I’ve received so much lovely feedback (fan mail!) recently I just had to share some with you (note I look much more excited than Meg does when I get mine!). It’s so exciting to be a part of our burgeoning naturopathic & integrative network. From Alyssa Tait a Brisbane based naturopath, clinical nutritionist & physiotherapist: “I am so appreciative of your mentoring and your professional development (e.g. recent Health Masters Live webinars). You make me really enthusiastic about being in this field, and you actually help me feel like I sort of know what I’m doing…most of the time!!”(more…)
So far this year I’ve been doing most of my presenting online which has been fantastic because we can all be in our PJs and no one’s the wiser (except now!!) but I do miss the face to face seminars where sometimes the real magic happens thanks to the two-way dynamic between you and me!
So guess what? I’m coming to Sydney on the 31st August (and then Brisbane 6th September and then Melbourne 13th September) to touch base with many of you again. I’m joining forces with Rachel McDonald from Biomedica to talk about the real world application of naturopathy in mental health conditions. (more…)
In spite of several advantages of salivary hormone assessment, one important piece of information you miss out on when you do this rather than blood assays, is the SHBG result. Sex hormone binding globulin is a protein produced in the liver that, as the name suggests, binds our sex hormones rendering them inactive and therefore buffering us against their full potency. They bind the sex hormones to different degrees – the androgens most potently and oestradiol to a lesser extent but curiously it’s higher oestrogen that represents the major hormonal driver of increased SHBG production (including synthetic oestrogens). (more…)
There are few complementary medicines that come onto the market with such a bang, opening up genuinely new therapeutic options for the effective management of such a broad range of health complaints. N-acetyl cysteine stands out for this reason and has changed the way I practice… seriously!
Recently I had the pleasure of presenting a webinar for Biomedica completely and utterly focussed on N-acetyl cysteine – its key actions, pharmacokinetics, applications and contraindications. In the process of researching for the webinar I learnt so much and to my surprise found even I was under-utilising my favourite supplement! How familiar are you with its application in cystic fibrosis, fertility, biofilm eradication etc. etc ? Not to mention, it’s incredible versatility in mental health. Recently, buoyed by some new research suggesting the efficacy in severe glutamate excess of much higher doses than previously studied for depression and bipolar, I have stepped up my doses in patients with some forms of addiction, OCD, refractory insomnia to 4g/d with great results! I could talk all day about NAC but perhaps for a starter if you missed the webinar you might want to listen to the recording? We have the Clinical Knack of NAC now available as a CD with audio and notes for purchase on the website:
This in-depth 1 hour webinar offers practitioners new to NAC, the practical knowledge and tools they need to start using it effectively and for the practitioner already dispensing it, to really broaden their understanding of indications , correct many misunderstandings and get the latest research on the why, when and how to use it. From reproductive to respiratory health, from heavy metal burdens to biofilms and athletes to addicts, this webinar covers the latest information about NAC’s real therapeutic potential. Having been a favourite nutraceutical/prescription of Rachel’s for some time, she punctuates the presentation with many of her own cases.
Globulins…ever thought much about them? Me neither really unless they were clearly below range which made me consider immune impairment but recently Dr. Michael Hayter, who I am co-presenting the Diagnostics Master Class (Health Masters Live) with, inspired me to take a closer look! Globulins are typically reported in your patients’ E/LFTs or standard chemistry and they refer to a big group of molecules including CRP, transferrin, lipoproteins and yes all the immunoglobulins/antibodies. (more…)
I often say that if my surname was Rubin I wouldn’t be able to resist calling my son Billy. I am sure the joke would be lost on 90% of people & certainly on my poor child who might never forgive me but never on me – I get a giggle every time 🙂 Recently, I’ve been reading a lot of scientific literature on bilirubin, previously regarded as simply the end waste product of haem, it’s now attracting huge interest as a biomarker of oxidative stress. There’s still lots of ongoing debate & contradictory research findings but here’s the general consensus so far…bilirubin is an antioxidant (particularly protective against peroxyl radicals & lipid oxidation although the latter is still being hotly debated). Not surprisingly then, several studies have shown that smokers for example, consistently have lower total bilirubin blood values, indicative of their greater oxidative stress & yes, smoking cessation leads to partial correction of this (O’Malley et al. 2014 Smoking Cessation Is Followed by Increases in Serum Bilirubin, an Endogenous Antioxidant Associated With Lower Risk of Lung Cancer and Cardiovascular Disease) A recent study also found a positive correlation between higher flavonoid rich fruit & vegetable intake and total bilirubin (Laprinzi & Mahoney 2014 Association Between Flavonoid-Rich Fruit and Vegetable Consumption and Total Serum Bilirubin).
On top of this, there is a wave of epidemiological research to currently surf, suggesting inverse relationships between total bilirubin levels and several diseases: hypertension & CVD, T2DM, metabolic syndrome, MS, renal disease, IBD, lung cancer and the list goes on. The sort of cut-off point being talked about is a result < 10 µmol/L being associated with the highest risk. What remains unclear is whether lower bilirubin levels are actually risk-promoting or whether they are just a signal of the individual’s oxidative stress.
Total bilirubin (aka Indirect or Unconjugated bilirubin) values are typically included in most pathology company’s basic general chemistry or E/LFT panels which means most of your patients already have had this test performed in the previous 12 months. So next time you’re looking at patient results check out their bilirubin values and if they have bilirubin levels consistently <10µmol/Lconsider how you might better support your patient manage their oxidative burden to reduce risk of future disease and if you’re hitting the mark the bilirubin level should rise 🙂
Want to know more about Bilirubin and Pathology interpretation in general – Rachel is collaborating with Dr. Michael Hayter to present an online Master Class in Diagnostics starting this week. For more information check out Health Masters Live https://www.healthmasterslive.com/product/clinical-diagnostics-masterclass/?mc_cid=cfd82dd367&mc_eid=014c831228
I briefly mentioned in a previous post Dr. Robyn Cosford’s inspiring opening speech at this year’s MINDD conference. A key point she made was the growing gap between what’s regarded as normal and what is actually healthy.
Having worked in general practice for decades, Robyn provided us with one illustration after another – Type 2 diabetes, previously called adult-onset diabetes, now not infrequently diagnosed in primary school aged children; delayed speech and learning difficulties in male toddlers which many increasingly regard as ‘normal’; precocious puberty in girls; escalating rates of depression and anxiety in children and adolescents…Robyn asked us as practitioners to be vigilant about helping patients to distinguish between what has become perceived as ‘normal’ and what is actually healthy.
In my MINDD presentation this year I talked about the mental health challenges faced by young men and I expressed a similar concern: that when we witness extensive aberrant behaviour in young men we are prone to rationalise it. Are we mistakenly attributing these signs of dis-ease in males as simply being an initiation into Australian culture? When you hear of young men exhibiting binge drinking behaviour, does it set off the same alarms as it would if your patient was female and if not….why not?
As part of a broader discussion of the issues, I presented two cases of young men with mental health problems – both from very different sides of the tracks, one gifted and the other a struggler but one of the features they shared included the way their use of alcohol & other substances had passively been condoned by society instead of being seen as a call for help. We can help these young men but only once we’ve acknowledged there’s a problem. So now I’m extending Robyn’s plea and ask you to be vigilant in making the distinction between ‘normal’ and healthy… when mothers relay stories of their son’s ‘antics’, when brothers, cousins & uncles temporarily ‘go off the rails’, when young men reluctantly present for a quick fix…
I’ve been curious about the push towards using so-called ‘active forms’ of B vitamins over the last 10 years in nutritional medicine – particularly with regard to B6 (pyridoxal-5-phosphate) and B2 (riboflavin 5’-phospate aka FMN) in light of substantial research demonstrating that these phosphorylated forms will in fact be dephosphorylated prior to uptake in the small intestine (Gropper, Smith & Groff Advanced Nutrition & Human Metabolism 2005) – so initially it seemed we were being encouraged to pay more for something that ultimately gave us less of the same vitamin. Funnily enough the only established scientific way to ensure uptake of the active forms in their intact active states is to use very high doses – however supplements containing either active B6 or B2 consistently offer very low doses compared with the regular supplements, so this seemed to rule this out as an explanation.
In spite of my scepticism & encouraged by the Pfeiffer approach, I got into using P5P and had to suspend my disbelief in the face of some good clinical results.
However finally at the MINDD conference last week, scientist Woody McGinnis at last made sense of this riddle for me!
McGinnis, who some of you might know as previously being a key researcher at the Pfeiffer Institute which specialises in nutritional and integrative management of mental health & behavioural disorders, confessed that he had also struggled with concept of P5P supplementation from a scientific perspective until Bill Walsh suggested that this form was particularly indicated for the ‘lean malabsorbers’.
What Woody essentially took from this was that patients with leaky guts could absorb the P5P intact & would ultimately benefit from this form. Adding to this is my understanding that the dephosphorylation process for P5P in the gut occurs via ALP – a zinc dependent enzyme found in the brush border of the small intestine…so here you have the double whammy – if your patient is a malabsorber AND zinc deficient (which of course commonly go together) they are the ones picking up the P5P perfectly and for the rest of us perhaps the pyridoxine will do.
Woody also attested to this with his story of his own pyrroluric son who initially only responded to P5P but in his teens (with significantly improved gut health) appeared to stop responding – at which point Woody switched him to the higher dose pyridoxine with fantastic results…..Aaahhhh at last my scientific curiosity has been quenched! 🙂
I was honoured to speak at the MINDD conference again this year. MINDD is an organisation that really sets itself apart by providing incredible hands on support for parents, carers and practitioners in the area of integrative mental health management and one of the key strengths is the sense of community they’ve developed secondary to this. A key message echoed by numerous speakers was the enhanced clinical benefits for patients when a truly whole health, multi-modality approach is taken – from naturopathy to psychology, from neurology to audiology, from building biology to biological markers and so on.
And just to put the brakes on the whole ‘genes are us’ movement that is currently sweeping Australian integrative medicine, Dr. Robyn Cosford (a highly-regarded integrative GP) kicked off the whole weekend with a presentation that included a study of some of the oldest Okinawan individuals and their genetic profiles. These individuals aged well over 100 and fighting fit each possessed hundreds of genes currently thought to be associated with chronic disease: cardiovascular, diabetes, cancer. Robyn reminds us all that while genetics loads the gun it is our diet, lifestyle and environment that actually pulls the trigger!
While I was inspired by the research and insight offered by clinicians and scientists from various modalities, I was reminded again, that no one individual can be across it all and to attempt is to fail or become exhausted in the process and this of course is where the communitybit comes in – we need a network of integrative individuals to refer between and support each patient & my experience this weekend suggests these events certainly build that community. Our job is to practice within our scope and know when and where these other therapies and approaches are indicated and to develop a good referral network. So many great speakers this year and this time I actually managed to sit still and enjoy some of these so I’ll be bringing you the highlights over the next couple of weeks so stay tuned! 🙂
Be warned…whinge ahead!One of the things I’m asked most often by naturopaths is about my experiences & interactions with doctors regarding shared care of patients. The question typically arises because they’ve been on the receiving end of less than ideal situations. We’ve probably all been there at some point. My usual optimism tells me that if we keep building the bridge by ensuring our communication is professional, accurate, respectful and always in the patients best interests, eventually we’ll bring the detractors around and those who make it clear they’ll never come around reveal themselves to be ill-equipped for shared care. Over this last week I’ve had a nasty reminder of the latter!
Here’s the scenario: I recently started seeing a female patient in her late 50s who has had unresolving diarrhoea for 3 months. Multiple trips to the GP and investigations revealed no explanation, however, the diarrhoea was severe, unprecedented and deeply concerning to my patient. After much discussion I organised a CDSA for her, the results of which confirmed extensive infection with Dientamoeba fragilis. This parasite is a well-known established cause of diarrhoea and its eradication is associated with resolution of these issues. There were also high levels of two gram negative bacteria which can be commensals (non-pathogenic, not infrequently found in human GIT), however, their population should be kept in check: Klebsiella pneumonia & Citrobacter freundii. As both of these bacteria are notorious for developing antibiotic resistance I did what I thought was best and communicated the findings of these results (plus copies) as well as a review paper from a mainstream scientific journal on Dientamoeba fragilis to her doctor in case we needed to pursue medical treatment of the parasite. Now this is where the drama begins. Did I mention this patient also suffers from anxiety? Upon receiving my communication, her doctor wildly informs her that Klebsiella pneumonia is lethal! Potentially true if found in your respiratory system, however, absolutely not in the GIT. He says has no idea about what I’m talking about (true!), with the suggestion that I don’t either & refuses to treat her. Understandably, I receive frantic calls from a very upset patient concerned about the lethal bit! What do you say? Here’s what I said: Unfortunately this GP has simply demonstrated his ignorance about GIT microflora. K. pneumonia is nasty in other parts of your body but quite common in the gut. I can send you some information about this to reassure you. In the meantime let’s get you in to see someone who actually knows something about GIT pathogens.
A week later after the same patient sees the GP I referred her to (who received the same referral letter and information) I receive an email from him saying essentially: Thanks for sending this patient and the information. According to the Centre for Digestive Diseases I think we can treat the parasite if necessary without risking resistance with the gram negative bacteria, however, right now she seems to be doing really well on the herbal anti-microbials you’ve prescribed so let’s delay any medical intervention unless really necessary. I’ll see her again in 3 weeks and keep you posted.
Let’s just recap…this is a regular GP with the same training as her original one the difference is he has an open mind and takes the time to keep abreast of new information in order to offer his patients the best care. In the space of one week and two GPs I’ve gone from ‘mad fish-slapping dangerous naturopath’ to a welcome & respected contributor in patient care. A good reminder that if you’ve done your best in terms of establishing good communication with doctors and other carers and they seem unable to respond in a way that has the patients best interests at heart…find another doctor! Ok – I’m done now 🙂
Seeing female patients with anxiety/depression, irregular menstrual cycles and perhaps marked PMS? How about male clients with decreased libido, low measurable testosterone and perhaps even impotence or infertility? All of these signs and symptoms could actually be the result of elevated prolactin.
Our patients are faced by more health & nutrition messages via multiple mediums than ever before yet escalating rates of obesity & lifestyle related disease highlight the failure of these. It would seem behavioural psychologists are right when they assert that information does not change behaviour in the majority of people. Therefore if we too simply add to our patients’ information overload, we’ve missed the point. One of my favourite & at the same time terrible illustrations of this was when I walked into a local café and saw a man sitting at a table by himself having just finished a cup of coffee and something sweet. On the table next to his coffee was a very recognisable ‘prescription’ from a naturopath he’d obviously just been to see.
It read:
Reduce coffee
Reduce sugar
Reduce fat
Increase exercise
Oh the power of such words!! If we spit out advice/instructions/directives at our patients, even with all the best intentions, we seem to make very little progress or only create short-term change. In contrast, if we take the time to focus in on each change we wish the patient to make, individualise the approach and solutions then we may have only given them a small fraction of the ‘advice’ we ultimately want to but at least this time it’s actually met it’s mark and created life-long healthy habits.
An understanding of the components behind successful behavioural change (readiness, empowerment, barrier identification & resolution etc.) is essential to improving patients’ health & wellbeing. If you want to hear more about how to successfully promote behavioural change in your patients follow this link https://rachelarthur.com.au/product-category/premium-audio/ to a premium audio download I recorded on this topic last February. I really believe it can make the difference between success and failure with individual patient’s treatment & the success of your practice overall. Enjoy and remember more information isn’t the answer!
Ok – I’m excited!! A recent meta-analysis of seventeen epidemiological studies (n=1,643 depressed individuals and 804 controls) investigating zinc levels and depression found that depressed individuals had lower plasma/serum zinc levels than non –depressed people (Swardfager et al., 2013) While the actual difference in plasma/serum zinc was found to be small, approximately -1.85 umol/L lower in depressed compared with control individuals, the effect size increased in individuals with more severe depression, inpatients and studies with more robust methodology.
It is important to note that the lower levels seen in depressed patients were typically still within the established reference range….and this is the bit where I get excited because in fact, all 16 studies that found a correlation between lower plasma/serum zinc and depression found a mean zinc level i.e. 10-14mmol/L that according to the reference range used here in Australia (9-19 umol/L) – would be deemed adequate!
This research suggests that a) the reference range for zinc testing needs serious review and b) when some health professionals insist that there’s nothing wrong with your patient’s zinc result because “it’s within range” – we now have a great piece of very significant evidence to support our different interpretation and the need for zinc supplementation.
If you want to hear more about these new findings and the key things you need to know about plasma and serum zinc testing and interpretation then have a listen to the latest premium audio here
The last two decades have seen the introduction and rapid rise in popularity of the proton pump inhibitors (PPI) for GORD & gastric ulcers. While clinical trials prior to their approval and release didn’t reveal much in terms of adverse reactions, being not dissimilar to the side effects of the previous acid suppressing drugs, more recent studies involving larger numbers of individuals and post-marketing surveillance have raised several concerns about their chronic use. The three key current areas of concern are
the potential for increased bone fracture
increased susceptibility to infections
altered gastric function – digestive and nutritional consequences
While more targeted research is needed to fully clarify any causal role of the PPIs, there is a growing body of evidence which points to potentially serious detrimental effects for some long-time users. Increased rates of small intestinal overgrowth (SIBO), Clostridium difficile associated diarrhoea (CDAD) and other enteric infections highlight the negative impact gastric acid suppression has on host defence & eubiosis. While the nutritional consequences, initially thought to be limited to impaired nutrient digestion and absorption are now extending to the sudden development of IgE food allergies in PPI–taking patients. There is also new information about how PPIs interact with other medications both within the GIT and via CYP450 system. If you’re interested in learning more about this widely prescribed class of drugs check out a recent Medscape review on the topic https://www.medscape.com/viewarticle/730747
Scenario:Patient presents with low baseline 25(OH)D levels, let’s say 40 nmol/L and you prescribe a high dose (e.g. 5000IU/day) bioavailable vitamin D supplement and retest in 3 months but the 25(OH)D levels haven’t improved…what do you do now?
Sound familiar? It does to me. Once we have ruled out the usual suspects like taking the supplement at the wrong time (must be taken with a full stomach to ensure optimum fat digestion & uptake), inadequate dose (keep in mind that due to altered pharmacokinetics individuals with obese BMI will require a significantly higher dose) etc. then according to new research from Deng et al. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III, we should be reviewing the patient’s magnesium status pronto! Deng et al remind us that magnesium is the co-factor for 3 critical enzymes central to vitamin D metabolism. Previous in vitro research suggests that magnesium status regulates both 1α-hydroxylase and 24-hydroxylase activity and the binding of vitamin D to its transport protein and 25-hydroxylase might also be magnesium dependent. You might remember as well that the synthesis and metabolism of PTH (the critical cue for activating 25(OH)D to 1,25(OH)2D are reliant on health magnesium status.
All in all this places magnesium front row for a starring role in vitamin D metabolism.
Only isolated previous research showed the strength of this relationship with a 1974 study describing ‘magnesium-dependent vitamin-D-resistant rickets’, which was effectively treated with magnesium & vitamin D, while vitamin D alone was completely ineffective.
This recent research has demonstrated in a large cohort inadequate magnesium intake was more potently related to the presence of vitamin D insufficiency in individuals than vitamin D intake!
While this is only epidemiological research at this stage – it’s certainly a scientifically plausible concept and adds another element to the strong relationship between low 25(OH)D levels and increased all-cause mortality which numerous studies point to.
So next time when a patient’s 25(OH)D levels appear non-responsive to vitamin D supplementation – ask yourself, ‘Have they got enough magnesium?’
Over the last year, I’ve seen paediatric patients with various presentations (alopecia, behavioural issues etc.) whose thyroid results have seemed out of whack e.g. TSH values in the 3s and 4s. I noticed as well that each pathology company provided a slightly altered reference range but on the whole they weren’t significantly different from expected adult results (0.4-4.8 mU/mL). It left me wondering if there should be in fact specific reference ranges for kids given the striking developmental endocrine milieu. So began a brief search of the scientific literature and lo and behold (!) there is such a thing and guess what? Kids’ thyroid results do differ from adult ones!! One piece of research that was intended to establish kids’ reference ranges was conducted in Austria, where routine results (serum TSH, fT3, and fT4) were collated from existing laboratory data of 2,194 serum samples from a hospital based population of children aged 1 day – 18 years (Kapelari et al. 2008 Pediatric reference intervals for thyroid hormone levels from birth to adulthood: a retrospective study. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645400/)) Granted, these children are in hospital and yet deemed ‘healthy’ – which is a bit befuddling, however, the ranges found by these researchers were consistent with other previous studies in different cohorts, which adds strength to their findings. They revealed that TSH should be highest at birth and in the first month (e.g. 3.5 is the 50th percentile for this age group) and progressively decline throughout childhood and adolescence. So 50th percentile results across the age groups looks like this:
Age
TSH 50th percentile values
TSH Range
0-1mo
3.5
0.75-16.89
1-12mo
2.85
1.30-7.09
1-5yr
2.1
1.00-5.42
6-10yr
2.3
0.90-4.40
11-14yr
2.1
0.09-4.10
15-18yr
1.7
0.70-3.93
While there is a clear pattern of declining TSH with age throughout childhood, there were less changes across the ages with regard to fT4 and fT3 values, with the 50th percentile value for fT4 being approx. 15 pmol/L in all ages except 1mo and fT3 being high 5s to mid 6s. These are more robust values than we’ve come to expect and accept in many of our adult patients.
So next time you see thyroid results for a child – check out where they sit according to these percentiles, because where there’s smoke there’s typically a fire and further investigation of a marginally high TSH can reveal, antibodies, incorrect T4/T3 ratios and deficiencies of critical thyroid nutrients which might be central to helping resolve the health issues.
This week, care of Health Masters, I am delivering the first part of a 3 part webinar called ‘Clinical Case Analyses in Women with Anxiety’.
I originally wanted to call this brand new seminar series Dis-ease.
The idea was in response to the large number of female patients who come through my clinic door, presenting mostly self-diagnosed with anxiety. Some of these women absolutely do have anxiety disorders and both the aetiology & maintenance of these fit with the regular psycho-social theories, however, many of them, upon further investigation, have something biologically going on that constitutes a plausible alternative cause of their dis-ease.
That’s where the interesting journey begins as
you start to identify what’s the physical source of sensations they have reinterpreted/translated as ‘anxiety’ and
you start to address these physical drivers and relieve their negative psychological affect and then finally
you see how the discovery and recognition of a biological rather than a purely psychological explanation behind their ‘anxiety’ challenges women to rethink their self-story.
It’s big and thrilling stuff to be a part of and one of the most satisfying aspects of my practice.
This is the latest instalment in mental health education from me but from an entirely fresh perspective.
I’ve buried my head in the journals & leant heavily on my colleague who’s a psychologist to bring to you the first instalment this week – understanding the long list of differentials for patients who present with anxiety and how to approach the work up.
The following two weeks are dedicated to presenting 2 amazingly anxious female patients of mine – with case summaries, all the pathology results etc. so that you can see the journey I took with them and why.
I hope to ‘see’ you there.
If you’re not on the Health Masters mailing list already and want to check it out click here.
Often I find practitioners are a bit mystified by the male hormonal milieu and their skills at interpreting androgen results are patchy compared with their confidence in female hormone investigation. Yet, just like in females, understanding the sex hormones is a critical part of the whole health puzzle in our male patients – leading us to a better understanding of possibly the cause of their presentation (impaired motivation and mood, subfertility or infertility & osteoporosis etc.) or perhaps the consequence of unhealthy behaviours & other health risks (e.g. obesity, excess alcohol, chronic inflammation etc.). The natural decline in androgen levels with ageing (so called andropause or PADAM) gets talked about a lot but when does it start (typically in the 4th decade), why does it happen (primarily due to reduced number, function & responsivity of testicular secretory cells) & how low does it go? Is it possible for men to age and not become hypogonadal in the process? Well the answer to the last question is emphatically, ‘Yes!’ according to Australian research. Often, however, I’m finding younger males with very low testosterone levels which require thorough investigation to determine any direct cause. When none emerge, we are left with the ‘canary in the mine’ scenario, whereby testosterone production, not considered essential for survival, will be sacrificed when the organism is ‘under threat’. To hear more about how to comprehensively assess & interpret androgens, the real causes and consequences of low testosterone and some treatment suggestions check out the following premium audio https://rachelarthur.com.au/product-category/premium-audio/
Professor Andrew Sinclair, a leading Australian nutrition scientist from Deakin University, has warned that some snack foods on Australian supermarket shelves contain high levels of trans fats acids (TFAs) and is calling for mandatory labelling of TFAs in processed foods.
Societies promotion of happiness and happiness campaigns puts expectations on people of how they should feel. Expectations of happiness may be making sad people feel worse.
