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Constipation is a very common clinical problem in our community, characterised by infrequent bowel motions or difficulty passing stool. It affects an estimated 24% of adults, with up to 18% of adults regularly using laxatives. Constipation may be secondary to slow colonic transit, pelvic dyssynergia, pelvic floor disorders associated with organ prolapse, or all of the above.  Slow transit constipation or colonic inertia reflects an abnormally long length of time for waste material to pass through the colon. This contrasts with pelvic dyssynergia, also referred to as anismus or obstructed defaecation, which is a functional defaecation disorder in which the muscles involved in defaecation fail to coordinate properly.  In pelvic dyssynergia, the anal sphincter and puborectalis muscle paradoxically contract or fail to relax adequately, resulting in difficulty evacuating stool. This is seen in 25–50% of patients with chronic constipation, is more common in women, and may overlap with features of irritable bowel syndrome.  Pelvic floor physiotherapy helps target the root causes of bowel dysfunction associated with pelvic dyssynergia by restoring the coordination, strength and relaxation of pelvic muscles. It treats conditions like faecal incontinence, dyssynergic defecation and incomplete colon emptying by using muscle re-training, biofeedback and postural adjustments. Importantly, pelvic floor physiotherapy helps to reduce reliance on medication or surgery and can be highly effective, with rehabilitation and biofeedback therapies showing significant symptom improvement in a large majority of patients.  Additionally, simple but highly effective adjustments are suggested to toilet mechanics, such as using a footstool to elevate the knees above the hips and leaning forward or backwards, which helps align the rectum and relax the pelvic floor. Further, incorporating breathing techniques with central core coordination by learning deep, diaphragmatic breathing and avoiding breath-holding helps to minimise dangerous downward pressure (straining) and relaxes the pelvic floor naturally.  In our gastroenterology practice, we see pelvic floor physiotherapy and rehabilitation as essential partners in the management of the conditions discussed above. To take a deeper dive into this subject, we are joined by physiotherapist Varsha Bhikha. Varsha completed her Bachelor of Physiotherapy at Monash University in 2013 and then went on to complete a Post-Graduate Certificate in Pelvic Floor Physiotherapy in 2016. She has gained extensive experience in both Musculoskeletal and Pelvic Health Physiotherapy and works in both the maternity ward at Saint John of God Hospital Berwick and within private practice settings. Varsha also has a broad-based experience in treating women prenatally and postnatally and has further expertise in Clinical Pilates.  Please welcome Varsha to the podcast.  References:  Varsha Bhikha  www.gihealth.com.au  PubMed Central  Park et al., (2026). Biofeedback therapy and pelvic floor physical therapy in the treatment of constipation and fecal incontinence are very different in real-world practice. Neurogastroenterology & Motility, 38(8), e70412. https://doi.org/10.1111/nmo.70412

Diverticular disease is both very common and largely asymptomatic. It is increasingly prevalent with age. Less than 10% of 40-year-olds have diverticulosis; however, the figure increases to 30–40% by age 60 years and 50–70% by age 80 years. It is more common in industrialised countries and associated with low fibre diets, obesity, sedentary lifestyle and smoking. NSAID use and corticosteroids are quoted to increase complication risk, such as bleeding and perforation.  The natural history includes 70–80% of patients with diverticulosis remaining asymptomatic lifelong. Approximately 15–20% of patients eventually become symptomatic, but with uncomplicated diverticulitis that may be managed as an outpatient with bowel rest, analgesia and antibiotics. Some 12–15% of diverticulitis cases, however, will eventually become complicated and require hospital care with administration of intravenous antibiotic therapy and potentially surgical review.  That is, overall, about 4–5% of patients with diverticulosis will eventually experience complicated diverticulitis during their lifetime, and of these, 3–5% will experience a diverticular bleed.  Diverticulitis has a tendency to recur, and the recurrence rate for acute diverticulitis ranges between 16% and 35%, with roughly 20% of patients experiencing another episode within 5 to 10 years following their initial attack. The risk of future attacks increases if the first episode was complicated or if it occurred in patients under the age of 50 years. The risk increases with each flare-up. After a second episode, the recurrence rate jumps to roughly 55% over a 10-year period. Younger patients (typically under 50) and those with more complicated presentations tend to experience higher recurrence rates. Pips, seeds and nuts are irrelevant to episodic diverticulitis, although they have grown to occupy myth status in this regard.  Major complications requiring hospital admission include acute diverticulitis warranting intravenous antibiotic therapy, pain management and bowel rest, abscess development, perforation, fistula development, bowel obstruction and peritonitis.  Some acute diverticulitis events may be secondary to micro-perforation, with inflammation developing in and around diverticula. Such cases typically present with left lower quadrant pain, fever, raised inflammatory markers and altered bowel habit.  Diverticular bleeding occurs with a ~3–5% lifetime risk and is usually painless, large-volume haematochezia. This is the most common cause of lower GI bleeding in older adults and is confronting for patients. Often, bleeding stops spontaneously (~70–80%), but with a recurrence rate of ~20–40%, which may require radiologically targeted embolisation or surgical intervention.  Abscess formation occurs in ~15% of acute diverticulitis cases. Both frank perforation and peritonitis are less common.  Other diverticular complications include fistula formation, with a frequency of about ~2–4%. The most common fistula is colovesical, presenting with pneumaturia, recurrent UTIs and faecaluria.  Whilst most cases of acute complicated diverticulitis can be managed conservatively without surgery, I like to involve surgeons early in the hospital management of patients. For a deeper dive into this subject, we are joined by colorectal surgeon Asiri Arachchi, who is frequently called for his expert advice and intervention and provides an excellent service for both emergency and elective care across all colorectal pathologies in Southeast Melbourne. Asiri trained in high-volume colorectal units at Monash Health Victoria, Austin Health, North Shore Hospital Auckland and Christchurch Hospital, and is proficient in laparoscopic, open and robotic surgery. Please welcome Asiri to the podcast.  References:  Dr Asiri Arachchi: caseysurgicalgroup.com.au  Colorectal Surgery Australia and New Zealand Charity PubMed Central  NIH – Diverticular Disease

Patients with ulcerative colitis (UC) and Crohn's disease (CD) involving the colon are at an elevated risk of developing colorectal cancer (CRC), secondary to long-term chronic mucosal inflammation. The level of risk depends primarily on disease duration, the extent of colonic involvement, and the presence and grade of precancerous cell changes (dysplasia) present.  While most IBD patients never develop CRC, the risk, compared to the general population, is significantly higher. For ulcerative colitis, the cumulative risk is generally estimated as 1% to 2% at 10 years from diagnosis, 3% to 8% at 20 years since diagnosis, and 7% to 18% at 30 years' duration. The risk also depends on the severity and extent of the colitis.  For patients with Crohn's colitis, a level of CRC risk similar to those with UC is noted when comparable extents of large intestine inflammation are involved.  During colonoscopic surveillance of patients with IBD, dysplasia is looked for histologically, reflecting abnormal, precancerous cellular changes, and is categorised into low-grade (LGD) and high-grade (HGD) forms.  Patients with LGD are approximately 3.5 times more likely to develop advanced neoplasia compared to those without dysplasia, in the absence of intervention.  HGD is very dangerous. Approximately 40% of IBD patients with initial HGD findings on endoscopy will progress to colorectal cancer over a 15-year period if untreated.  Risk magnifiers include disease duration of 8 years or longer, colitis activity, and extent of disease involvement, including colitis that extends beyond the rectum into the left side of the colon or involves the entire colon (pancolitis).  Due to these risks, guidelines recommend starting surveillance colonoscopies 8 to 10 years after symptom onset. The gold standard technique for dysplasia detection at endoscopy involves the engagement of high-definition chromoendoscopy, followed by targeted biopsies of visible lesions rather than relying solely on random biopsies.  Routine surveillance every 2 years helps identify dysplasia early, enabling proactive management and preventing progression to cancer.  If PSC is diagnosed, annual colonic surveillance is recommended.  To discuss this subject in further detail, we are joined by Dr Ali Eqbal. Ali has expertise in advanced colonic interventional endoscopy and inflammatory bowel disease. He completed a two-year advanced endoscopy fellowship at King's College Hospital, London, where he developed expertise in the diagnosis and management of complex colonic polyps using techniques including endoscopic submucosal dissection (ESD) and endoscopic mucosal resection (EMR). He also undertook a clinical research fellowship in complex IBD at the Austin Hospital in Melbourne. He is widely respected and recognised for his advanced technical skills and commitment to minimally invasive treatment options. He has published and presented both nationally and internationally.  Please welcome Ali to the podcast.  References  Ali Eqbal:  https://www.gihealth.com.au  Gastroenterological Society of Australia (GESA)  NIH  PubMed Central (PMC). Primary sclerosing cholangitis as an independent risk factor for colorectal cancer in the context of inflammatory bowel disease: A review of the literature. https://pmc.ncbi.nlm.nih.gov/articles/PMC4112886/

Colon polyps develop on the inner lining of the large intestine or rectum and are medically significant, as a small percentage may subsequently develop into colon cancer.  They affect roughly 15% to 40% of all adults and become increasingly frequent with age. Whilst we are now observing an increasing prevalence of polyps and colon cancer in young adults, they are still relatively uncommon before the age of 40 years.  Colorectal polyps are found in about 25% of adults aged 45 years. By age 50 years, approximately 40% to 50% of people will develop at least one polyp, slightly more in men than women.  Polyps generally fall into two main categories: non-neoplastic, including hyperplastic polyps, inflammatory polyps and hamartomas; and potentially neoplastic polyps, which include adenomas and sessile serrated polyps. While harmless initially, adenomas and sessile serrated polyps are considered precancerous and may develop into invasive cancer over time. Fortunately, only a small minority, approximately 5% to 10% of conventional adenomas and an estimated 2% to 6% of isolated non-dysplastic sessile serrated polyps (SSPs), will ever progress to malignancy.  Conventional adenomas progress to cancer via a traditional adenoma-to-carcinoma pathway, a relatively slow process that may take 10 to 15 years.  By contrast, sessile serrated polyps (SSPs) develop through an alternative biological pathway. They are flat, often hidden under a mucus cap, tend to be more right-sided in location, and are historically difficult to spot during a colonoscopy.  For an isolated non-dysplastic SSP, the 10-year cumulative risk of becoming cancerous is relatively low, at around 2% to 6%. When dysplasia is present, however, the malignant potential is much higher.  The bottom line is that colorectal surveillance by colonoscopy is essential. Colon cancer surveillance and screening have been shown to reduce colorectal cancer (CRC) incidence by approximately 50% to 90%. This dramatic reduction is achieved primarily because colonoscopy allows direct detection and removal of precancerous polyps before cancer development.  To discuss this important topic in more detail, particularly focussing on large colonic polyp management, we are joined by Dr Ali Eqbal. Ali has expertise in advanced colonic interventional endoscopy and inflammatory bowel disease. He completed a two-year advanced endoscopy fellowship at King's College Hospital, London, where he developed expertise in the diagnosis and management of complex colonic polyps using techniques including endoscopic submucosal dissection (ESD) and endoscopic mucosal resection (EMR). He also undertook a clinical research fellowship in complex IBD at the Austin Hospital in Melbourne. He is widely respected and recognised for his advanced technical skills and commitment to minimally invasive treatment options. He has published and presented both nationally and internationally.  Please welcome Ali to the podcast.  References  Dr Ali Eqbal, www.gihealth.com.au  GESA   National Center for Biotechnology Information (NCBI). Colonic Polyps. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK430761/  PubMed Central

In the preceding episode with Dr Peverelle, we reviewed pharmacologic approaches to obesity management. In this episode, we review an alternative approach to bariatric surgery referred to as Endobariatrics. These are endoscopic interventions sitting between lifestyle-pharmacotherapy and bariatric surgery and are suited for patients with BMI’s between 30-40 kg/m2 who don’t want surgery or are not surgical candidates.  The main interventions include:  Intragastric balloons, which are temporary devices associated with 10-15% weight loss. Endoscopic sleeve gastroplasty, reducing gastric volume with 15-20% efficacy and currently the preferred Endo Bariatrics technique. Duodenal mucosal resurfacing and duodenal-jejunal bypass liners. To discuss these options with us in more detail, please welcome back Dr Matthew Peverelle. Matthew is a gastroenterologist who completed his advanced training in gastroenterology at Monash Health and Austin Health, including the Victorian Liver Transplant Unit. Matthew went on to complete a hepatology fellowship at the prestigious Kings College Hospital in London and has developed a strong interest in both hepatology, luminal gastroenterology and Endobariatrics. Thank you for joining us as he brings his expertise to the podcast.  References:  Dr Matthew PeverelleEndoscopic Weight Loss Options, Danse & Jirapinyo. Endocrinol Metab Clin N Am 54 (2025) 149-162 https://pubmed.ncbi.nlm.nih.gov/39919871/ Endoscopic Bariatrics: Current Therapies and Future Directions. Reja et al. Transl Gastroenterol Hepatol. 2022 Apr 25; 7: 21. pmc.ncbi.nih.gov Outcomes of Endoscopic Sleeve Gastroplasty: A Systematic Review. Vargas et al. Medicina. 2025 Oct 11; 61(10): 1821 https://www.mdpi.com/1648-9144/61/10/1821

Australians who are either overweight or obese are increasingly turning to pharmacological approaches coupled with dietary measures to achieve their weight loss goals before considering bariatric surgery. These therapies are typically considered for adults whose BMI’s are equal or above 30 kg/m2 or above 27 kg/m2 with associated comorbidities and include the following: Incretin based therapies including dual incretin agonists (most effective) Appetite suppressants-central acting drugs Dopaminergic/opioid pathway modulation therapies Nutrient absorption inhibition therapies The most effective pharmacologic treatments available in clinical use are synthetic incretins. Natural incretins are gut derived hormones released after eating that enhance pancreatic insulin secretion in a glucose dependent manner. Examples in clinical use include: Exenatide (Byetta, a synthetic version of a peptide found in the saliva of the Gila monster lizard), Semaglutide (Ozempic-approved for type 2 diabetes, Wegovy-approved for weight loss with dosing up to 2.4mg per weekly dosing), Liraglutide (Saxenda with daily dosing). Another well-known GLP-1 is Dulaglutide (Trulicity). When applied for weight loss Semaglutide and Liraglutide lead to 10-15% body weight reduction. Benefits beyond diabetes and weight loss include a 30% reduction in the risk of heart attacks and strokes. These drugs also show promise in treating conditions such as fatty liver disease, obstructive sleep apnoea, and kidney disease. Side effects include nausea, vomiting, diarrhoea, gallstones and pancreatitis (0.2-0.3 % in most studies). They are contraindicated in patients with medullary thyroid cancer. Another incretin in clinical practice is Gastric Inhibitory Polypeptide (GIP) also known as Glucose Dependent Insulinotropic polypeptide. Like the GLP-1 incretin, GIP also stimulates insulin release in a glucose-dependent way, though it was first named for its weaker ability to inhibit stomach acid. The synthetic so called “twincretin” or dual action incretin called Tirzepatide combines GIP and GLP-1 agonist actions and further increases weight loss outcomes. Marketed as Mounjaro, clinical trials demonstrate it producing 20-22% weight loss for patients. Discontinuation rates for patients using incretin therapies for weight loss is quoted between 50-75 % in one year with factors including expense and side effects influencing this statistic. Recent data also points to significant weight regain over a two-year period after medication withdrawal. The centrally acting appetite suppressants include Phentermine which is a sympathomimetic noradrenergic agent used short term over weeks-months and increases noradrenaline and dopamine in the hypothalamus to reduce appetite. These therapies can expect an 8-12 % weight loss. Naltrexone combined with Bupropion acts on the POMC neurons reducing appetite and food cravings. Nausea, seizure activity and hypertension are side effects for a quoted 5-9 % weight loss. Orlistat is a gastrointestinal fat absorption inhibitor inhibiting pancreatic lipase and decreasing fat absorption by about 30 %. Steatorrhea and loss of fat-soluble vitamins are side effects for only 3-5 % weight loss. To discuss the application of these therapies in more depth we are joined by gastroenterologist Dr Matthew Peverelle. Matthew completed his advanced training in gastroenterology at Monash Health and Austin Health including the Victorian Liver Transplant Unit. He then continued his studies abroad completing a hepatology fellowship at the prestigious Kings College Hospital in London, subsequently he has developed a strong interest in both hepatology, luminal gastroenterology and Endo bariatrics. Thank you for joining us as he brings his expertise to the next two podcast episodes. References:  Matthew Peverelle Australian Family Physician, Pharmacotherapy for obesity, Lee & Dixon Vol 46,7, July 2017 Niddk.nih.gov Obesity Evidence HubObesitymedicine.org Pmc.ncbi.nlm.nih.gov

Medical cybercrime refers to criminal activities involving cyber-attacks on healthcare systems, devices and data. These attacks can range from ransomware and data breaches to the exploitation of vulnerabilities in medical devices, posing serious threats to patient safety, data privacy and the stability of healthcare operations. According to the Office of the Australian Information Commissioner in 2023, the healthcare industry tops the list for cyber-attacks. Healthcare became the most reported non-government sector for cybercrime incidents in FY2023–24 with more attacks than financial services, education and other critical infrastructure industries, highlighting its vulnerability, further ransomware attacks targeting the Australian health sector are growing. Highlighting this point 41% of healthcare organisations in Australia experienced a cyber-attack in 2023. This marks a significant rise in the targeting of this critical sector with a 71% year on year increase in global cyber-attacks targeting healthcare organisations. 32% of healthcare cyber incidents involved compromised accounts or credentials, others included malware infections (17%) and compromised network infrastructure (12%). Patients are also concerned, in one survey 82% of Australians indicated they were worried about unauthorised access to personal health records and consider health information security when choosing healthcare providers. 33% said they were “very to extremely worried” about the security of their health information. In December 2022, Medibank, the Australian health insurance giant, was the victim of a major data breach, affecting the personal details of 9.7 million customers. The attack was believed to be linked to a well-known ransomware group based in Russia, the REvil ransomware gang. Eastern Health an operator of 4 Melbourne hospitals subsequently fell victim to a cyberattack causing certain elective surgeries to be postponed at the time. Another notable incident targeted Melbourne Heart Group. Reinforcing these concerns tech giant Microsoft has also stated that the healthcare sector (and aligned industries) is one of the top targets for cyber criminals. Types of Medical Cybercrime include: Ransomware Attacks: These attacks encrypt a healthcare organisation's data, demanding a ransom for its release, potentially disrupting critical services and delaying patient care. Data Breaches: Cybercriminals may steal sensitive patient information, including medical records, financial data, and personal details, for various malicious purposes. Medical Device Exploitation: Vulnerabilities in connected medical devices, such as pacemakers or insulin pumps, can be exploited to compromise patient safety or disrupt treatment. Supply Chain Attacks: Cybercriminals may target the healthcare organisation's supply chain, compromising vendors or partners to gain access to the primary target. Phishing Attacks: These attacks involve tricking individuals into revealing sensitive information or installing malware, often through deceptive emails or websites. Social Engineering: Attackers use psychological manipulation to gain access to systems or information. Impact of medical cybercrime on patient safety, data privacy, financial losses, operational disruptions and erosion of trust cannot be overstated. To explore and discuss this topic in more detail we are joined on this podcast by both Dave Vosnakes and Stephanie Way from The Australian Government National Office of Cybersecurity who provide an expert overview of the growing problem. Please welcome them to the podcast. References: Office of the Australian Information CommissionerAct Now. Stay SecureAustralian Signals Directorate

It is now increasingly recognised that women’s health care needs at menopause have been both under-recognised and under-treated by medical practitioners, and that menopause management has not been emphasised adequately in graduate and post-graduate education. Considering that half the world’s population spend about a third of their lives after menopause, this unmet need must be recognised and addressed. I was curious to explore this subject in greater detail and welcome the opportunity to review some basic science and definitions. Menopause, also known as the climacteric, is the time when menstrual periods permanently stop, marking the end of the reproductive stage for females. It is often defined as having occurred when a woman has not had any menstrual bleeding for a year. Perimenopause is the natural stage in a woman’s life occurring before the final menstrual period, or menopause, when a woman's body transitions away from its reproductive years. Based on these criteria, perimenopause starts when there are persistent differences in cycle length of seven or more days between consecutive cycles and continues until 12 months after the last menstrual period. During this time, the ovaries gradually become less functional, leading to changes in menstrual cycles and potential infertility. Perimenopause is a time when risk factors for chronic disease need to be considered, including acceleration of bone loss, increase in cardiovascular risk arising from adverse changes in lipids and altered glucose metabolism. Cancer screening programs, including bowel, breast, and cervical cancer should also be discussed with patients at this time. Medical treatment of perimenopause and menopause is aimed at ameliorating symptoms and to prevent bone loss and is centred on the use of menopausal hormone therapy (MHT) with replacement of oestrogens either alone, in the case of previous hysterectomy, or combined with progesterone when the uterus is present. Many of the concerns about MHT raised by older studies are no longer considered barriers to its use in healthy women. The risks arise around discussions of breast cancer, uterine cancer and cardiovascular disease including thromboembolic events and strokes. For cardiovascular disease the evidence pertaining to MHT risk relates to timing and the use of oral rather than transdermal oestrogen. If oral or transdermal oestrogen therapy is initiated within 10 years or earlier since menopause or less than age 60 years, there may be a slightly reduced coronary heart disease risk. With this background I would like to introduce Dr Sugandha Kumar. Dr Kumar is an Obstetrician and Gynaecologist committed to providing comprehensive women’s health care in the south-eastern suburbs of Melbourne. Sugandha did her early specialist training at a prestigious medical institute in India (PGIMER, Chandigarh) and completed her advance training in Obstetrics and Gynaecology in Australia (Monash and Eastern Health). She holds specialist appointments at Box Hill Hospital and has a strong focus on improving outcomes for her patients by offering up-to-date and evidence-based treatment options. She provides obstetric and gynaecological and is expert in advanced laparoscopic surgery including laparoscopic hysterectomy and endometriosis surgery as well as having specialist interest in menopausal hormone therapy. Please welcome Sugandha to the podcast which we will present in two parts. References: Dr Sugandha Kumar : Create Fertility: ⁠www.createfertility.com.au⁠ ⁠https://www.thelancet.com/series/menopause⁠ Swan Study: JAMA 2015;175:531–39

It is now increasingly recognised that women’s health care needs at menopause have been both under-recognised and under-treated by medical practitioners, and that menopause management has not been emphasised adequately in graduate and post-graduate education. Considering that half the world’s population spend about a third of their lives after menopause, this unmet need must be recognised and addressed. I was curious to explore this subject in greater detail and welcome the opportunity to review some basic science and definitions. Menopause, also known as the climacteric, is the time when menstrual periods permanently stop, marking the end of the reproductive stage for females. It is often defined as having occurred when a woman has not had any menstrual bleeding for a year. Perimenopause is the natural stage in a woman’s life occurring before the final menstrual period, or menopause, when a woman's body transitions away from its reproductive years. Based on these criteria, perimenopause starts when there are persistent differences in cycle length of seven or more days between consecutive cycles and continues until 12 months after the last menstrual period. During this time, the ovaries gradually become less functional, leading to changes in menstrual cycles and potential infertility. Perimenopause is a time when risk factors for chronic disease need to be considered, including acceleration of bone loss, increase in cardiovascular risk arising from adverse changes in lipids and altered glucose metabolism. Cancer screening programs, including bowel, breast, and cervical cancer should also be discussed with patients at this time. Medical treatment of perimenopause and menopause is aimed at ameliorating symptoms and to prevent bone loss and is centred on the use of menopausal hormone therapy (MHT) with replacement of oestrogens either alone, in the case of previous hysterectomy, or combined with progesterone when the uterus is present. Many of the concerns about MHT raised by older studies are no longer considered barriers to its use in healthy women. The risks arise around discussions of breast cancer, uterine cancer and cardiovascular disease including thromboembolic events and strokes. For cardiovascular disease the evidence pertaining to MHT risk relates to timing and the use of oral rather than transdermal oestrogen. If oral or transdermal oestrogen therapy is initiated within 10 years or earlier since menopause or less than age 60 years, there may be a slightly reduced coronary heart disease risk. With this background I would like to introduce Dr Sugandha Kumar. Dr Kumar is an Obstetrician and Gynaecologist committed to providing comprehensive women’s health care in the south-eastern suburbs of Melbourne. Sugandha did her early specialist training at a prestigious medical institute in India (PGIMER, Chandigarh) and completed her advance training in Obstetrics and Gynaecology in Australia (Monash and Eastern Health). She holds specialist appointments at Box Hill Hospital and has a strong focus on improving outcomes for her patients by offering up-to-date and evidence-based treatment options. She provides obstetric and gynaecological and is expert in advanced laparoscopic surgery including laparoscopic hysterectomy and endometriosis surgery as well as having specialist interest in menopausal hormone therapy. Please welcome Sugandha to the podcast which we will present in two parts. References: Dr Sugandha Kumar : Create Fertility: www.createfertility.com.au https://www.thelancet.com/series/menopause Swan Study : JAMA 2015;175:531–39

Australians in their 30s and 40s are experiencing unprecedented rates of at least 10 different cancers. Between the year 2000 and 2024, for 30- to 39-year-olds, early onset prostate cancer increased by 500%, pancreatic cancer by 200%, liver cancer by 150%, uterine cancer by 138%, and kidney cancer by 85%. Australia is a world leader when it comes to bowel cancer and, again since the year 2000, the rate of bowel cancer in 30- to 39-year-olds has increased by 173%, and the stage the cancer is at when diagnosed is often advanced. DNA mutations in young onset colorectal cancer are very specific, including those involving mismatch repair genes and the P53 tumour suppressor gene, suggesting particular factors or exposures might be implicated. Although the cause for young onset cancer is not known, experts believe environmental toxin exposures maybe interacting with specific vulnerable genes to cause malignant changes. A person with nonvulnerable genes exposed to the same toxin would be unaffected. The Human Exposome Project is documenting and studying these exposures and encompasses environmental factors as well as lifestyle and their connections and interactions in an attempt to explain the causes of different diseases. Other factors considered relevant to the increased onset of young cancers may include: Childhood obesity and increasing obesity in young adults Alteration of the microbiome through antibiotic use and eating ultra processed foods, as well as through caesarean section. Being borne by caesarean section could result in the acquisition of a microbiome different to those born vaginally. Interestingly, E coli colonisation of the colon at an early age may be relevant in this respect by way of exposure to colibactin, a potentially mutagenic bacterial toxin produced by E coli. Microplastic exposure including polychlorinated biphenyls (PCB’s) and poly fluroalkyl substances (PFAS), which are found in nonstick cookware, food packaging and some cosmetics. These have been referred to as “forever chemicals” because of their very long environmental persistence. Thinking about this emerging problem, I was curious to learn more about the trending incidence and to seek advice regarding how we should be counselling our patients regarding appropriate recommendations for the age of entry to cancer screening programmes. It was a very special honour to have Prof Keefe from Cancer Australia accept my invitation to be a guest on the Podcast. Prof Keefe is the CEO of Cancer Australia and an honorary Clinical Professor in the School of Medicine at the University of Adelaide. She has enjoyed an illustrious career as a Medical Oncologist and Professor of Cancer Medicine and has a special interest and expertise in gastrointestinal toxicity of cancer treatment, supportive care in cancer, and both medical leadership and health reform. Her pedigree of publications, awards and commendations is enviable and her commitment to improving cancer outcomes through her clinical work, professorship and role at Cancer Australia is exceptional. I am so pleased we can welcome her to the podcast. References Professor Dorothy Keefe. researchers.adelaide.edu.auCancer Australia. www.canceraustralia.gov.auWhy Is Early Onset Cancer on the Rise? National Cancer Institute. Cancer.govEarly-Onset Cancer. canceraustralia.gov.auThe Alarming Rise of Early-Onset Colorectal Cancer. Markey, Srinath. www1.racgp.org.auThe Latest Research on Why So Many Young Adults Are Getting Cancer. Piersol. mskcc.orgDr Norman Swan, ABC. (July 7th, 2025)

A pandemic is defined as a new disease or new strain of an existing disease spreading worldwide. An ‘outbreak’ refers to a localised epidemic – something that affects hundreds, sometimes thousands; an ‘epidemic’ refers to an illness or infection that is in excess of normal, and ‘pandemic’ is an epidemic that occurs over a very wide area, crosses international boundaries, and touches thousands or millions. The enormous health and financial impacts of epidemics and pandemics are made worse through human foibles like fear, denial, panic, complacency, hubris, and self-interest. Experts advise we can end epidemics by facing up to them and by applying concrete actions ensuring, building resilient health systems, fortifying 3 lines of defence against disease including prevention detection and response, and ensuring timely and accurate communication, investing in smart innovation and spending wisely to prevent disease before an epidemic strikes. Pandemics have far reaching effects as we have recently witnessed with Covid -19, and I was curious to reflect on the way we responded to this threat as a community from the psychological perspective. Humans have had to respond to many pandemics over the course of recoded history, notably the so-called black plagues or black death spread by rats carrying yersinia pestis infected fleas hidden within their pelt. A series of black death pandemics dramatically and profoundly affected European and Middle Eastern populations both in the 6–8th century plague of Justinian and 14th–19th century, killing up to half the local population (over 100 million people), but paradoxically bringing about cultural and economic renewal. Before this was a deadly smallpox pandemic called the Antonine Plague during the time of Marcus Aurelius around 160–180 AD, killing an estimated 25–30 % of the Roman population and no doubt far more through Eurasia (between and 5 and 20 million). In the 16 th century between 1545 and 1548, the so called Cocoliztli epidemic in Mexico and Central America, caused by an unidentified pathogen, reportedly killed 5–15 million. Fast forward to 1918 – Spanish Flu caused by influenza H1N1 with between 17–100 million dead, the HIV epidemic responsible for approximately 44 million deaths with fortunately treatments now available, and not forgetting bird flu and swine flu, our most recent pandemic experience with Covid 19 claiming 7–36 million lives. When I came across Dr Robert Kaplans excellent article in the May edition of the GUT REPUBLIC discussing pandemics and the often-flawed human response where fear, emotion and disinformation easily crowd perspective, I was keen to invite him to talk on this subject on Everyday Medicine. Rob is a forensic psychiatrist and clinical associate professor at Western Sydney University, as well as a keen historian and author with a sharp wit and eye for the arcane. His latest book is The King who Strangled his Psychiatrist and Other Dark Tales, but he also has a deep catalogue of publishing including the books Medical Murder: Disturbing tales Of Doctors Who Kill and The Exceptional Brain and How It Changed the World amongst others. He is a sort after speaker and key thinker in forensic psychiatry and serves on the Professional Advisory Panel Victim’s Services. Please welcome Rob to the Podcast. References Dr Robert Kaplan: www. rkaplan.com.au The End Of Epidemics. Dr Jonathan D Quick. Scribe Publications 2018The Little Book of History. www.dk.com Wikipedia

Memory is the cognitive process of acquiring, storing and retrieving information. It's the mind's ability to encode, store and recall experiences and knowledge, allowing for learning, adaptation, and the formation of personal identity. There are different types of memory, including short-term memory, where information is held briefly and long-term memory, where information is held for extended periods. There is sensory memory where information relating to senses such as sight, sound and smell are retained, explicit memory recalling memories or facts and events and implicit memory that influences our behaviour without conscious awareness; for example, like riding a bike or driving your car. Memory storage involves multiple brain regions, but the hippocampus is crucial for forming new memories, especially long-term memories and acts as a gateway for encoding and consolidating memories. The cerebral cortex and prefrontal cortex also participate in memory storage and retrieval. Without memory, our enjoyment of life’s wonderful pleasures and diversity is severely compromised. Unfortunately, memory loss is also a key feature of dementia and is often cited as an early clinical marker of cognitive decline in a patient who is starting to have difficulty coping with the complexity of life, their medication schedule, shopping lists and daily tasks. I was curious to understand how we may improve and maintain our own memories whilst also providing advice in terms of exercises that may benefit our patients coping with early cognitive decline. The history of memory recall starts in Greece with Simonides of Ceos in ~500 BC. Simonides is credited with developing the ‘method of loci’ or ‘room method ‘of memory recall after an earthquake collapsed the roof at a banquet he had just attended, killing all inside. Relying on his visual memory, he was able to accurately identify the corpses by precisely recalling their seating arrangements as he had noticed them while he was reciting poetry to the guests. This method, now popularised by many teaching memory techniques, highlights the value of linking things we need to remember together to enhance their recall. It is also interesting that memory for music and songs is often retained until late in cognitive decline. In an attempt to explore the ideas behind the complex subject of memory in more detail, it was an honour to have Dr Natalie Grima accept an invitation for the podcast. Natalie is a clinical neuropsychologist based in Melbourne and the founder of Neuro Psychological Counselling Australia. She is a senior clinical neuropsychologist at Monash Health and has published widely, completing her doctorate at Monash University and undertaking advanced clinical training at Harvard Medical School. Natalie has a special interest in the diagnosis of dementia, psychiatric conditions and cognitive rehabilitation following acquired brain injuries. She also has an expert knowledge on the subject of memory. Please welcome her to the podcast. References: Dr Natalie Grima: www.neuropychconsulting.com.au https://mocacognition.com/ Simonides of Ceos-Wikipedia

Obesity has reached crisis levels in Australia, with 67% of Australians classified as being overweight or obese (2022 data). BMI measurements have been used in epidemiological studies to define overweight individuals with a measurement of 25 kilograms per metre squared and obese individuals with a BMI measurement of more than 30 kilograms per metre squared. It is now recognised, however, that BMI-based measures of obesity may both underestimate or overestimate adiposity and provide inadequate information about health at the individual level and subsequently undermine medically sound approaches to healthcare and policy. A recent Commission of 58 experts in this field reported a consensus in The Lancet defining obesity as "a condition characterised by excess adiposity, with or without abnormal distribution or function of adipose tissue and with causes that are multifactorial and still incompletely understood". They subsequently teased out the diagnosis of obesity to include preclinical and clinical definitions, where: Pre-clinical obesity is defined by excess fat accumulation as measured by direct means with DEXA or indirect anthropometric measurements such as waist to height, waist circumference or waist to hip ratio measurement. This group of patients have no clinical disease or end-organ damage or symptoms as yet, but an increased risk of developing clinical obesity and conditions such as type 2 diabetes, cardiovascular disease and some neoplasms. The treatment focus in this group includes counselling and the introduction of measures to prevent progression to the next subgroup, which is clinical obesity. Clinical Obesity is defined as a chronic, systemic illness characterised by alterations in the function of tissues, organs, the entire individual, or a combination thereof, due to excess adiposity. Clinical obesity can lead to severe end-organ damage, causing life-altering and potentially life-threatening complications. The main focus of management for this cohort is to improve end-organ dysfunction as a priority rather than to focus on weight loss alone. Treatment options include lifestyle modification through diet and counselling, and rely on established pharmacology such as GLP-1 receptor agonists, which are likely to be used as a long-term treatment strategy. For a select number of patients, however, these medications can induce nausea, vomiting, diarrhoea, constipation and reflux. In more serious cases gastro paresis and pancreatitis are described. Non-responsiveness and high cost may be a limiting factor amongst some patients. Consequently, surgery remains the cornerstone for safely and effectively managing obesity and includes both gastric sleeve and bypass operations. To discuss this new definition of obesity and approach to thinking about obesity, as well as to review surgical options, I was curious to open a discussion with Dr Melissa Beitner. Melissa is a fellow of The Royal Australasian College of Surgeons; she is American Board of Surgery certified, a fellow of the American Society of Metabolic and Bariatric Surgery and is a diplomat of the American Board of Obesity Medicine. Melissa is incredibly well credentialed, having undertaken bariatric surgery fellowships at Mount Sinai Hospital in New York, Royal Brisbane and Women's Hospital and St. George Hospital, Sydney. She has special areas of interest in bariatric surgery and obesity medicine, and is also highly skilled in hiatus hernia and anti-reflux surgery, cholecystectomy and general surgical removal of lumps and bumps. Please welcome Meissa to the podcast. References:  Dr Beitner, Weight Loss Solutions: www.360surgery.com.au Definition and Diagnostic Criteria of Clinical Obesity, F Rubino et al. The Lancet Diabetes and Endocrinology Commission. Vol 13, Issue 3, P221-262, March 2025

Molecular pathology combines molecular analysis with traditional morphology and immunohistochemistry to understand disease at its most fundamental level. The field continues to evolve as new discoveries enter clinical practice. Through molecular pathology, our knowledge of genetic mutations and targeted therapies has expanded. It is now rare for a tumour report to omit genetic findings. This discipline, while distant from daily clinical work, underpins treatment algorithms and prognostic models. The ten hallmarks of cancer include: genome instability and mutation, resistance to cell death, sustained proliferative signalling, evasion of growth suppressors, replicative immortality, angiogenesis, invasion and metastasis, altered metabolism, tumour-promoting inflammation, and immune evasion. Normal DNA contains proto-oncogenes that promote growth and tumour suppressor genes that restrain it. When balanced, they regulate healthy proliferation. Mutations in either disturb this balance, driving uncontrolled growth. Germline mutations are inherited and present in every cell, while somatic mutations are acquired, often influenced by smoking, ultraviolet exposure, or diet. When proto-oncogenes mutate, they become oncogenes. The RAS and BRAF oncogenes are key in molecular pathology. RAS controls upstream signalling that triggers cell growth, differentiation, and survival. Mutated RAS genes cause constant activation, leading to excessive signalling. The three RAS genes, HRAS, KRAS, and NRAS, are found in 20 to 25 percent of all human tumours and in 90 percent of pancreatic cancers. The BRAF gene, on chromosome 7, regulates downstream signalling and cell growth. BRAF mutations occur in about 10 percent of colorectal cancers, up to 50 percent of papillary thyroid cancers, and 27 to 67 percent of melanomas. Other oncogenes include MYC, EGFR, and HER2. HER2 amplification is seen in some breast and ovarian cancers. These findings are vital as targeted treatments, such as JAK inhibitors and monoclonal antibodies, act on these pathways. A single mutation can activate an oncogene. Tumour suppressor genes perform repair functions including correcting DNA mismatches, regulating the cell cycle, and promoting apoptosis. As telomeres shorten with age, mismatch repair errors increase. Mutated genes lose this ability, causing abnormal protein synthesis. Reports often describe mismatch repair proficient (no mutation) or mismatch repair deficient (mutation present), particularly in colon cancer. Key tumour suppressor genes include BRCA1, BRCA2, and the Lynch syndrome genes MLH1, MSH2, MSH6, and PMS2. When mutated, they increase the risk of breast, ovarian, prostate, colon, uterine, and pancreatic cancers. While often inherited, mutations can also arise spontaneously or through epigenetic silencing. Each gene has two copies; both must be affected before suppression is lost. This two-hit hypothesis, proposed by Knudson in 1971, explains tumour development with ageing. Methylation, sometimes noted in reports, refers to chemical modification of CpG (cytosine-phosphate-guanine) sites within a gene, often influenced by epigenetic factors. Abnormal methylation disrupts DNA repair, leading to failed tumour suppression. This is a brief overview of a complex and evolving field. Joining me is Dr Pranav Dorwal, Molecular and Anatomical Pathologist at Monash Health, also working in Diagnostic Genomics. Dr Dorwal is an examiner for molecular pathology, researcher, and author of over 60 publications. He has held positions at MD Anderson Cancer Center (Houston, USA) and Memorial Sloan Kettering Cancer Center (New York, USA), completed a fellowship at ANU Canberra, and received the Chancellor’s Gold Medal for Clinical Pathology. Please welcome Dr Pranav Dorwal to the podcast. References: Dr Pranav Dorwal – www.monashhealth.org | www.genomicdiagnostics.com.auOncology at a Glance, Graham Dark, Wiley-Blackwellwww.pmc.ncbi.nlm.nih.gov

Each year in Australia, there are about 1,800 new diagnoses of ovarian cancer and over 1,000 deaths, making ovarian cancer the fifth most common cause of death from cancer in women. The lifetime risk is about 1.6%, increasing to 5% if a first-degree relative is affected, and 45% and 25% respectively if the BRCA1 or BRCA2 mutation is present. The median age of diagnosis is 63 years, with two-thirds of patients diagnosed at 55 years or older. Histologically, tumour cells may arise from the outer epithelial lining cells of the ovary (60%), the germ cells (30%), or sex cord stromal cells (8%). Epithelial tumours of the high-grade serous type are now thought to spread to the ovarian surface after arising from secretory cells at the fimbria of the fallopian tubes, acquiring a TP53 mutation there before metastasising to the ovary as clinically evident ovarian cancer. Serous carcinomas represent the vast majority of primary malignant ovarian tumours (75%–80%) and are composed of columnar cells with cilia. These tumours are subdivided into high-grade and low-grade serous carcinomas, which has particular relevance for BRCA-associated ovarian tumours. As with many internal diseases, clinical presentation may be late, with vague pelvic discomfort giving way to pain and bloating, followed by more systemic symptoms as the disease advances. The tumour marker CA 125 may only be elevated 50% of the time in early disease, rising to 80% in advanced cancer; however, false positives may occur with benign ovarian disease, leiomyomas, and endometriosis. As with tumour markers used in the follow-up of other cancers, its utility in screening and early diagnosis is limited. The disease is advanced in 75% of cases at the time of diagnosis. Five-year survival is about 41% when local spread is detected, reducing to 30% or less with distant metastases, compared to 89% survival or above with early detection when the disease is localised. Given the importance of this condition, I was curious to consult Professor Thomas Jobling once more on current practices of surveillance, approaches to detection and management, and how to manage risk in first-degree relatives. How should we approach an ovarian cyst found incidentally during abdominal imaging? What symptoms should we, as clinicians, be mindful of in triggering our suspicion to investigate further? I know you will find this conversation with Professor Thomas Jobling interesting. Tom is a gynaecological oncologist, ex-AFL footballer, and medical researcher with a highly respected reputation in Melbourne and internationally. He has extensive experience with minimally invasive surgery, including robotic surgery, for gynaecologic cancer. His main research area is ovarian cancer, for which he received an Order of Australia Medal in 2017, and he is currently Head of Gynaecological Health and VMO at Peter MacCallum Hospital. Please welcome Professor Jobling to the podcast. References: Professor Tom Jobling: [email protected] Ovarian Cancer: Cancer Australia Pathobiology of Ovarian Carcinomas, Chinese Journal of Cancer, 2016 Jan; 34 Ovarian Cancer Research Alliance: https://ocrahope.org/