little quirky which again this is my kind of color really really obsessed with it. So overall I am just so in love with the colors in here and the ColourPop Super Shock formula like you can't deny. It's a really fantastic formula. It's extremely affordable. So the Going Coconut collection was a big hit for me. I didn't think everything was amazing but these two items in particular I have been loving this month. Also what I'm wearing that I know you guys are going to ask me about what's on my lips and again this lip is my color story. So these are the Christian Audet and Mel Thompson collaboration items. So in the collaboration there were two lip liners and two lipsticks. So what I'm currently wearing right now is the Smooches Gel Lip Liner and you guys this is one of the best lip liner formulas because it is so smooth and creamy going on the lips. It feels just like a ColourPop lip liner just that really creamy feeling but it sets down and it doesn't move. This is one of the most long wearing lip liners but it's also creamy so you definitely get the best of both worlds where it just sets down and it lasts forever but it also is just so easy and comfortable to apply and I love this color. It's the perfect lip defining color for a good nude lip and on top of that I have the Beauty Lipstick which I just these two are a match made in heaven. I am so obsessed with these colors Mel you did such a fantastic job. I cannot stop wearing these colors. Also in the collection there's a little bit more of a light nudie pink lip liner and kitten again something super great and wearable. This color is so fun. This is Puffin right here. If you love these super neon red orangey kind of colors you are really going to love this one. This color is just so beautiful and honestly it's very unique in my collection but you guys know I'm such a nude lip lover that I'm honestly obsessed. Definitely check out this collection. The formula on these are super good. The packaging is very luxurious feeling and the lipstick formula is lovely but I gotta say these lip liners are A1. Let me talk about another lipstick that I've been loving. This is from Essence and it's only a few bucks but I've been obsessed with it. I can't believe it's as cheap as it is. This is the lipstick and this is nude and it's just such a really pretty wearable nude shade and I cannot believe the quality of this given the price. Now previously in past years I had tried Essence lipsticks and I just was not impressed. So I believe they reformulated because these are so nice. Now I don't know if it's just this color in particular or this is the bold shade so maybe it's just the bold formula. Whatever it is this lipstick is working. I am interested in trying other lipsticks from the line to see if they're as good as this. But these are the perfect lipsticks to throw in your purse because if you lose them it's just like whatever but the colors are actually very pretty and the quality is super good as well so I'm very impressed with this. So if you're ever at Ulta I would definitely say pick up some of the Essence lipsticks because I am pleasantly surprised. So again another nude lip that your girl loves. Next up let's do a powder foundation that I've been loving. It is a bit light for me right now but it's super good. This is from the brand Jaycat and it is the Aqua Insurance Compact Foundation. As you guys know I wear powder foundation every day to work and this one is so good. Now it is a little bit more loosely packed so it can get very messy. I play it with the Esum X57 and I get so much coverage with this. This is probably the heaviest coverage of powder foundations that I personally own and it's a drugstore powder foundation. Mine by the way is in the shade natural. I think I would go a shade deeper if I could. But this makes the skin look super smooth. It really buffs into the skin and coverage on here is amazing. Definitely comparable to the Makeup Forever Powder Foundation. I don't know which one I like more but this one is significantly cheaper. So I've just been using this one a ton and it is amazing. So if you're looking for a good drugstore powder foundation order this Aqua Insurance foundation from Jaycat, incredible. Moving on, here's an eyeshadow palette that I've been absolutely loving. This is the Vizzy Art Dark Edit eyeshadow palette. Now it's not the newest item on the market but it is quite incredible. I've dug into it a lot recently and I just I'm so obsessed with this palette. It has the most amazing fall tones. I find this palette to be extremely unique. Just given the palettes that have come out lately, this one is so unique. It's so pretty. The colors are very cohesive in a very unique way. Like you can create so many looks. You can create a purple look, a super orange look, a gold look, a smoky eye, a green look. You can really just do so much with this little guy and the quality is amazing. Right now Muse Beauty Pro is having a deal where this is included. So I definitely recommend you check that out because this is one of the best eyeshadow palettes that Vizzy Art has put out and the quality is just so amazing. And it's a great way to try their formula in mini forms so you pay a little bit less. And it's just worth every penny. I've just been loving this and I just recently did a rankings video and a lot of you guys love this as well. So there you go. So last makeup item that I want to talk about is actually the highlighter that I am wearing right now. And this is from the brand Kaleidos. Now Kaleidos is an indie brand, but they are so good. They did send these to me, but like they're so good. First of all, let's talk about the packaging of these. These are the cutest things I've ever seen. They are so amazing. They create like the cutest products ever. Now, the one that I'm wearing is Ray Rider. Now the collection itself, now all of the highlighters are wearable. Some of these are really fun, funky, glittery, cool colors that my boring self wouldn't wear. But Ray Rider, look how pretty that is. The quality of these are really phenomenal. Another really wearable one that I like is Star Surfer. So if you want to try out these items, Ray Rider and Star Surfer are the most wearable. If you are into really fun, unique kind of highlights, this is Laser Glazer. Thinking incredible. Some of these have more of a smooth formula. Some of them have more of a glittery formula. You just don't know what you're going to get. And it's so amazing. I really, really think they did a phenomenal job. And you should definitely check out all the other things they have on their website. They come out with the coolest things. Like this brand needs to be huge. They're eyeshadow palettes. I mean, hold on, how freaking cool. I just every time they come out with a new item, I'm just like, so cool. Okay, anyways, that was the last makeup item. Don't really have too, too much to talk about really. Just, I don't know, there's just so much makeup that it overwhelms me. And I only use like two things. I don't know if anybody falls into a rut like that, but I will not lie. November was a bit of a makeup rut for me. I was feeling very overwhelmed and I just needed to chill out and use the products that I really wanted to use. So that is everything that I love this month. So let's talk about my channel of the month. And that one goes to my friend, Jessica. If you look up Jessica Lee-Mohaz Ken here on YouTube, but you will find her channel. She's just the sweetest and cutest person ever. She has such amazing makeup skills. She does so many things that I could never do. And I feel like she sees makeup from a really fun, unique standpoint. So she just does these fun makeup looks that I love watching. I love hearing her opinions on makeup. And she has a very similar taste in makeup that I do.  So you will definitely like Jessica's videos.  So I did wanna give her a quick shout out because she's amazing. I love you, Jessica. Make sure you go to her channel, check her out and subscribe. You can definitely feel how much she loves makeup just through watching her videos and it just makes it that much more enjoyable. So that is all I have for this month's favorites. I hope you guys enjoyed it. Let me know what your favorites were for this month. I'm gonna be continuing to use a lot of makeup. I have a lot of fun video ideas in store for you. So I have winter break coming up in a couple weeks and so I have like 10 days off. I'm just gonna be filming and filming and filming. I'm so excited. So thank you guys so much for tuning in. If you aren't subscribed to my channel yet, I sure do hope you take the time to do so and I will see you guys in the next video. Bye guys, have a good one.


I'm gonna stay good morning, good afternoon, good evening, wherever you may be, across the planet, around the world. My name's Greg from in5d.com and in5d.net. And today we're gonna be talking about the metaphysical reasons why you may be unusually tired. I don't know about you, I can't speak on your behalf, but yeah, I am. How are you guys doing? Have you felt this? And I will be explaining why you're feeling this and some of the explanations are really quite fascinating. I just wanna say too, a quick shout out to everyone that has been joining us lately, like for example, last night on the global predictions with my wife, Ally and me, and we do date night as well on Tuesday nights. We're literally having people from all around the world joining us. So I encourage you, if you're watching this right now, we have some people checking in right now on the live chat to tell us where you're from. And this way maybe it can help you make those connections as well with people in your area, right? So when I say good morning, good afternoon, good evening to start the show, it really is that to specific people all around the world. It's a beautiful thing that we are global and we are making these connections everywhere. When I sell the N5D quantum tie-dye shirts, I always put some 99.9% quartz crystal sand on top of the shirts before I mail them out. I believe this sand is from Atlantis. And what it's doing is it's going all around the globe. I just had a sale in Australia, New Zealand, Canada, all over Europe as well. So what this is doing is creating these Atlantean points of light all around the world. So it's a really beautiful thing to see happening. And just a quick reminder too, before we jump into this. We do have all of the shirts at N5D quantum tie-dye are buy three, get one free and that includes any ones that are on sale. These are, if you just go to click on shop and you'll see they're sorted by the latest ones that we have and these are the latest styles that I have that are on sale. The solar plexus crown chakra, third eye and throat chakra, they're all on sale for $25. This is the one I'm wearing right now. This is the exact one I'm wearing. As a matter of fact, it's called be beautiful quantum tie-dye and here you see like the quantum earth element which looks amazing and all of these. I mean, this is another one of my favorites, the cosmic lightning. Yeah, so lots of amazing styles on sale, buy three, get one free. Also, I've added a bunch of them to, well, if you're on a laptop or an iPad, just go to the right hand side under product categories and you'll find underneath the X discounted, each particular size. So, if you're looking for like a men's large, just click on that and you'll see all the men's large shirts that are on sale right now. And obviously these are also buy three, get one free. Any combination of any shirts, buy three, get one free. So, check that out at n5d.net. And yeah, when you get your shirt, it'll be packaged in one of these kind of envelopes, but there'll be CSZK, 99.9% quartz crystal sand in there. So, when you dump it out, you will see the quartz crystal sand. I can't put a ton of sand in there because it'll affect the shipping weight, but I put enough in there that you will notice it. So, it's really cool. And we're sharing that energy all across the world, basically. Yeah, so, Ellie and I did date night last night and that was fantastic. As always, my beautiful wife Allie and I do global predictions every Tuesday night as well. And on Friday, we're starting the monthly global predictions and we have a bunch of things that we're gonna be covering and we're gonna be taking requests from you guys as well. So, stay tuned to that. We're gonna be doing that, I believe. That's gonna be at eight o'clock on Friday. So, stay tuned, it's gonna be the first Friday of every month that we'll do the monthly global predictions and we'll continue to do the weekly global predictions on Tuesday night as well. So, quick shout out to people who have joined us here tonight so far, hi to Tina Lee and that Vaporama. That's a new one. I love that name, that's a great name. Yeah, and Tina's already saying that sleep issues yesterday and then again, I didn't get much sleep either night before. Wow, she's in Northern California. Hi to Von Craig and Jeanie, who's checking in on Facebook with us and CJ, hi to CJ and up three, Janet. She's checking in on Facebook as well. Thank you for joining me as well. Here on a lovely, what is it? Wednesday night, Wednesday, June 29th. Sometimes I have a hard time remembering what day it is. So, for the last two weeks or so, I've been unusually tired. Let me know if you guys have been. If you're watching this right now live, check in on the chat. Let me know if you've been feeling unusually tired. If you're watching this on the recorded version, make a comment below. But it's been about the last two weeks that I've been slammed. And I'm like, what the hell's going on right now? You know, in the Northeast and Northwest of the United States, they have what's called seasonal effective disorder, right? The acronym is SAD. But I'm thinking, you know, I live in Florida.  They're gonna have seasonal effective disorder in Florida, right? Oh, Jesus, the sun again?  Sunny again? I can't believe the sun's out. So, yeah, that's not very prominent here in Florida. But that is in like the Pacific Northeast and Northwest where the sun plays on the psyche. Yeah, I used to be a child and family therapist before I was started doing this full time. And I did see that in the Northeast of the United States. You know, when everything is gray from probably late September, you know, until April or May, and you rarely see the sun. You see the sun probably at best half as much as we see the sun in Florida. And, you know, that might just be a partly sunny day compared to a fully sunny day here. It plays on your psyche, you know? And when you wake up and you see the sun and you think it's gonna be a great day already, you know? You just feel good because everything is illuminated when you see the sun. So, yeah, it does play on your psyche. Here, I'm in Sarasota on the Gulf Coast. Oh, there's a lot of noise outside. But I'm on the Gulf Coast in Florida and I'll go to the beach, I'll play my bocce ball and, you know, rest and take a little swim, do my walk of gratitude. I do my work while I'm out there, both for physically and spiritually as well. But even on the beach, I found that I'm taking a nap. I'm needing a nap, thankfully.  And I can fall asleep under there for like a couple hours if I wanted to and still not get sunburned. But yeah, I'm finding that I'm needing a lot of naps. The other day, I was talking to Ally where we were doing FaceTime and I think I called her up early because, I mean, normally we talk later at night, but lately I've had to call her earlier because I'm just tired, I'm exhausted. I gotta get some sleep. So I ended up getting off the phone around 10.30 a.m. And fell asleep immediately. I woke up about 7.30, I made breakfast and then went back to bed and slept until 11 a.m. So I slept at least 12 hours, maybe a little bit more that particular day. Today I woke up, made breakfast, fell back asleep after breakfast. And then I took a second nap around one o'clock today. Now there could be a reason for that today and we'll get into that in a second. Just wanna check in, see how everyone's doing here. So, paper Rama saying, yeah, feel more tired lately. And so is Janet. Hi, Elizabeth, thank you for joining us. Tina Lee says, being in triple digit heat doesn't help either, yeah, I bet. Triple digit, oh wow. Yeah, we don't, here in Florida it gets hot but it never gets into the hundreds here, never. I mean, like the all-time high, like today might be 93 or something like that. And CJ is saying yes and lots of people that she knows or lords of people that she knows. But I'm pretty good at reading Typhonese. And up to you say, not tired but very little sleep. That's interesting. So, that reminds me of that article I have on N5D called 30 Ways You're Wired Differently. And it's something along that line. I can't remember the specific title, I'm paraphrasing but for example, I used to have ADHD. I was given Adderall which is an amphetamine. I could take an Adderall and go to sleep within an hour. So, it does the exact opposite. So up three, that's maybe you're getting that as well. Being wired differently. And Rob's checking in saying, you've been feeling that way for weeks now. So yeah, you're not alone, brother. Yes, and lots of people I know have been feeling it. Well, this is interesting. Jeannie's saying I was for years, recently got a CPAP machine to stop me from apparently snoring. The device seems to be helping me sleep better. Maybe you aren't sleeping well due to your sleep apnea. I don't know. I don't know. I think I've had sleep apnea in the past and I don't think it's really affected me as much as just the, because I'd still have normal sleep patterns. Now that my sleep patterns are abnormal and maybe that is something after chronic sleep apnea for years. I don't know, but when we're looking at all the comments here, it looks like, well, it looks like there's a lot of other people that are experiencing that like you're Suzy. Yep, and taken afternoon naps lately. Denny's saying hi to everyone that's joining us here. Hi, Denny. Same here, longer sleep and still napping in Georgia. Hi to Chrissy. She's checking in saying working seven days a week is making me so tired. Wow, you gotta find a little time off there sunshine. And hi to, hi to Susan. Thank you for joining me up threes. Yeah, I'm wired differently. The human spikes jack me up and we will be talking about that. Huge purging going on CJ. Paper on my sleep great at night, but tired all day. Yeah, lots of karma clearing. So yeah, we're seeing a little pattern here, aren't we folks? A lot of people are feeling that the tiredness and we're gonna be getting into why this is happening. Hi Donna, I'm gonna say Greg. So grateful you are broadcasting. The energies are extremely intense. Yeah, they are, there's a lot going on right now. And it's, we're trying to understand it all too and process everything. And you're gonna get a really good idea of what exactly you're processing here in a couple of minutes. This is my sigil glass. The sigil says all of my codons are open. So I put that energy into whenever I drink and I'm consciously thinking all my codons are open. And so, you know, we only have 20 of the 64 codons in our DNA open. So if somebody can figure out how to open up the remaining 44 codons, you can do anything. You can have abilities that we haven't even thought of yet that they only have in higher dimensions probably. So there's an, I put a link in the more info section for that article, how to change your DNA right now. And I think, I'm pretty sure I put my glass in there in that article too. And then I also included a couple one hour meditations that you can just listen to when you're going to sleep at night that reinforce that. And basically what the, what they're saying is all of my codons, all of the beneficial codons in my RNA and DNA are now open. I can do anything. I promise to use these new abilities responsibly in humanity's best interests. And it loops over for like an hour. One video has that with just me saying that. And the second one has me just saying that plus ambient music, ambient music in the background. So, check that out. You might want to even, you know, do it yourself, record something like that and loop it around. I have a program called MixCraft that I use for my guitar. I can plug my guitar basically into the computer and record music that way. But I can use it with vocals as well. So what I did was I just recorded myself saying that one time and then just copy and pasted that enough times to cover an hour's worth of MP3 sound.  Other people you're like, oh, wow, cool. I want to try that. So yeah, that's what I have, MixCraft. And that's how I made those videos. Well, let's hop into it right now. The first thing I want to talk about is the Schumann resonance. And let's go take a peek at it right now. So I'll do a screen share here. Where did it go? Okay. Oh, here it is. Okay. So as you can see, we have a little whiteout going on right now. And we had some going on in the past as well. But right now we're in the midst of a Schumann resonance whiteout. As you can see over here. And each Schumann resonance energy wave seems to carry a specific signature that can be interpreted on many levels. Yet many of these signatures are so obvious that they're hard to miss. What we also know is that there is a correlation between the Schumann resonance spikes and how they affect consciousness. As you can see, there were no spikes yesterday, but yet I still needed a nap. So the Schumann resonance can cause you to be tired, but there has to be other explanations if the tiredness is still occurring without any Schumann resonance whiteouts. Okay. So let's get back to the main screen here. Have you guys felt anything differently today because of the Schumann resonance whiteouts? Because they do play on our psyche. And I noticed because we are in the midst of one, you may be specifically picking up something right now because of that. And it's curious, with all these different energies coming in, and I'll be explaining some of these other ones as well, they have to be doing something to the human body, right? So thank you everyone for joining us right now. So the Schumann resonance can cause you to be tired, but there has to be other explanations of the tiredness, right? Because it wasn't happening the other day, and now it's happening right now. It wouldn't surprise me if there are people sleeping right now because of the Schumann resonance, but if we turn our attention to the sun, we know how the sun affects the human psyche. For example, as I was mentioning beforehand, seasonal affective disorder is prominent in the Northeast and the Northwest sectors of the United States where they don't get as much sun as in like California or here in Florida.  Josie's saying, screaming, go home and rest. As we know, the pineal gland affects human consciousness as well. The pineal gland regulates our circadian rhythm and melatonin production, right? Melatonin is what makes us sleep, right? So the pineal gland regulates that and it's sensitive to the magnetic fields, which may include coronal mass ejections, solar flares, emissions from the great central sun, Alcyon and galactic core emissions. I was reading an article regarding solar storms and CMEs where it's stated that solar storms are known to desynchronize our circadian rhythm, which means to throw it out of whack, right? And which is the internal biological clock that controls our sleep and wake times. Our pineal glands are affected by this electromagnetic activity and produce an increase in melatonin, thus disturbing our sleep and impacting our intuition. We may have enhanced intuition and psychic awareness during CMEs and solar storms. And I think that would include emissions from the great central sun, Alcyon and the galactic core emissions as well. So what's happening energetically? There are no significant coronal holes on the earth side of the sun right now. So we can rule out our tiredness due to coronal mass ejections and solar flares. There was no unusual human resonance activity yesterday. So we can rule that out as well unless lingering human resonance energies still existed from previous whiteouts. With that being said, many of us are receiving higher dimensional downloads when we sleep, which are basically DNA upgrades. So when we're sleeping, our bodies are adjusting to these frequency upgrades. And because these upgrades are coming in so often and frequently, it's quite possible that they're directly coming from Alcyon or the galactic center because we're needing additional sleep to absorb these energies. So bear with me a second. As our bodies are going from carbon to crystalline, it's quite possible that this takes place in our sleep. I have an article by Rosie Neal called, This Is What Happens As Your Light Body Activates in which you can see physical light body activation occurring in many of us. And let me, I'll put a link to that. There's a link in the more info section, but let me put a link to that here as well. Bear with me. I'll show you guys some pictures of what was taken. Okay, so do a screen share. So what happens when your body goes to crystalline, right? Well, this, check it out. And like I said, I just put the link in the chat and it's in the more info section. But do you see the glitter, the light shining on here? And here's some more pictures. That glitter of the light body, the light coming through, basically the pores of the skin. You see that? Check out this video. So, I mean, you can see like the little glitters spots that are going on right there and it's pretty wild. So, I mean, that's happening to many of us right now. The carbon-based body is turning into the light body. So, what's happening is your light body takes energy to create and form and nothing just happens for no reason, which is a double negative, meaning that everything happens for a reason. And much of this is happening while we sleep. Your pineal gland is in control right now. If you're sleeping a lot or have been unusually tired lately, then rest assured, no pun intended, that your pineal gland is not calcified and is working to give you these upgrades as we speak. So, there's a lot of different ways that things are going on right now. We have the human resonance, we have the sun, the solar mass ejections, I'm sorry, coronal mass ejection, solar flares, energies from the Alcyon, great central sun and energies from the galactic core all coming in. And why are they coming in? They're coming in to give us DNA upgrades and to create this light body from our carbon bodies right now. So, there's many things that are going on with our bodies right now. I'm gonna check out the chat real quick. Lucas, is it just me or someone is having insomnia? It's the opposite of insomnia, if anything. As Tarek time says, never nap, but I've been napping over three hours a day several times a week recently. Yeah, welcome to the club, brother or sister. Not sure, can't tell from the name or image. We're doing a lot of work in other dimensions when we sleep and we are becoming more aware of that which could explain why we feel tired more exactly. Suzy says, thank you for talking about this, Grace. Good to know that everyone else is going through this as well. And that's one of the main reasons why I love coming on and doing broadcasts is we're all experiencing some things that if you talk to somebody else, they'll say, oh, you're just f'ing crazy but we know there's something more going on. We're seeing physical and tangible proof like of the pores lighting up in the skin, the carbon body turning to light body. And no, you're not crazy. We're all in this together. I heard about this thunder who was saying last Sunday, the human resonance stopped for 15 minutes.  Let me go back to the human resonance. We'll see if I can, where is it? Oops. Oh, you can't see it anymore. It was right over here though. I brought it up the other day. It might've been on, yeah, it was probably when Ellie and I were doing the global predictions or date night but there was a thin strip of black and it was, it's off the chart right now but I don't see it anymore. I wonder, is that what you were talking about? I wonder if that was the 15 minutes and why it stopped for 15 minutes would be another question. That's Tarek time saying that dreams are becoming more memorable, kind of more accessible to wake into. Awesome. And hi to Star Price from Sydney. Welcome aboard. I love seeing new names coming in here and you're always welcome to join us anytime and thank you for being part of our N5B family. Star's watching us on Facebook right now in chrysalis pods ready. I'm not sure what that means. Star says you're feeling so tired. Thank you so much for being here. Okay, so CJ is saying I have those markings too of the light emanating from the pores. It's just a beautiful thing. Yeah, so it's not, a lot of people are experiencing that. This is the transition that's going on as we turn from carbon to crystalline beings. So that's all I basically wanted to cover tonight. I'm so grateful that you guys had a chance to join in with me as well. And if no one told you this yet today, please allow me to be the first. You are loved. You are appreciated. Thank you for your service to humanity. I'm gonna leave it off at that until the next time. I'm Greg from n5d.com and n5d.net sending you all infinite love and light. Namaste everyone.


Today, on A Better Way, we'll have a food price outlook for the months ahead and offer some suggestions on managing your food budget in 1980. We'll take a look at how the telephone, presently and in the future, can help to conserve energy. And Agriculture Secretary Bob Bergland will comment on the future economic and social structure of American agriculture. For our young viewers, we'll look at soil, the foundation of life. Nuts are not only tasty but nutritious. We'll offer some tips on using them in your family meals. Finally, we'll visit a U.S. trade fair in Japan, next on A Better Way. Most of us are acutely aware of inflation every time we go through the checkout line at the grocery store. For an idea of what we can expect in the way of food prices in 1980, Larry Quinn has this report. Inflation will continue to be a major concern for consumers in the year ahead. Food prices will average about 11 percent higher in 1979 than they were in 1978. That's about the same as the general inflation rate for the year. With us to take a look at food prices in the year ahead is Dawson A. Halter, the U.S. Department of Agriculture. Dawson is chairman of the World Food and Agricultural Outlook and Situation Board. And Dawson, as we begin to think and look about, look at 1980, what do you see for food prices? Larry, we see the inflationary pressures that are permeating our economy, pushing up the cost of food at the retail counter in 1980. We expect food prices in the year ahead to average somewhere between 7 and 11 percent higher than they did in the current year. Most of that increase will be due to inflation itself as it pushes up the cost of processing and marketing food after it leaves the farm gate. What will account for most of those food costs? You said inflationary factors, but will farm prices increase that much? Will it be marketing costs? What will? The main source of the increase will be increased marketing costs. The largest component there is labor, but higher prices for energy, packaging, transportation, all of the cost of moving food after it leaves the farm gets added in and is going to be the main source of the increase as we look at the year ahead. What about the pattern of food price increases for this coming year? Will we see about the same as we've had this past year or will it be somewhat different? At this stage we look for a much different pattern in 1980. Right now we are seeing record levels of pork and poultry production. We expect that pattern to continue into next year running at very large levels through the first half of the year. Thus consumers should be able to get very good buys on those products in the first half of the year while in the second half by that time producers having been squeezed by the inflationary pressures that are above their returns will have made adjustments and meat supplies will perhaps be much tighter in the second half of the year. Perhaps a consumer will be filling up their freezers with meat during the first six months of the year. I believe that would be a good strategy for consumers to follow particularly with purchases of pork and poultry meat in the first half of 1980. What about the red meats? What do you see there for 1980? Beef prices will average higher in the year ahead. Supplies will be about as large as they have been in 1979. But we don't expect to see as much of an increase in beef as we do in pork and poultry. Let's talk about a couple of other basics that of milk and eggs. What do you see there? Eggs should continue to be a good buy next year based on our supply prospects at this stage. However, dairy products are going to continue to go up perhaps not much different than the overall rate of inflation. Breads and cereals? Breads and cereals will increase roughly in line with the overall rate of inflation because those products are highly processed and labor packaging costs get built in to those items as they move to the retail counter. What about fruits and vegetables? Fruits and vegetables have been a good buy this fall because we've generally had good crops. We're having our record citrus crop coming on, lots of oranges coming out of Florida this season. So we expect particularly the fruit crop to be quite large and some pretty good buys in some of those products. What about vegetables? Fruits and vegetables have something like oils and sweeteners that we all use. The vegetable oil situation is a bit uncertain at the moment partly due to the fact that the monsoon was erratic in India this year and India is the world's largest importer of vegetable oils. That could have some effect on the cost of oils available for consumers in this country. But perhaps a modest rise over the current year. Prices for sugars and sweeteners will move up pretty much in line we think with the rate of the general rate of increase in food prices. What are the basic factors that could quickly alter just what we've been talking about the food price outlook? It does change rather quickly sometimes. Food supplies of course are vulnerable to sudden changes in weather and we have had two very bad winters the past two years Larry as you know. We're sure hoping that we get to this year without unusually cold weather and also we hope we can avoid getting a cold snap either in Florida or California in the winter months because we depend on those states for the bulk of our produce during that season of the year. Weather is an important factor and can inhibit farmers ability to move their livestock to market which can tighten up supplies quickly in the short run. What tips would you give a consumer that might help them manage their food budget for this coming year? Well consumers will have to continue to look for the best buys and to take advantage of the specials that stores are offering. If you look at the ads you see wide divergences in prices among products at the various stores. It's getting more costly to shop from store to store but you still can take advantage of specials that stores are offering each week. That's what I think consumers need to look for. Dawson A. Hall, chairman of the World Food and Agricultural Outlook and Situation Board for the Department of Agriculture. Most of us are probably familiar with that slogan made famous by the L-Pages called Let Your Fingers Do the Walking. Well when that slogan came into use about 20 years ago even then the idea was energy conservation. My guess has some thoughts on how today's telephone service can help to conserve energy. Joel Bab is with the USDA's Rural Electrification Administration. Joel what are some of the ways that the telephone can cut down on using gasoline and other types of energy? Well I think we've got to take that old slogan, let your fingers do the walking and go just a little bit further than what the slogan was probably originally designed for. The slogan was probably designed to sell yellow page advertising and to help the shoppers locate the items that they wanted to buy. But I think with today that with our energy conservation that we have and I would like to say that our agency, the Rural Electrification, is certainly interested in conservation. We're primarily in the electric program but yet a lot of people don't know of our telephone program but we are vitally interested in both of these energy conservations in it. The ways that we can save it is that we're going to have to change some of our habits probably from we want to talk to mother or we want to go across town or we want to go look and see something or we want to go find out if something is there we should stop and think and stop. Do we really need to take this trip or should we pick up the telephone and do our visiting with the telephone? I think I would prefer to call around to different stores to find out they have the item than to just take the time and go look for it anyway. That's true and you know Don we might think that just this one little trip won't count but yet we have made loans to probably 4.4 million real telephone subscribers and if we could just save a mile a day how much energy would that be in a year's time? Sure even a mile a month with 4 million people would be amazing. That is quite amazing. Outside of the obvious the idea of using the telephone rather than getting in your car and driving around or verifying that indeed a store has what you're looking for what are some of the new features offered through telephone service not only in rural communities but in our urban suburban areas that are oriented toward energy conservation? Well the telephone should be well pleased because they can get the same features as the people in the urban areas and they're coming with many things. We've gone a long ways from the old crank telephone system and the two longs and three shorts with the 12 or 14 people on the line. Today we've got many many of our... Sometimes you had 12 and 14 people on the line at once too in those days. We certainly did. In fact I made a call the other day and it was to a five-hour long distance and the operator said well we got four of the other parties but we couldn't get the one you wanted to see but we don't have that today because we can. We do have many of them in the one party. I think that our features that we are going to have and as I say there that we can come that we have the same as in the urban and the rural as we have call transfer. Call transfer is this if you want to go, some housewife wants to go visit her mother she can transfer calls over there. If a business feels that they have some very important calls coming in they can transfer their calls to the house when they go to lunch and that we have call waiting. The call waiting is you receive a little buzzer or a little beep or a little tone signal and you can push one button on your telephone and transfer your call to the incoming call when you're through with that push back and get the other party that you were talking to. It also gives you an excuse to break off a long minute telephone conversation too. If you need an excuse, yes. The other thing is in addition to that is conference calling that maybe you have a couple of friends that you want to talk. You don't have to just call one person, you can call two people. We've gone into the automatic dialing with the DDD today and almost any parts of the country. I think you and I were just discussing and both of us got in our telephone bill and then we can dial direct to 74 foreign countries. These are some of the things that are coming down the pike. Joel, what about some of the features outside of telephone conversations that many telephone customers might not be familiar with? Some of the data transfers. I think the greatest move that I see in the telephone industry is the use of the computer. We're using the computer inside of the telephone in but I think the computer is going to be coming to the home and be used into the home. I think we're going to be doing a tremendous amount of purchasing with a computer. Many times today that you'll call up and you'll ask if you have a certain item at the store, it'll take a long time to get a clerk and then the clerk will have to go search. In some places you can call up on your own telephone if you have a terminal or a data set in your home, put it into the cradle, get access to the computer and the computer can tell you what's available. You're going to be able to do your purchasing with a computer. You're going to be able to do price comparison with a computer and many more things with a computer. That is rural energy conservation. When you figure the amount of gasoline it'll be wasted just in the trips to the bank and to the store. We serve many, many rural areas and I think one of the very important things in the rural areas is going to be in the medicine because we might not have all the expertise with the doctors and the fancy equipment that we have. Today we can hook up an EKG and you can be in one place and the doctor can 2,000 miles away and an expert can be sitting and making an analysis of that EKG from somebody in a little hospital way out in some far place in the country. This is something we have today using the existing telephone lines? We have that today using existing telephone lines. We do have the slow scan X-ray transfers of transferring X-rays so that the X-rays can be analyzed real quick. But I think the medicine is coming along with the computer that we are going to be able to use that computer in the telemedicine and that is going to be one of the most important or going to become very, very important especially in the rural areas. One final question that really isn't directly related to this but is important. Many urban suburban telephone lines are now buried underground. What advice do you have or precautions for the homeowner that they should be aware of? It's very unfortunate that where they used to probably where the telephone company wants to bury their line is probably where that homeowner wants to put his mailbox.  I've seen them put in fence rows and fence rows it just so happens that you want to put the fence row right down where the cable is. In fact it gets very expensive not from a standpoint of maybe just coming out and fixing it but some of these cables carry a tremendous amount of volume of business. I had one friend that was out demonstrating a backhoe and he cut the cable and just for the loss of business until they could switch that it cost him about $42,000. Don't cut the cable. Thanks very much Joel Babb with the Rural Electrification Administration being with us taking a look at the telephone as an energy conservation tool. Today on Better Way for Kids we begin a new three-part series on soil and why it's important to us. I'm Tom Leverman with the Soil Conservation Service. You've all heard the word soil you probably see soil every day but how much do you really know about soil about its development how humans use it and abuse it. This little bit of soil takes away a piece of history. The result of natural processes that began thousands of years ago and continue even today. Soil isn't all the same. Here are two examples of soil both from Maryland. It's quite easy to see the difference between these two soils. The cellum has a very shallow topsoil indicated by the dark soil colored soil which is about three and a half inches deep. The color from the topsoil down is the same. At about 29 inches rocks are found. The Hagerstown cellum has a dark brown layer about nine and a half to ten inches deep. There are a few small pebbles found in this layer. Notice the distinct color change between the first layer the topsoil and the subsoil. The color is about the same all the way down to the bottom where we find some large rocks. This is about 36 inches deep. These are only two examples of nearly 70,000 soils found in the United States. That's right, 70,000 different soils. Now here's a quick two-question quiz to test your knowledge of soil. Question number one. Soil is made from rocks, plants, animals, glaciers or all of the above. The process to manufacture soil is extremely complicated. Every activity of nature including glaciers which slowly moved across the land to the death and decay of plant and animal life all have a part in creating the material we call soil. Question two. Which of the following is found in soil? Sand, silt, clay, air or all of the above? A close investigation of soil reveals a great diversity of materials. The primary building blocks of soil are sand, silt and finally clay. The thin layer of soil that covers the earth's surface ranges from just a few inches to four or five feet in depth. The soil is where all human and natural forces eventually meet. On the soil we grow crops, build highways, homes and businesses. The soil is the foundation of our lives. We're in an electron microscope lab. You can see grains of sand magnified one hundred times. Now I'll zoom the lens in closer and you can see the grains of sand magnified one thousand times their original size. And once again I'll zoom the lens in closer and you'll see the grains of sand magnified ten thousand times their original size. Soil scientists, people who study soil, say that about fifty percent of the space is composed of air and moisture. Now here's another way to take a look at our example of sand.  This peak shows the amount of silicon contained in our sample of sand. But by the way, how did you do on your soil quiz? The answers to both questions are all of the above. I hope you visit me again to learn more exciting things about soil. The holiday season may have left you with a lot of leftover nuts. The eating kind. Nuts contribute rich flavor and a crunchy texture to many kinds of foods. They're not only tasty, but nutritious as well. Nuts in the shell keep well in a nut bullet room temperature for a short period of time. For prolonged storage keep them in a cool, dry place. Shelled nuts will keep fresh for several months if you store them in a tightly closed container in the refrigerator. Nuts are filling because of their fat content and may prevent between meal hunger pangs which encourage nibbling. Most common nuts contain about 10 to 25% protein and can be an added source of protein in meals. Peanuts are highest in protein with 25%. Nuts are versatile and may come to the dinner table in a variety of ways as an ingredient in cooking or as a garnish. If you'd like to find more ways of using nuts in main dishes, soups, salads and desserts send for this copy of nuts and family meals. Write to Agriculture TV, Washington DC 202-50 Japan is one of the major customers for U.S. food products. Recently our reporter Wally Dudney visited a United States food fair in Japan. Here's his report. Eating habits are changing in Japan. More Japanese are eating out and western style foods are becoming more popular. This includes many consumer ready foods from the United States. Sales of these foods to Japan totaled nearly $1.5 billion last year. To see and sample these products Japanese food importers gathered in Tokyo for an American foods exhibition part of the big international hotel and restaurant show. Phil Holloway assistant U.S. agricultural attaché in Japan describes what they saw. In this exhibit we have at least 50 exhibitors which come from almost all states in the union. Among them are many fruit and vegetable some of our cooperator organizations such as the American Soybean Association, the Poultry and Egg Institute of America, the U.S. Meat Export Federation, California Cling Peach Advisory Board among other organizations here. Buyers attending the show represented all segments of the Japanese food trade. Many of them represent hotel and restaurant trade but also we have people here from the Japanese school lunch program from mass feeding units of major Japanese corporations and other institutional feeders and we are quite pleased with the quality of the visitor that we are receiving from them. Japanese food buyers were able to taste a wide range of American foods. Many of them knew to the Japanese market. Sales of these consumer ready foods accounted for about 15 percent of the 4.4 billion dollars of American agricultural products sold to Japan last year. Japan is the number one overseas market for U.S. farm products but there is strong competition for U.S. food producers who are actively promoting their products. Phil Holloway comments on the future of American sales. With the tremendous demand for U.S. consumer ready food products in Japan, I expect sales to double in the next two years. Wally Duttony reporting for the U.S. Department of Agriculture from Tokyo. There's a very good chance that you're watching this program on a Japanese made television set and you probably listen to a Japanese camera or you might be one of millions of Americans who drive a Japanese automobile. The thing to pay for these imported goods are American agricultural products. You know, in less than 200 years our nation has developed the most efficient and abundant food production system in the world. We progress from hand power to horse and ox to complete mechanization. The quality and quantity of our yield increases each year. We feed not only ourselves but also a substantial part of the planet. Where do we go from here? What's the future of American agriculture? What are the concerns? Larry Quinn has this report. The economic and social structure of agriculture directly affects all Americans. The income farmers make, the jobs of people in the marketing chain, the quality of life in rural communities, the price of food, even the value of the dollar in foreign trade are affected by our food and agriculture system and how it operates. That means that the consequences of a given farm structure pose critically important issues of public policy. The term structure is an economist word used to describe such things as the number, size, and control of farms. The relationship between farmers and their suppliers and markets and other institutions that make up our food and agriculture system or influence how it operates. Secretary of Agriculture Bob Bergland has called for a dialogue between American agriculture to re-examine the forces which has shaped agriculture as we know it today. A broad-based public discussion of these issues will occur in a series of 10 meetings in late November and December. Agriculture Secretary Bergland outlined areas of concern that will be discussed. Well, looking at trends in land ownership, for example, everyone is concerned about we're going to look carefully at how that farm is situated and what's happening. We know that in the last 10 years there are about a million families have retired from farming and during that period only half a million new starts. Will that be a good or a bad thing if it continues? We're going to look at then commodity policy, credit policy, and all the rest including tax policy to see whether these policies make sense in the long run. Are there any social and economic issues involved here? There are. The social issues are, for example, trying to measure the worth of having a policy in which people are given a chance to own the land they live on. And we know that 100 years ago with the Homestead Act that was the roots of the policy at that time. If you lived on the land, you had a chance to own it. And since then, of course, the way from that basic concept about half the land in the United States is now tenant farmed. Nothing really wrong with that. But if the rate tendency towards increased tendency continues what then will we have land owned by a relative handful and is this a good thing or a bad thing? Of course the farmers and the rural citizens have the most at stake in a dialogue on this subject but we all have something about one family and four in the United States lives in a rural place. Now, only about one fourth of those live on farms but we are a rural country. And so the question of the future of small farming in the country is an important issue. One and a half million farms in this country are too small to provide full-time employment for the family but they have non-farm jobs and there have been some people who criticize the rural development programs in the grounds that they're either not effective or we don't need it or for whatever reason and we want to examine the social and economic implications in the role of these small-scale farms in the country. Today we seem to think in terms of large-scale farming, mechanization, automation, efficiency and hard-charging output all of which has served the United States very well and we don't mean to find fault with any of this. We're simply looking to see whether these programs are doing what it is that we want to do and if the small-scale farming has a role to play in this country maybe we should design programs to accommodate that need as well. Next week, Agriculture Secretary Bob Bergman will be back with us to discuss the problem of using marginal land. We're going to focus on the importance of soil conservation and how it affects all of us. Debbie Reader, I didn't realize there are so many different kinds of peanuts. Oh, there are many, many kinds. That's it for a better way. We'll be back in seven days. Join us.