The Root Cause of Medically Unexplained Symptoms | Part 1 | Chronic Fatigue Syndrome

Hi everyone, and thank you for joining us for part one of our three-part webinar series on finding the root cause of the medically unexplained. Our webinar will be starting very shortly. I appreciate it's a beautiful warm day today, so thank you, and we are very grateful for you joining us.

Before we kick off with today's session, just a small piece on the series itself. We are often in conversation with a lot of practitioners, and we feel there is a growing awareness around us. People outside of functional health are starting to take note of what functional medicine can really do, and we just want to fully explore and celebrate that a lot more.

According to the NHS, about one in four people who see a GP have physical symptoms that can't be explained: headaches, stomach troubles, physical pain, fatigue, and heart palpitations, all of which, at best, are worrying to our patients, but at worst, life-altering and immobilizing to some. Just because general practitioners are currently unable to access those resources to help them find a condition causing these symptoms, we know that it doesn't necessarily mean that nothing can be done to help.

So, our webinar series is, as it says in the title, all about finding the root cause for the medically unexplained and taking the experience of reputable fellow health professionals to explore client case studies and innovative treatment processes that go beyond symptom management.

Today's session will be all about chronic fatigue syndrome, and following that, we'll have a session on IBS and fibromyalgia as well. If you haven't yet registered for all of the sessions and you would be interested, please just visit our website or the Instagram bio to register. Alternatively, you can access them all using the link that you've just joined us with today.

So, without further ado, I'd love to introduce our host for today's session, Lauren Windas. Lauren is a renowned registered nutritionist, naturopath, author, and co-founder of a holistic well-being company specializing in wellness and non-toxic self-care products. Lauren works a lot with clients who suffer from CFS, ME, and post-viral fatigue-related conditions, as well as those struggling with their weight or poor relationships with food. Lauren is also qualified as a master practitioner in eating disorders and obesity with the National Center for Eating Disorders and is additionally trained in NLP.

Lauren journeyed into the world of well-being and nutrition at university and has recently published her book, "The Chronic Fatigue Syndrome: Your Route to Recovery," which I'm sure Lauren can tell us more about later. We're thrilled that she's joined us today. If you do have any questions, please just drop them in the chat box throughout the session; we'll come around to them at the end. But for now, I've spoken too much, and I'm going to hand over to Lauren.

Hi, Lauren.

Hi, Amelia. Thank you so much for that introduction. Let me just swipe onto my next slide, which, to be fair, you've already done the intro for me, but I'll just kind of reiterate. So, hi everyone, my name is Lauren Windas. I'm a registered nutritionist, naturopath, and also the author of "Chronic Fatigue Syndrome: Your Route to Recovery," which is obviously very aptly titled in terms of the talk we're discussing today, which we'll go on to discuss in depth. I'm also co-founder of a holistic well-being company. We specialize in a private wellness clinic; we have nutritional therapists, psychologists, one-to-one private practice, and we also have self-care products.

I very much specialize in personalized nutrition and all those areas listed on the screen here, as Amelia already discussed. You can find more about me on Instagram; those are my handles below. Of course, today we're going to be talking and kicking off this webinar series, which is all about medically unexplained syndromes.

Medically unexplained syndromes refer to a group of conditions that are essentially characterized by chronic symptoms that lack a clear or consistent organic medical cause, despite having thorough medical investigations. These syndromes can often overlap in terms of their symptomology and also be quite challenging in terms of diagnosis and treatment, especially from a medical point of view.

We've got the common examples listed here below, and of course, every week for the next three weeks, we are kicking off with a different topic. Today's chronic fatigue syndrome, I believe next week is IBS, and then the final week is fibromyalgia, if I'm correct.

So, of course, today we're going to be talking in more depth about chronic fatigue syndrome and really where this issue has taken place in terms of medically. There has been a lot of misunderstanding and stigma around chronic fatigue syndrome, so we're going to go into a bit more depth about CFS, about the naming of the condition, and also how, as functional practitioners, we can really stand in good stead with patients and really support them in terms of functional medicine support and really digging down into the root cause.

But just to define the word syndrome, a syndrome refers to a constellation of signs or symptoms, and the word comes from the Greek "syndros," which means running together. Symptoms of a syndrome may not always be 100% consistent between patients, and they can also change over time, so they can have this kind of relapsing and remitting pattern. They don't always have a medically identifiable cause, so they can kind of overlap in terms of, for example, the list that we've seen on the previous slide; a lot of those symptoms can certainly overlap.

So, chronic fatigue syndrome, just to kind of define it, is a complex chronic illness that significantly impacts the lives of those who experience it. It impacts various bodily systems, including our neuroendocrine system (our hormonal system), our nervous system, our digestive system (our gut microbiome), and also our immune system. What we're starting to see is that, obviously, yes, there's a lot that we don't know in terms of CFS, but there is a lot of evidence that we are starting to mount up in terms of our understanding of CFS, which is that there is really this kind of dysregulation between these systems, and these functional systems really help to explain the cluster of symptoms that we see in chronic fatigue syndrome.

Some key symptoms that we're seeing in CFS: I think one of the first symptoms, of course, is persistent fatigue, which is obviously the first thing to say, where you're waking up and not being refreshed by sleep, and you're just in a constant state of exhaustion. But one of the actual hallmark symptoms—and that's why I've highlighted it here—is this idea of post-exertional malaise, and that is kind of the key cardinal defining symptom of CFS. It's part of the diagnostic criteria that is needed for making a diagnosis of ME/CFS.

Post-exertional malaise is essentially where that person really goes past their energy envelope, so past their energy threshold, and they are met with, I call it, "payback," this kind of payback of symptoms or crash, so feeling worse after exertion. It doesn't have to be necessarily like a high level of physical exertion; it could be something as simple as walking to the other end of your garden or going up the stairs, for example. It also doesn't necessarily always have to be physical activity; it could also be cognitive or mental tasks that are also causing these post-exertional payback symptoms.

But broadly around that, we also tend to see a pattern of cognitive impairment, so things like memory problems, brain fog, trouble recalling the right words in a sentence, loss of balance, and vertigo; sensitivities to chemicals, smells, sounds, and lights; heart palpitations; flu-like symptoms; and we also see orthostatic intolerance. That's essentially where we feel worse upon standing up. It broadly crosses over a little bit into the POTS category, so postural orthostatic tachycardia syndrome, which is an abnormal increase in heart rate upon standing. We tend to see people feeling worse upon standing up and moving around.

Muscle pains as well, stress-related symptoms, so difficulties tolerating stress—kind of that stress threshold has been lowered—food and alcohol intolerance. Very interestingly, as I said earlier, with these medically unexplained syndromes, we're also seeing that, actually, with CFS, for example, and IBS, there is actually an overlap. There was a study published in the Archives of Internal Medicine that found 92% of CFS patients experience irritable bowel syndrome, so in most cases, actually, IBS had preceded the onset of chronic fatigue syndrome. There is a real big overlap.

I forgot to mention my own journey; the reason I got interested in CFS and why I work clinically with chronic fatigue cases is because of my own journey with chronic fatigue syndrome. For me, it was when I was at university, over about 12 years ago now. I had a viral infection, and it was a classic "never been well since" scenario, with all of these symptoms. But I'd also had a history of IBS, so it's very interesting how the studies are starting to showcase this overlap.

We do tend to see these GI symptoms of bloating, constipation, and alternating bowel habits, so very much overlapping with IBS. It's important to also say that with CFS, it's a spectrum disorder, so not every patient that has chronic fatigue syndrome presents the same way. On one end of the spectrum, you have those mild sufferers—those who are maybe mobile, still in work or education, but struggling with their functioning and daily symptoms. They're really struggling to get by; perhaps they go to work on Mondays or Fridays and spend the weekends crashing and sleeping because they're almost running on exhaust fumes, trying to get through the week.

Then you've got moderate sufferers, and that's those with reduced mobility—maybe they've stopped work or education, or they've had to make some adjustments, like working part-time. Then, unfortunately, we have the severe end of the spectrum. This is 25% of the total CFS population. If we think of chronic fatigue syndrome in terms of how many people it affects, it's estimated to be 250,000 people in the UK and 24 million people globally. However, I would say that that figure is perhaps underestimated, especially due to the problems with diagnosing this condition and also the overlaps now, obviously, with post-viral fatigue and long COVID since the pandemic.

So, 25% of this patient population are either housebound, wheelchair-bound, or bedbound, and some can have difficulty with speech and swallowing. It can be very, very severe in 25% of this population. It's also important to say that because chronic fatigue syndrome is a spectrum disorder, I think it's really important that we're all more aware of this. In my case, I was met with stigma because I was ill with it, and I was met with the assumption that because I wasn't in a wheelchair and I was, I'd say, mild to moderate, I wasn't severe. But because I wasn't severe, then I wasn't classed as having it, so people kind of negate the illness.

There's so much misunderstanding around it; as they say, it's a functional disorder, and it really impacts our ability to function, but that can vary on a spectrum—more so for some people and less so for others. But that doesn't mean to say that on either end of the spectrum it's not debilitating. Just because you're not severe and you're mild, it's very much impacting these people's lives and my clients' lives. So, just something for us to be more aware of.

A bit more background in terms of the terminology: CFS has been known by various names throughout its history. We see myalgic encephalomyelitis, which we'll go into on the next slide, post-viral fatigue syndrome, and even it was colloquially referred to as "yuppie flu" during the 1980s due to its widespread prevalence among young working professionals in the city. More recently, we see this term "long COVID" coming into the mix since the pandemic.

Often, it was associated with people who had been unwell with, I'd say, kind of an often mild SARS-CoV-2 infection. They weren't hospitalized; they were ill at home with the infection, and thereafter, they started to mirror the classic symptoms of chronic fatigue syndrome. While experts are still actively researching whether long COVID is a distinct condition from chronic fatigue and ME, there is a substantial overlap between the two, with many patients receiving a diagnosis of post-COVID ME/CFS. The jury is still out on that one; obviously, we are seeing this huge overlap, so I think it's all part of this umbrella.

Going into a bit more depth in terms of the name, as I say, you hear this a lot: ME/CFS. To break down myalgic encephalomyelitis, my is a shortened form of "myo," which means muscle; alic is the adjective form of "algia," which means pain; and then we have "itis," which means inflammation. So, if we were to break that down, it's basically saying that this is an illness of muscle pain and inflammation of the brain and spinal cord. That was a term introduced by The Lancet after an outbreak at the Royal Free Hospital in London in 1955, but it's not a pathologically proven explanation for what is going on within this illness.

So, yet we're still left with this long and confusing name. On the other hand, we see chronic fatigue syndrome, and this also has a bit of stigma attached to it in the sense that, for a lot of the patient community, it's been thought to trivialize their level of suffering. I often say it's a bit like saying someone without cystic fibrosis has chronic forgetfulness syndrome because it's trivializing the debilitating nature of that patient's experience, especially if there's somebody, you know, that's severely housebound, wheelchair-bound, or bedbound. It's not just "being tired all the time." I think that's where that kind of comment comes from, from people who tend to see, you know, when they hear about chronic fatigue or post, "Oh, isn't that just where you're tired all the time? Oh, well, I'm tired too." But it's a totally different level of debilitating and obviously impacting your ability to function.

Some experts posit that ME and CFS are slightly distinct from one another as conditions, maybe in the same way people think long COVID could be slightly distinct. But actually, I'd say it's too premature to say that these are distinct from each other, and in fact, the medical literature often refers to the two synonymously. So, you've got ME/CFS, and I just refer to it as chronic fatigue syndrome, despite my qualms about how it trivializes it, just because it's the most kind of easy to, I guess, access for people to get their head around for the time being. As we learn more, maybe this might change.

You see all these other different terms thrown around: yuppie flu, systemic exertion intolerance disease, adrenal fatigue, burnout. Interestingly, burnout is not actually a medical condition; it was a term coined by a psychologist in America in the 70s. It's a list of symptoms a few similar to CFS: fatigue, exhaustion, low mood, but more resulting from severe stress and high ideals that are induced by a professional setting. So, it's more an occupational phenomenon rather than a medical condition per se.

As I say, you've got this huge kind of list of names, but we're going with today's chronic fatigue syndrome, and it all forms part of this umbrella. While we don't know fully in terms of a medical standpoint what causes ME/CFS, we are starting to find evidence pointing towards genetic links. We're seeing infectious triggers, cellular immune-driven problems in the body, including problems with the mitochondria (those energy-making factories within our cells), and also within our gut microbiome, as well as our hormone function. I'll go into detail about that later on.

One of the reasons that ME/CFS is such a hard illness to understand is because we may be looking at this kind of umbrella of etiologies and subtypes within this cohort of patients. Each patient presents with a nuance behind their symptom clusters. If you look at this kind of here within this umbrella of chronic fatigue syndrome, patient A perhaps has one kind of driver that's maybe more distinct from patient B. Yes, there are potential similarities and patterns that we're seeing, and the evidence is starting to showcase that, but there may be slight nuances. This is why medics, researchers, and scientists are finding it so challenging to really understand.

That's where us as functional medicine practitioners can really come into our own because, for us—and certainly for me clinically—it's about working with each patient as an individual. That person sitting in front of me is entirely unique to the next person, and that's really where functional testing has its place, which we'll go into.

In terms of this root cause approach, the way that I like to talk about it—I talk about this in the book in more detail—is that CFS follows a three-prong structure. We have the predisposition, we have precipitating triggers, and we have perpetuating factors. The predisposition is this kind of genetic predisposition. We know now from studies that there are genetic links that make somebody more predisposed to developing chronic fatigue syndrome. In fact, in 2020, there was a large study in Norway that looked at two versions of genes called the alleles, and these are part of the HLA (human leukocyte antigen) family. These help to make proteins essential for the immune system to recognize different pathogens.

What scientists have found is that these are more common in CFS patients than in healthy people, and this is a finding that points towards issues with the immune system in CFS. There's also a huge study happening now in the UK called the Decode ME study, and it's looking at genetic links into what makes somebody more or less likely to become unwell with ME/CFS. We do know there is this kind of genetic component; we have twin studies that have backed that up as well.

Then, also, precipitating triggers. One thing that is clear is that, you know, there is often—more cases than not, I will say—not always, because sometimes clients and patients find it hard to ascertain why they or how they've become unwell at which point. Whereas others, there's very much this distinct classic "never been well since" scenario. For a study that was recently done on precipitating triggers, 72% of patients reported an infectious illness upon becoming unwell with chronic fatigue syndrome.

Whether that's the SARS-CoV-2 virus, it could be Epstein-Barr; I suspect in my case it was Epstein-Barr virus. It could also be various other infectious agents like the Coxsackie virus and cytomegalovirus. There's a whole host of different pathogens, even potentially microbial or parasitic, that can trigger the onset of CFS. We also know that 28% of patients had no apparent infectious trigger but instead reported a traumatic event, such as a car accident, a fall, or surgery.

I recently had a gentleman come to see me; he was perfectly healthy all the way up until his mid-30s, and then he had an operation and had a metal plate put in his wrist for an injury he'd received at work, and he has never been well since then. We've also seen in the studies that stressful life events have also been reported to be very common in the year preceding the illness, and that's certainly the case in the case study that I'm going to talk about later on.

In my clinical experience, approximately, I'd say about 90% of the patients that come to see me report having had a recent trigger infection, but in some cases, it could be a vaccination that's potentially made them unwell, and surgery, like breast implants, as well. So, you have this trigger episode, and then what we see is these kind of perpetuating factors—these driving mechanisms of what's still kind of driving the situation and has potentially been set going by this trigger episode, whether it's the infection, the surgery, the trauma, or the stressful event.

This is the idea of dysregulation, also these chronic stressors, and we can group these into deficiencies and toxicities, which I'll explain more about on the next slide. Dysregulation: every single day, our body is faced with certain demands. We have internal demands, like having to break down our food after eating a meal, regulating our sleep cycle (our circadian rhythm, for example), just functioning our brains so that we're alert and able to process things, and also recover from physical exercise, in addition to that, we can also encounter injury or infection, which are more of these additional internal demands.

Then we have external demands that are related to our environment, so coping with whether it's kind of toxic pollution in the environment or whether it's pollen in the summertime or even changes in gravity as we're moving around, our posture, our body temperature. We have all these different physiological feedback loops and systems that work in a tightly controlled manner in order to handle the various demands sufficiently, and this is a form of balance known as homeostasis.

As one thing changes, something offsets that, and that's how our physiological feedback systems work in this kind of homeostasis pattern. What happens in ME/CFS is this idea of dysregulation, which is where the body systems are becoming imbalanced. If we look at that seesaw at the top there, homeostasis is kind of at that level playing field, but in dysregulation, we see the seesaw tipped, but it's not coming back into balance. The body is somehow unable to handle basic daily demands due to disruptions in these physiological mechanisms.

If you look at that web that I've just showcased, which is a diagram from my book, these are kind of all the areas that we're now starting to find evidence of issues going on within CFS patients. We talk about the autonomic nervous system; we're actually seeing evidence that showcases that CFS patients are almost in this state of sympathetic nervous system arousal predominance. This idea of dysautonomia—the nervous system is not quite firing correctly; it's not going back into this parasympathetic state, but actually, it's almost that autopilot is this fight or flight response.

In addition, we're also seeing digestive system imbalances, so issues within the microbiome, for example. We're seeing evidence of reduced levels of these commensal bacteria—these friendly bacteria within the gut—and also specifically a species called Akkermansia, which is very important to regulate our immune system. We're seeing reduced levels of those in CFS patients.

In addition, GI infections are also quite commonly associated with CFS, so things like parasites, such as Blastocystis or D fragilis, candida for yeast, and also viruses. We have this whole community of viruses that live within our gut, and that makes up the gut virome, and we're also seeing imbalances there that potentially are giving us insights as to how this is impacting these widespread symptoms.

The mitochondria—those energy factories within our cells—are also seeing reduced levels of the ATP molecule, which is that energy currency molecule that they produce. That can actually be a big explanation as to why we're seeing this symptom of post-exertional malaise. This idea of feeling worse upon exertion is because, actually, the body is not recycling ATP quickly enough. The body's energy demand is exceeding energy delivery, so we're having this slow ATP recycling and a reduced level of ATP, so the mitochondria aren't able to produce enough energy, essentially.

Also, the immune system, of course, we know infections are a big part of this puzzle piece. Whether that's acute or chronic, an infection could be acute; you could have cleared the infection, but your body's still having an ongoing immune reaction to it, so this autoimmune response. If it's chronic, perhaps the virus is laying dormant and reactivating, so it's kind of relapsing and remitting. It's really about getting the terrain right so that we can deal with these pathogens appropriately.

We're also seeing increased levels of inflammatory cytokines, so inflammation is a huge part of this puzzle. When it comes to hormones, we're seeing in some patients with CFS reduced levels of T3 and T4 hormones in the absence of a diagnosis of autoimmune thyroid conditions or even hyperthyroidism in general. We're also seeing lower levels of cortisol, especially after a period of what we can see initially of high cortisol levels, so a period of really this kind of low cortisol, which is essentially where the adrenals have started to flatline, where we're seeing adrenal insufficiency.

That's just a little bit of a web of dysregulation. In addition to that, we kind of group it into this chronic stress pattern, where we're also potentially seeing added to the mix maybe nutritional deficiencies, stress, and trauma are also a huge part of this pie, and also toxic agents. Sometimes clients can come to me after maybe it's an exposure to mold, like sick building syndrome—they've moved into a new house, and there's a lot of mold around, and then they've developed this illness—or whether it's pesticide exposures, potentially if they work in agriculture on a farm, for example.

That can also be part of the mix. Really, as I say, it's about finding the needle in the haystack. For us as practitioners, these are the root drivers that have been correlated at the heart of CFS. Clinically, for us, it's about unpicking that mosaic of fatigue and really understanding what are the perpetuating factors for that person in front of us and what are the driving agents.

Ultimately, while there are similarities between cases, we have to consider that each patient is entirely unique. Our job is to really apply our functional medicine detective lens to consider what is going on for them as an individual and what that third P is, as I said, using scientific evidence and functional testing.

Just a final note on the NHS and this kind of medical approach is that, first of all, the diagnosis of ME/CFS is a diagnosis of exclusion. When your doctor can't find anything wrong with you, ME/CFS is kind of the only explanation left if you match a certain symptom criteria for a period of three months. The reason being is because there are no standard NHS medical tests for ME/CFS.

We do have studies now going into—I mean, Stanford University in the US is looking at a test at how the immune system cells are responding to stress, almost as a future diagnostic test. But of course, we don't have a specific test to say, "Yes, you have it; no, you don't have it." It's really about following distinctive patterns and features in terms of symptoms. Not always will all the symptoms match from one patient to another, but there is a list of diagnostic criteria within the NICE guidance system.

It's about matching that, obviously excluding out any other possible causes of fatigue. Fatigue is a huge broad symptom that crosses over into many different categories, so it's excluding any other causes and then seeing where you fit. There's no international agreement on classifying these symptoms as well or even what to call the condition.

Within the US, there's a different diagnostic criteria against the NICE system, which is in the UK. As they say, this is where the NHS, I guess, falls short in terms of its support. These are the kind of medical approaches that you see within the NHS for ME/CFS. We know that the NHS care model is not particularly well set up for chronic illness and chronic disease management. It's currently crippled as a service, and we know that as nutritionists and functional practitioners, we can really hone in on this because long-term, we offer that hand-holding, that really focused one-to-one support for patients to feel heard and supported.

We're looking into those root drivers, so we're asking the right questions. You can see here that you've got cognitive behavioral therapy, which is a form of talking therapy that works to support changes in the way people think and behave. It's used in a lot of other conditions as well, but actually, it was previously positioned as a curative therapy for ME/CFS. It was used alongside graded exercise therapy, which has since been scrapped from the NHS due to controversy.

These therapies gained momentum because of a study in, I think it was 2011, called the PACE trial, which was funded by the UK Medical Research Council. The theory behind using CBT and graded exercise is essentially a structured exercise program where you increase physical activity levels without listening to patient feedback. If the patient feels worse, we've still almost been told to keep increasing.

Essentially, it was found that patients were feeling worse upon doing this; it was making their ME/CFS a lot worse. The theory behind using these was almost based upon the view that patients were feeling their symptoms because of inactivity and deconditioning, as well as holding negative illness beliefs. Of course, that really fails to take into account the fact that this illness is physical. It's not psychological, and it's this idea that, "Oh, we're simply thinking more."

You know, thinking more positively, should I say, and moving more is the better way to go to get better. But of course, this was then investigated further, and there was a lot of outcry from patients, researchers, and charities about it making patients worse, especially the graded exercise therapy, which was then taken off the NHS support program.

Now they use CBT, but more as it's been reframed as a support tool for the psychological effects of dealing with a chronic illness. I think that reframe has been very welcomed among clients of mine. I also just wanted to kind of pinpoint this, which I saw on a leading CFS charity, is that they used this term: "There's no effective drug treatment, and full recovery is rare, but symptoms can stabilize and improve over time with careful management and special support."

Just kind of highlighting there, full recovery is rare; it's a very pessimistic way of looking at ME/CFS. I think when you do go online and look at a lot of the stuff that you tend to see online with ME/CFS, it is very pessimistic, and it's very doom and gloom. I think it's really important that we have the context here: what is that going to say to a person who's newly diagnosed, and how will that shape their beliefs on recovering their health back?

It's so important that we're optimistic and that we challenge any negative attitudes or beliefs on them recovering. We know that it's possible for patients to recover. I'm an example; my clients are examples, and there are so many people out there that do get well. I think just really kind of challenging that, and I think this quote is very important to hold on to: "If something is not impossible, then all of a sudden, by some margin, it becomes possible."

So, we really need to hold on to that positive outlook, especially as we're beginning that journey and that chapter in recovery.

Let's move on to my case study. My client, Lucy, is 34 years old. She was a senior consultant working in the city. She had taken a leave from work around November time of last year due to poor health and had three bouts of COVID close together in 2023. She was struggling with a "never been well since" situation. She came to see me in early 2024, and the symptoms she was experiencing were chronic fatigue, post-exertional malaise, brain fog, light sensitivity (so every time there was bright light, she was feeling triggered, and it was making her symptoms worse), dizziness, memory problems, concentration issues, sinusitis, GI issues, and also anxiety and low mood.

The ones in yellow I've highlighted were kind of her main presenting symptoms that she was really wanting to work on. She did have a medical diagnosis of CFS, so she'd ruled everything out with her doctor, and she also had a history of IBS prior to this, which was very interesting as well. She was also an A-type personality, so her self-esteem was intrinsically connected to her work achievements, and she was keen to get healthy so she could get back to work ASAP.

She was really kind of driving herself, like, "I need to get better so that I can get back to work." There was a little bit of nervous system tension I could sense just upon meeting her; she was very tense and just very stressed about the fact that she was off work and that she'd taken this time off work. She really wasn't giving herself permission to have a period of convalescence, which was interesting. That stress picture certainly seemed a big thing for us to investigate.

In our initial consultation, we had a thorough health assessment. I asked her to complete a food diary before seeing me, and we went through all of that, really delving into everything from her past health, any medication she was taking. I also requested a battery of GP tests as well, just to make sure that we knew exactly what her levels were of things like B12, vitamin D, folate, for example, and also iron, her thyroid, etc., just to rule out any anemias or nutrient deficiencies, which, of course, is a really good first point of call.

We also looked at what those key antecedents were—the triggers and the drivers—and really what warranted more investigation. For her, it was a stressful time of pushing herself work-wise. You could see that she just did not let herself rest. She was also on a frequent battle of antibiotics because she was constantly getting unwell with infections. Of course, then the big straw that broke the camel's back was this SARS-CoV-2 infection or a multitude of them over the course of late last year.

What I could certainly observe from her driving pointers was that she was stressed; she was resisting the situation; she was really impatient to get back to work, as I said. She was also undereating as well. She didn't have an eating disorder as such, but she had a sister who had an eating disorder, and she'd kind of followed a similar pattern in the sense that she was not eating a lot of food, and she was aware of it.

That was certainly something that we really wanted to focus in on. There were also obviously these suspected food intolerances; she noticed fiber was a big trigger for her, so we wanted to investigate that. She had these gut symptoms as well, so again, thinking we really need to look at what's going on within the gut.

So, what did I recommend as the next step? I recommended Genova's chronic fatigue screen test and also Genova's GI effects test. The reason for this approach was really kind of identifying the key symptoms that she had and also exploring that personal health history and considering the best test, of course, also understanding the means and her budget and really where she wanted to go with this.

But she was really keen on doing some testing to really gain more answers and insights. Obviously, her symptoms were the fatigue, the gut symptoms, the cognitive symptoms, and also the anxiety. This really gave me an insight into kind of where I made my decision. If, as a practitioner, you are just struggling to make a decision on what test is best for your client or your patient, then Genova does have a really fabulous service on their clinical education portal where you can book a call or consultation to really find out what might be the best test for your case or for your client, and you can get some support that way.

Essentially, I went for the chronic fatigue screen; this is two tests in one. It's an adrenal stress profile; it has the option for a cortisol awakening response add-on, and then also the organic acids test. The organic acids test is essentially where we're looking at these urinary metabolic byproducts that accumulate within your urine, and they give you an insight into various different levels of your functional health, from your mitochondria and your citric acid cycle to specific cellular demands in terms of nutrients, what we need.

But also, we're looking at toxic exposures and liver health, and we're looking at the GI tract as well in terms of what might be going on there and oxidative stress. We can see a lot in terms of understanding how this can fit into the fatigue picture.

Knowing what I know about CFS and the picture of root causes, why I've recommended these tests, of course, she had a chronic stress picture, so that was certainly the case that we needed to look at her adrenals and cortisol levels. There were suspected cellular stresses due to the viral trigger, working in the city again, organic acids—we can look at the mitochondria, her nutrient demands, inflammation, oxidative stress, and of course, her history of IBS, the antibiotics that she was on, and these frequent gut complaints that were really bothering her.

This was the need to gain a better insight from really looking at her gut status and gut function. Functional testing gives us an insight into a client's functional systems, really delving into those biochemical imbalances, which is really important for complex unexplained medical illnesses like CFS and COVID. This is where these two tests really provided a point of reference for these chronic stresses and a pathway for personalization.

We were really able to delve into exactly what we've identified and picked up. So, the results: this is her adrenal stress profile. We're looking at her cortisol levels, her DHEA—these are kind of her two major stress hormones. Wow, you can see just how high and elevated her stress response is. The first box on the left is her cortisol awakening response, so that's basically her morning time response of cortisol, which is essentially meant to follow this kind of triangle pattern of we see this rapid rise in the morning and then starting to taper off as we move throughout the day.

What you can see for her is that already on waking, it's very, very high, but it's not actually rising that much; it's then starting to taper off, but it's not throughout the rest of the day. As you move into this box here, she's very, very stressed. You can see that cortisol activation, and even just into the 10 p.m. to 12 a.m. slot, she is really firing sky-high there. She's not really having any kind of recuperating effects from that stress response either because her DHEA is also on the low side.

So, you've got a low DHEA level and a DHEA/cortisol ratio. DHEA almost has this kind of—they're like a bit of yin and yang, cortisol and DHEA. DHEA basically counterbalances the catabolic effects of cortisol, and it has this kind of anti-inflammatory ability, but she's not really getting any result from that or response from that, and it's just this wear-and-tear effect on her system.

Then we look at her GI effects. We'll move on to the organic acids part in a moment, but her GI effects showed that she had elevated levels of fecal fats and also protein breakdown products in her stool. Now, she wasn't eating a very high-fat or protein diet, and of course, she was really following a pattern of really undereating.

So, for her, I was suspecting this was related to the fact that she had a very high secretory IgA. Secretory IgA is your gut's most abundant antibody. The fact that this was firing very high suggested to me that she had picked up a pathogen, which we'll showcase later on in a moment, but that she's got this very high immune activity, but also that can be really impairing the integrity of the gut lining.

This is where I'm thinking, okay, compromised gut barrier, intestinal permeability could be driving those scores high on the digestion and absorption scales. Her short-chain fats were good; her beta-glucuronidase was within range. But as we move on to her commensal pattern, actually, this is pretty good. She had a relatively good balance of commensals, although kind of low levels of lactobacillus, which we do know play a role in digestive health and also helping with the integrity of the gut barrier.

Interestingly, her levels of bifidobacterium, which you can see here, were also within range, and that's actually a good thing because, as I say, we know they're really beneficial for supporting and educating the immune cells to work. Actually, studies have showcased a pattern that they tend to be low in ME/CFS cohorts, but for her, this wasn't the case.

So, really, just looking on this page, not too worrisome. But as we move on to the kind of parasitology and the pathogenic microbes, we picked up Blastocystis, which is basically a protozoa—not bacteria—that can be associated with a lot of GI complaints, so abdominal pain, bloating, flatulence, IBS symptoms, and of course, has also been associated with chronic fatigue syndrome.

There is some controversy around the fact that parasites can be detected in healthy and symptomatic patients, so sometimes there's controversy around whether we do anything about it in terms of if you went to a GP. However, if we know that we've detected this and we know she's got these medically unexplained symptoms, why are we not going to go in and really address it? We certainly should, so it's something we've spotted, and it could certainly be driving what's going on.

It's really good that we've detected this. We've also seen levels of a potential pathogen, Entamoeba coli—I can never pronounce these correctly, so forgive me if I'm mispronouncing any of them—and then levels of Citrobacter and Candida albicans were detected, not at a high enough level to become problematic, but they could become opportunistic in the future.

Again, it's really about thinking about how can we deal with this environment and support that. Her organic acid results were showcasing the B vitamins and manganese. We know that B vitamins are very important as co-factors for ATP production within the mitochondria. Even when we're stressed, we deplete levels of B vitamins, so due to her chronic stress picture, we really need to be thinking about B vitamins for her.

If we look more broadly at the kind of organic acid markers, I'll whip through this very quickly, just being mindful of time, but essentially, you can see a few of her malabsorption markers just up here were elevated, which linked with her stool results. The dysbiosis markers were relatively elevated as well, and I think this is not specifically related to the fact that her commensals were obviously—we know her commensals were fine—but actually, those dysbiosis markers of the potentially pathogenic bacteria and the parasite that we detected on the stool test could be driving these organic acids up.

We also see her yeast and dysbiosis markers elevated as well, so that also points to that pattern. This ratio here is looking at the kynurenine and quinolinic ratio. Because this is out of range, we know that this has a capacity to be associated with neurotoxicity, so neuroinflammation. Because she had a lot of cognitive symptoms, this was speaking to me a lot in terms of, okay, this could potentially be showcasing that we have not just inflammation happening within the body, but actually inflammation happening within the brain, and this could also be driving what's going on in terms of the brain fog, the cognitive impairment.

That's definitely something we really wanted to work on together. She had high serotonin breakdown product markers; she was on an SSRI, and also she did have those raised dysbiosis markers, so there could be a link between that, I think, potentially the SSRI medication.

Toxin and detox markers were not hugely elevated, but there was some exposure to petrochemicals. Again, sometimes we can't always do a lot of that living in the city, for example. But what this does showcase is that we can really go in with some support in terms of her cells and looking at antioxidant support.

So, again, just further on the oxidation point, she had moderately elevated levels of 8-hydroxy-2'-deoxyguanosine. I've never pronounced that correctly. That's basically a marker formed when DNA is damaged by reactive oxygen species. We know that, as I say, that's elevated; we are seeing some oxidative damage to DNA. We really want to support her cells as much as possible because, of course, everything that's happening within the body is happening on that cellular level.

Energy manufacture is being done on a cellular level. If that cell is being in any way damaged from a DNA perspective, but also from their outer layer perspective when we look at these lipid peroxides, then we're not able to manufacture proteins efficiently, we're not able to repair things, we're not able to produce ATP effectively, and do our jobs.

So, this is where this really comes in. As I say, we can see moderately elevated urine lipid peroxides, and these are a class of free radicals that damage that fatty coating on our cell membranes. All of these things that we picked up are really feeding into that picture of chronic fatigue syndrome.

So, what did we do? We went in with a protocol of antimicrobials, so berberine and oil of oregano for a period of eight weeks. We really wanted to give that enough time; sometimes they can have a high FB resistance or drug resistance, Blastocystis, so it's really thinking about making sure we go in strong with that for a period of eight weeks.

Of course, going low and slow, so really just making sure that she's responding well to those and not having any negative feedback to the supplements, because sometimes we do get a bit of aggravation, and sometimes you do have to taper that approach. We also went in with a methyl B complex for the family of synergistic B vitamins as a mitochondrial co-factor.

We know that a lot of people have the genetic polymorphism where they can't methylate effectively, so that's where we went into the methyl B. Another thing that's really powerful—we talk about the urine lipid peroxides and also the oxidative stress markers—is phosphatidylcholine, and it can really help to restore the integrity of that fatty coating on the cell membrane.

So, it's really going to be supportive for cell function, neural firing, and just really kind of coating and protecting those cells. Ashwagandha we used as an adaptogen to really support and balance her cortisol response. NAC was used as a precursor to the body's master antioxidant, glutathione.

Interestingly, a specific type of it, augmented NAC, is being studied as useful for denaturing the spike protein in SARS-CoV-2 infection. We went in with an augmented version, and then we switched after about six weeks' time to a more cost-effective version because the augmented version is a little bit more expensive.

But this was fantastic for not just supporting her liver detoxification pathways and that oxidative stress, but also helping in terms of citric acid and Krebs cycle and supporting with that ATP production. It's just a general, really fantastic thing to add in because it's just supporting your cells and supporting the mitochondria.

Dr. ribose is another fantastic mitochondrial agent, which I use in pretty much most of, if not all, of my CFS clients. It's a powder, so you can take one teaspoon and then start to titrate it up. With Lucy, we managed to titrate to two to three teaspoons a day within the three-month period.

That is something that really does have a fantastic effect when people are experiencing post-exertional malaise. Zinc carnosine is really useful for restoring integrity to the gut barrier and dampening down inflammation, and that can also support that high kynurenine/quinolinic ratio we saw in her organic acid report.

It can also bolster stomach acid levels, so we need to get stomach acid levels strong to prevent reinfection of future parasites or pathogenic microbes. That's also another factor of where the zinc carnosine came in. Omega-3s for cognitive support, reducing inflammation, and just fantastic in terms of brain health.

What we did afterwards: we did the eight weeks of weeding with the parasite, and then we went in with a multi-strain enteric-coated probiotic complex, which had a multitude of different strains. Of course, her commensal pattern was already pretty good, but because we've done some antimicrobial work, it was really about making sure we supported with a broad range of bacterial species.

We went in with those for a period of six weeks, and actually, we're now moving across to partially hydrolyzed guar gum, which is a prebiotic fiber. It's a non-FODMAP, so it's basically going to help to support microbial diversity going forwards, and it's a really useful and versatile supplement to have going forwards.

In terms of what we did nutritionally, we made sure that she was consuming more in terms of daily calories, consuming three meals a day, high in protein, high in those good fats, and also at least a little bit more complex carbs than she was consuming previously.

I asked her to do a food and symptom diary to look at any FODMAP triggers, so things like garlic, onion, and meats actually came out as really bothersome for her in terms of those GI symptoms. We slowly, over time, once we managed to kind of rebalance those, really reduced them after a period of removal but at a much lower level according to where her tolerance level sat.

Blood sugar was also a key part of that, and that's always a key part I ask clients of mine: how does a meal make you feel? Do your energy levels feel better after eating, or do they feel worse? That's such a key thing to ask because it can give you an insight as to whether somebody is hypoglycemic or hyperglycemic. She was on the hypoglycemic spectrum, so we really needed to look at meal timing, making sure she was eating regularly, and just anticipating any blood sugar dips.

We made sure that she was chewing food, making mealtimes a ritual, and having enzyme-rich foods to really support those absorption markers we saw in her GI effects test. Dietary diversity was a big part of this, so making sure she was getting a cocktail of different fibers every week, not just eating the same foods on repeat.

Fermented foods, of course, after we've done that weeding period, have been a really important part of her protocol. Things like bone broths—I asked her to do, you know, whether she's making some chicken or rotisserie chicken or anything like that, or making it at home or buying some and freezing them in batches and just drinking three cups a week to support the GI lining.

Those will contain things like amino acids, like collagen, glutamine, glycine, and gelatin—things that all really help to nurture and support the integrity of that GI tract, and that's going to really help to counter any inflammatory processes going on.

Green leafies—just trying to rotate those because we know they're very dense in energy and offer key fighting nutrients, things like B vitamins and iron, things like magnesium, for example, folates. We just really need to think about getting those in, which we did. Anti-inflammatory herbs, lots of fluid, and of course, manganese-rich foods, which she was demanding more of on her report.

I'm just going to briefly brush through this. Pacing was about getting through that boom-and-bust cycle. The boom-and-bust cycle is where you have a good day, you overexert yourself, then you have the payback post-exertional malaise, and then you're left with no choice but to rest. It's about anticipating that from happening, finding your baseline, and dropping down your levels of activity to a point of really incorporating rest and convalescence.

Giving yourself permission to rest as well was a massive part of her puzzle because she just wasn't giving herself permission. Scheduling rest between taxing activities and making sure she's doing energy-giving things each day—so just really kind of getting a hold on that boom-and-bust cycle.

Pacing her activity levels and finding what activities—I asked her to do an activity diary to really kind of see, okay, what's building you up energy-wise, what's breaking you down energy-wise, what's energy-giving, what's energy-draining, what's energy-neutral? How can we do more energy-giving things, and how can we prioritize what's important in terms of the energy drainers and how can we chop and change that?

It's about really working with her routine. Mindset was also a big part of our work together, dealing with the emotional ups and downs. Crashes are bound to happen; it's part and parcel of chronic fatigue syndrome. It can be a bit of a game of snakes and ladders, so for us as practitioners, it's about how we can help clients bounce back from a crash. What are the learnings we can take?

Reframe them as a learning experience in their journals or their thought diaries. Really working on those achiever patterns—the A-type personalities—and all of these other different fabulous tools of, you know, nervous system support. Giving herself permission to rest, as I say, was really important.

Three months after our work together, where Lucy is today: along the journey, of course, yes, crashes did take place, and that's totally normal, but we did see an observable symptom reduction. Actually, it's amazing now because she's able to start to get out of the house again; she's going out, meeting friends, and her physical capacity is improving. She is no longer in that boom-and-bust pattern, so that's something we've really managed to get a hold on, and her body is more tolerant of activity again.

She's increasing her daily step count without the crashes, and concentration is also restoring. In terms of her gut, we're still seeing a little bit of bloating going on, but we're now starting to correlate that a lot more with stress and anxiety triggers, and she has seen some relief there since she's incorporated antimicrobials for the parasites and also identified those FODMAP triggers.

What we're also looking to do going forwards is to try and taper off some of those supplements in the next few months, and that is a sign of progress. We don't want her to be on supplements forever and ever and ever. We're looking to retest the GI effects and also specifically the organic acids towards the end of the summer to review her progress on her adrenals and the eradication of the Blastocystis parasites.

She's not currently going back to work just yet, but this certainly might be on the cards towards the end of the summer. I think, for her, she's just had to really lean into this period of convalescence because it's so important for her. She's taken the time off work, but she wasn't mentally allowing herself to. I think now she's really invested in all that she's done, you know, development-wise and in terms of the testing and all the things that we found out and these mechanisms that we put in place in terms of her nutrition, her supplements, and her lifestyle.

I think this is all kind of starting to look good, and actually, you know, she continues to go onwards and upwards, so it's really, really positive to see how she's doing.

That's a little bit about chronic fatigue syndrome in a nutshell and also really how, as practitioners, we can really delve in using a functional medicine model in terms of understanding those root drivers. It really is about that kind of personalization approach because each person that comes to us with CFS perhaps has other comorbidities going on as well, but really they are all unique, and it's all about how we can delve into that understanding.

Thank you for listening. Here's a little bit more about where you can find me, where you can find my book, and I will leave it now for Amelia to jump on and ask any questions if we have them.

Thank you, Lauren. That was such a great presentation, and I think all of us get so much out of hearing those protocols and client case studies, especially. So, thank you so much. We do have quite a few questions, which is great to see. If anyone does have to jump off at this point, don't be worried; you will receive the Q&A as part of your post-event recording as well.

So, just to jump straight in, someone has asked here, when you're looking at the protocols, can you re-explain what the reason might be for your patient's high levels of fecal fats?

The fecal fats, yes. So, she had elevated levels of secretory IgA. One of the reasons why she could have had high secretory IgA was because of the fact that she had the parasite and the pathogenic microbes, so that was amping up her immune activity. But sometimes, once the inflammation is quite high, what it can do is impair that intestinal barrier, and then that can drive up those levels of fecal fats or products of protein breakdown as a result of that impaired gut lining. So, that was kind of what basically was the basis for that.

Great, thank you. And then we've got another question: what is the rationale for using antidepressants, and the SSRIs in particular?

Well, for her, it was kind of really—she was on it because of the fact that she had low mood. I probably wouldn't be able to medically comment on that one; obviously, that was under the care of her doctor. But it was really to support kind of the serotonin in her brain and the levels of that. Of course, we did see elevated markers on her organic acid report, which, as I say, I think would have been explained by that medication.

Yeah, great, thank you. Oh, and how many COVID shots had your patient had, by interest, if you knew?

I think she'd had one or potentially two. I need to look back at her report, actually, but I know she definitely was vaccinated. It wasn't that she had the kind of classic "never been well since" after vaccination; it was the infectious agents that were the trigger for her.

Great, and then there's another question here: could you please list the genes involved? I think this might have been asked right at the start.

Yes, so the human leukocyte antigens, so the HLA family, and it's two versions of those HLA genes, basically. They make proteins for the immune system to recognize different pathogens, and they've been linked with autoimmune disease as well. I can't off the top of my head remember the specific type of HLA gene, but I can—I think I've listed it in my book, actually. I go into depth in terms of the genetic links of those, but as I say, they're really important for the immune system. What we've found is that patients with CFS have these more common in those than in healthy cohorts, potentially impacting the way the immune system is functioning.

Great, thank you. And then another question: when you mentioned fermented food, do you recommend home-fermented as recommended by Dr. Greger, or to avoid excess salts?

In terms of what food companies have added, for example, I mean, yes, there is certainly a benefit of home fermentation because, obviously, you've done it yourself; you're much more in control of what's going into it. But what I would say is that, obviously, if you've got chronic fatigue syndrome, you probably don't really have the energy to be doing those sorts of things.

So, I think just starting kind of low and slow, you know, if you can access or you've got the means to pay for—I know they're a bit more expensive than making things at home—but, you know, things like—I think the brand I like is Vadasz, if you can. V-A-D-A-S-Z, I think it's spelled. That's the one that does the beetroot kimchi and the normal spicy kimchi and different sauerkrauts and things like that. They're a very good brand.

But, yeah, I mean, I certainly encourage if it's within the client's means, but obviously, if you've got chronic fatigue syndrome, it can sometimes be a challenge to do all that sort of stuff.

Yeah, and it helps if they like it as well. Love kimchi, but it's very love or hate, isn't it?

Yeah, it really is. I often say to clients, if you're struggling to kind of get it in around meal times or with your meals, for example, because you don't like the contrast of the savory versus sour, I just say just have it when you're eating or just about to have a meal. Just literally have a tablespoon from a clean spoon from the tub, or one or two, do you know what I mean? So instead of having it combined with a meal, because sometimes people just don't like the combination of savory versus the sour, just have it on its own if you like as well.

Yeah, absolutely. And we've got a question here about Genova testing and how we can interpret the results.

If you've got any questions about our testing specifically, you can head to the gdx.net website, and we've got a full list of our product ranges there. Or you could also email us at info@gdx.net, and you can get put straight into contact with one of our clinical education team, who can talk you through the different testing and what might be useful for your client or your case study.

Another question here: you mentioned about crashes and how do they tend to look for a client, and how do we build them back up after that?

Yeah, so crashes can be different for each CFS patient because they all vary, right? A common crash would be kind of the worsening of the fatigue after maybe they've gone out and they've gone for lunch with somebody, or maybe it's something as simple as they've just gone up the stairs and they've maybe done a bit more housework than they normally would have done.

But for others, it could be that they maybe—the brain fog is getting really bad; they're struggling to recall sentences, concentration is bad, maybe their GI complaints are getting a little bit worse, or potentially the muscle joint aches and pains. As I say, we're talking about these medically unexplained syndromes; the symptoms can very much be, I guess, diverse.

With the crashes, in terms of navigating them, it's about really what I like to get clients to do is kind of complete an activity diary. Find out what things are energy-giving in your daily or weekly routine, what things are energy-neutral, what things are energy-draining or energy-giving. If I didn't say either, it's about trying to understand and ascertain the things that you're doing on a weekly basis that are really contributing to your energy levels or draining them down.

There will be certain tasks that potentially, you know, I say you're part of this boom-and-bust pattern. If you have a crash, of course, it's important to stop. What's also important is getting clients to spot the warning signs because symptoms can often start to present themselves. As clients, I find I'm working with clients, they become much more in tune with their bodies over a period of time of working with me, and then they start to be like, "Honestly, I used to go to the gym and smash out a session, and then I'd be on the floor afterwards."

But before that, they wouldn't notice. Or they do loads of things after that, and then they'd be on the floor, like, "Crash." But as then, as I'm trying to say, you just don't notice that you have these increasing warning signs of symptoms. Whereas they're becoming more in tune with their body, they start to realize.

So, I think as that happens, the pacing narrative is about really kind of pulling back before you continue doing more and more. That's where you work on really kind of finding activities that they can do in their day. Non-sleep rest is a really good one, which is really finding ways to take 10 to 15 minutes, whether it's doing a guided yoga or something where literally you're almost doing nothing; you're just focusing on the breath or a body part for a 15-minute period that takes you into the present moment and allows you to rest.

Because people sometimes think that they're resting, but they're not. Or they're not fully giving themselves permission to rest. Maybe they're sat on the sofa watching TV, but they're neurologically not resting. So, it's thinking about also the cognitive aspects as well—not just the physical, like, "Okay, you've gone to the coffee with your friend and you've crashed," but perhaps maybe they've done something else, and they've crashed, and they've not realized what it was.

Like, "Okay, I was on Instagram scrolling for ages and ages, and my brain was just frazzled with information, and then I crashed." So, it's trying to kind of piece back what caused it, spot the warning signs, give yourself the convalescence and the rest, and figure out how we can incorporate scheduled rest going forwards. That's what pacing is all about, but I go into more depth on that in my book in terms of how you can pace activity levels better because it's a big, big minefield.

Yeah, for sure. Thank you so much. I think we had time for just one more question before we get to like 10 past. To what extent do genetic predispositions play a role in CFS? Are there specific risk factors that we should be aware of?

I think what was the science is still kind of ongoing; it's still in its infancy. What we do have confidence to say is that, you know, there are genetic links. There are twin studies as well that showcase that, you know, it's more kind of likely for—in terms of our genes—that somebody can be predisposed to becoming unwell with ME/CFS. How that looks, we don't fully know.

Obviously, we talked about these HLA gene families that potentially make you more predisposed. Then there's also the Decode study that's now finding out more information, so I'd maybe point you in the direction of them to kind of have a look and find out more further as they're gaining more nuggets and insights there. But we still just don't know enough. What we do know is that there are genetic links in terms of potentially what can make us more fed to those; we just don't know exactly what is being pointed there.

Yeah, for sure. Well, thank you so much, Lauren. That is all we probably have time for today. Next week's session is going to take place on Wednesday next week at 1 p.m., so you can join us for that using today's session link, or you can re-register online to receive a new link as well.

Thank you, Lauren, for your time. It was such a great presentation, and we've got so many questions, so I'm sure everyone agrees with me as well. Thank you all for joining us today. Enjoy the rest of your very sunny afternoon, and we'll see you soon.

Yeah, I hope everyone enjoys the sunny afternoon. I'm going to get myself outside.

Great! Thank you so much, Lauren. Thank you.