Friday, 15 December 2017

YOU contain multitudes!

Bacteria have lived on our planet longer than any other being by billions of years.  They have evolved during this time to live in some of the most inhospitable environments imaginable and continue to evolve as the planet changes.  They are to be equally admired and feared, and they will ultimately outlive all other living beings.  Throughout history bacteria have claimed more lives than all of the world wars combined and simultaneously (an often in an unrecognized manner) facilitated better health for most humans on the planet.  Think about it, how many deadly ailments are bacterial in nature?  Leprosy, tuberculosis, malaria, cholera, meningococcal disease, typhoid fever, tetanus, botulisim, listeriosis, bubonic plague, necrotizing fasciitis, Legionnaires' disease, scarlet fever, dysentry, bacterial pneumonia...the list goes on.  It's no surprise that during the 1950s and 1960s tremendous effort was invested in the development of antibiotics.  This 'antibiotic era' is responsible for some of our best defenses against harmful bacteria which include glycopeptides (ex. vancomycin), tetracyclines (ex. sumycin), macrolides (ex. erythromycin), polymyxins (ex. neosporin), β-lactams (ex. methicillin), etc. yet bacteria continue to evolve and adapt.  On the heels of the antibiotic era was the era of antibiotic resistance - we currently battle some of the most evolved pathogenic beings including MRSA (methicillin-resistant staphylococcus aureus), VRSA (vancomycin-resistant staphylococcus aureus) and even instances of chlostridium difficile infections for which no known antibiotic is effective.

So is it all doom and gloom when it comes to bacteria?  Far from it - these little guys are also responsible for helping us live happy and healthy lives, and you are covered in them! In fact, the average human has ten times as many bacterial cells in and around their body than human cells which make up the body.  The largest concentration of bacteria in the human body is found in the digestive track, second only to the skin.  The past decade has brought about an increased appreciation for the microbes within us as study after study links our gut microbiota with a variety of ailments.  Huge movements to eat more bacteria in an effort to increase our microbiome diversity has brought foods like kimchi, sauerkraut and kombucha (all having been used for hundreds of years by a variety of cultures for their digestive health benefits) from the 'oriental' isle at the grocery store to the main display.  And, of course, if you put the phrase 'improves gut health' onto almost any product you can expect customers to pay at least two to three times its actual worth.  Go look in any drug store - you will be overwhelmed by the number of supplements containing a zillion strains of utterly unpronounceable bacteria all claiming to provide some benefit.  However, the question remains: how much do we (this is a collective we, including scientists) truely understand about the precise role of bacteria in the pathophysiology of disease?

This is one of the questions frequently brought up when discussing whether or not the FDA should play a role in the marketing and administration of probiotic supplements.  A recent policy piece in Science summarized the state of affairs with respect to the role the FDA could play in the probiotic supplement industry, and it really boils down to how you define 'probiotic supplement.'  Is it a food or is it a drug?  Is it sold with the intention of supporting gut health or influencing a disease state?  It is certainly a challenging question to answer, and most likely one which will not be answered anytime soon.  Research into this area is still in the 'information gathering' phase.  So what do we know so far and how can we make positive changes to promote our gut health with this limited information?

1.  We need both probiotics and prebiotics to support our gut microbiome.  The probiotics are the 'good' bacteria - we need a variety of bacterial strains in a variety of ratios for optimum gut health.  Everybody and everybody will have a different probiotic profile which fits them the best, and this profile likely changes over the course of life.  For optimum support of your own personal microbiome, you need to feed these little guys!  This is where prebiotics come into play.  Prebiotics are food sources on which the probiotics feed and YOU are responsible for feeding them the right sorts of foods.  Examples of prebiotics include garlic, oats, onions, asparagus, leeks, flaxseeds, bananas, cocoa, etc.

2.  Consistency is KEY! The most significant time for microbiome development is during birth, when an otherwise sterile and undisturbed environment is introduced to the world and its microbes.  After this event, especially as significant spans of time pass, the established microbiome becomes much more challenging to shift.  There is not a 'one-size-fits-all' microbiome fix in a pill which can be taken daily to fix a gut-related problem.  To truely influence your gut microbiome, diet and lifestyle modifications are a must!  A plant-based diet (not necessarily excluding meat!) supplemented with lots of probiotic rich foods (think greek yogurt, kefir, kombucha, kimchi, tempeh...) adopted consistently as part of a reduced-stress and moderately active lifestyle is the best thing you can do for your gut!

3.  This process takes time - don't expect to immediately feel like your younger, care-free self in 24 hours.  Explore new foods, keep a food and feeling diary, go outside and play, incorporate relaxation techniques and indulge in treats every once in awhile!  Look back after a few months and then compare how you generally feel.  This is an inside job.

4.  To further get to know your gut microbiome, pick up a copy of I Contain Multitudes by Ed Yong.  Your multitudes will thank you!

Friday, 28 April 2017

Could a silent virus trigger celiac disease? Scientists say...maybe...

The gluten-free lifestyle has moved from relative obscurity to mainstream use.  For most individuals, a gluten-free diet will be a passing obsession (although one which may result in increased attention to what is in food - which is a very good result) but for those with celiac disease it is a welcome societal movement.  Celiac disease is an autoimmune condition which presents with gastrointestinal distress (pain, bloating, cramping), steatorrhea/diarrhea and malabsorption.  Sounds a bit like IBS, right?  Many of the clinical symptoms of celiac disease and IBS are identical, making a true celiac disease diagnosis challenging for both patient and practitioner.  A person with true celiac disease has a specific and measurable autoimmune response to the ingestion of dietary gluten.  IBS symptoms are often non-specific (i.e. varying severity, length, location, etc.) and worsen with a virety of triggers (gluten may be a trigger for IBS symptoms, but other dietary (lactose, soy, fructose) and lifestyle factors (chronic stress) influence this condition).  Fortunately, diagnostic tests for celiac disease are becoming more common and often begin with a simple blood analysis - unfortunately, however, IBS has not lent itself to reliable diagnostic measures.  Several specific criteria are used to confirm a diagnosis of celiac disease, although every body and everybody is different: 

1) HLA-DQA1 or HLA-DQB1 gene variants (this is very important - if you do not have the 'celiac gene mutation' you do not have celiac disease; non-celiac gluten sensitivity is a related condition which does not invoke a true autoimmune response but has been described as a gluten-related inflammatory response)
2) Elevated antibody levels (tTG, IgA, IgG - these are the 'gluten antibodies' which can be quantified in the blood and used as a diagnostic marker for the autoimmune condition)
4) Vitamin A, D, E and K deficiencies (fat-soluble vitamins are less readily absorbed due to intestinal damage)
5) Damaged (atrophied) intestinal lining confirmed by small bowel biopsy
6) Environmental trigger resulting in decetable immune response

Common factors 1-5 are easily tested for and confirmed by a gastrointestinal specialist - most of them are quantifiable and/or visually informative.  The 'environmental trigger' aspect of celiac disease (6 listed above) has remained the most elusive requirement for disease onset.  How do we even know that an environmental trigger is important?   Scientists agree that environmental risk factors are likely to be a cause of consideration based (so far...) purely on statistics.  Celiac disease occurs globally in 1 out of 100 people.  However, only 3-4% of individuals who carry the HLA-DQA1 or HLA-DQB1 gene variants ever develop celiac disease - what happens or does not happen to the other 96-97% who never progress?  These values are reported in a recent study published in Science which reports the first experimental observation of celiac disease onset after exposure to a known environmental trigger.  Their study, titled 'Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease' describes a controlled experiment in which genetically susceptible mice, living on a gluten-containing diet but showing no clinically diagnostic celiac disease symptoms, are exposed to a known reovirus.  Onset of celiac disease after viral exposure was confirmed by a measurable increase in immune response pathways, specifically those which promote the production of T-cells (immune cells) which specifically respond to the gluten antigen.  This particular immune response pathway is triggered by HLA-DQ2 and HLA-DQ8 molecules, which are coded for by the HLA-DQA1 or HLA-DQB1 gene variants.  

So, the mice had these genes and consumed a gluten-containing diet but did not show signs of celiac disease prior to viral exposure.  What this study shows is that the externally applied environmental factor (the reovirus - which is avirulent and causes no 'viral symptoms') has 'turned on' the mutated gene (just like a ligh switch).  When the gene variant is 'turned off,' it is still there but it is not physiologically active, whereas when the gene is 'turned on' downstream physiological changes have been shown induce disease progression.  Now, would the mice have eventually developed celiac disease if they had not been exposed to the reovirus?  Maybe.  Would they have developed celiac disease from some other environmental trigger?  Maybe.  What this study provides is only one piece of the enormous jigsaw puzzle describing celiac disease - and most of the pieces are still scrambled in the box!  There are likely thousands of additional environmental triggers which influence disease progression, and not every genetically susceptible individual who encounters a reovirus will go on to develop celiac disease.  However, direct demonstration and observation of environmentally triggered change in gene expression promoting the development of celiac disease is a HUGE step towards understanding the complicated relationship between food and the immune system.  I'll raise a glass of (gluten-free) beer to that!

Monday, 10 April 2017

Spotlight on Anthera and AzurRx for next-generation PERT

The impact of FDA-approved pancreatic enzyme replacements cannot be overstated.  In fact, the World Health Organization (WHO) includes pancreatic enzymes on the 'Model List of Essential Medicines' for both adults and children.  These 'living' lists are assessed and updated every two years to identify the 'minimum medicine needs for a basic health care system, listing the most efficacious, safe and cost effective medicines for priority conditions.'  For many, especially those with cystic fibrosis or living without a pancreas, replacement enzymes are lifesaving and life-sustaining.

Research into next-generation replacement enzymes seeks to improve upon current challenges for those who use PERTs in whatever capacity - from supportive care, such as in mild to moderate pancreatic insufficiency, to life-long dependency.  Amongst the concerns of those either making (R&D sector) or taking (patients) replacement enzymes are:
  • Dosing consistency/individualized dosing - there is no one size fits all method for prescribing enzymes (especially when there are three types of enzyme in each pill!), most individuals on pancreatic enzymes benefit most from the lipase
  • Enzyme source - due to personal or religious reasons, enzymes derived from pigs is not an available dietary addition
  • Side effects - bloating, gas, stomach pain, diarrhea, constipation and nausea are all listed as side effects for replacement enzymes at normal dosing regimes; although rare, long-standing enzyme overdose can lead to a condition called fibrosing colonopathy
  • Additional required medication - it is very common to co-prescribe a proton pump inhibitor alongside replacement enzymes to regulate gastric pH (and these come with their own list of side effects!)
Two up-and-coming biotech companies are slowly gaining attention in the PERT community and market.  Their research is addressing several of the challenges listed above and is made possible by the smallest of creatures - bacteria and yeast!

Anthera Pharmaceuticals is a small biotech company in California focusing on a next-generation  pancreatic enzyme replacement therapy which aims to reduce patient pill burdenThe most common ways for PERTs to fail is patient non-compliance, fundamentally forgetting to take enzymes prior to every meal and snack.  This often means taking up to 6 pills 4-5 times per day, every day, to ensure therapeutic benefit.  One way to reduce the quantity of daily pills is to improve the quality of the enzymes in each pill.  The proprietary enzyme blend in Anthera's Sollpura drug candidate is biologically engineered (this means made from a biological organism such as a bacteria - no pigs involved!) and features crystalline and cross-linked enzymes.  Crystallization and cross-linking bring stability to the enzyme molecules, ensuring that low gastric pH and the presence/absence of bile salts do no effect their availability.  In addition, Sollpura has been formulated into both a tablet and sachet (water-soluble!) form, the later being particularly attractive for pediatric cystic fibrosis patients with pancreatic insufficiency.   The Sollpura formulations are currently in two clinical trials.   

AzurRx BioPharma is a publically traded biopharmaceutical company working in the areas of gastrointestinal and microbiome-related disorders and diseases.  Their drug candidate, MS1819 lipase is currently in phase IIa clinical trials (to profile the safety and efficacy in comparison with currently available PERTs).  As the name suggests, this produce is either a lipase-only enzyme capsule or one which features a significant percentage of lipase with respect to amylase and protease.  As described on their website, although amylases and proteases are produced alongside lipases in the pancreas, only supplementation of the lipase is thought to be necessary for treatment of EPI.  In fact, proteases in currently approved PERTs have been implicated in the cause of fibrosing colonopathy, a rare but very serious side effect of taking replacement enzymes.  Looking to the microscopic world for answers, MS1819 lipase has also been biologically engineered - but this time from yeast rather than bacteria!  Yes, the same microorganisms which serve us by fermenting wheat to make bread, grapes to make wine and hops to make beer have been engineered to produce highly potent and stable lipases for treating EPI.    

Anthera and AzurRx are just two of a growing number of biopharmaceutical companies approaching pancreatic enzyme improvements using non-traditional (biological) methods.  The use of microorganisms such as bacteria, yeast and algae for the production of valuable materials including antibiotics (many of which are also on the WHO's Model List of Essential Medicines), food and even crude oil demonstrates the viability and influence of biologically-derived products.  A biological approach to enzyme production may provide not only a renewable and reliable method for enzyme production (with the potential to tailor enzymes on an individual basis) but may help alleviate the burden we place on animal-derived healthcare products.

Wednesday, 8 March 2017

PERT - Pancreatic Enzyme Replacement Therapy

So what is the deal with all of these enzymes?  There are loads out there - you are very likely to find at least 20 different plant-derived enzymes at your local health food store.  Many are coupled with a cocktail of probiotics and additional nutritional support, labeled with the words vegan, vegetarian and all natural to distinguish them from their porcine-derived cousins.  Many individuals report very positive results from taking these enzymes and probiotics, but the jury is still out as to whether this is a quantifiable test or another well documented case of the placebo effect (which is not bad, by the way - I once recovered from an aggressive bout of bronchitis only after a reluctantly written prescription for the world's weakest and most ineffective antibiotic, just the thought of having medicinal help improved my health almost overnight...).  Certainly a combination of digestive enzymes and probiotics never hurt anyone and in fact, a little digestive help is always appreciated.

The enzymes and probiotics you find in the store are different to those available by prescription - in quite a number of ways!  The first and most obvious difference is the requirement for a prescription (or not), meaning the FDA has become involved.  I was astonished to learn that the first FDA approval for porcine-derived pancreatic enzyme replacement therapy was in 2009!  Until 1991, replacement enzymes sailed along on the free market - and there were loads of them.  Inconsistencies in formulation and quality, resulting in adverse side effects, eventually caught the attention of the FDA.  As of 2012, there are only six FDA-approved replacement pancreatic enzyme formulations:  Creon, Zenpep, Pancreaze, Ultresa, Viokace and Pertyze.

A second, and equally obvious difference between store bought enzymes and prescription enzymes is the price ($$!!).  In order to be approved for use in chronic disease (such as Cystic Fibrosis), pharmaceutical companies must formulate a supplement which delivers the appropriate enzymes in the appropriate amounts at the appropriate time.  This is no small feat.  The internal environment which the supplements must withstand before reaching the duodenum is severe - the pH of stomach acid is between 1 and 3.  Your gastric acid, which can be destructive to other tissues such as your esophagus and intestines,  provides a massive service for the rest of the body.  Not only does it help to break down complex proteins in food (a low pH value is required for this!) but it also serves as a primary defense against bacteria and viruses.  Not many lifeforms can withstand the stomach acid, but one common exception, helicobacter pylori, has been linked to a variety of gastric ailments.  The enzyme supplements therefore must hold up against this acid - many lipases (which help with fat breakdown) are irreversibly deactivated by stomach acid.  This is why replacement enzymes are often prescribed with a proton pump inhibitor (PPI) to help raise gastric pH to the 3 or 4 level.  The price you or your insurance pays towards replacement enzymes is not driven by the enzymes themselves but by the protective (enteric) coating required to ensure proper enzyme concentration in the duodenum.  In addition to completely protected tablet formulation, each tablet contains enzymes which are further encapsulated in microspheres or microbeads.  More enzyme protection means more background R&D which is supplemented by the price of their product.

One final difference between store bought and prescription enzymes is the enzyme source.  Most (but not necessarily all) over the counter digestive enzymes are plant derived.  Prescription enzymes are solely porcine-derived, meaning that there are currently no FDA-approved pancreatic enzymes which are harvested from anything other than pigs.  Why pigs?  It turns out that pigs are a very close model for humans in many ways, including their pancreatic enzyme composition.  Animal-derived enzymes and molecules are commonly used in the production of food and medical therapies.  For example, rennet is a collection of enzymes produced by cows which is used for making cheese.  The commonly prescribed blood thinner Heparin is also derived from cows - although formulations of Heparin may be prepared from other farm livestock, the FDA approved and regulated Heparin is solely bovine-produced.  Porcine and bovine derived products have been deemed safe and effective for human use, but they pose a problem for select groups of people including those allergic to pork or those who do not consume pork or porcine-derived products.  Recently, a few small biopharmaceutical companies have taken up the challenge and have demonstrated production of digestive enymes from yeast (AzurRx MS1819 in phase II clinical trials) and bacteria (Anthera's Sollpura studies).  Although Anthera's bacterially-derived enzymes failed to show improvement over currently available therapies (which meant clinical trial failure), interest in non-porcine derived enzymes has hit the drug development pipeline!

Your enzyme prescription and therapy response rate depend on a number of factors, including diet and lifestyle, weight, underlying condition and often preference of your GI doctor or insurance.  Under dosing can lead to further pancreatic problems including fibrosis and calcifications while over dosing burdens the colon and can result in fibrosing colonopathy.  It is therefore imperative that patients are open and honest with physicians about symptoms (even if the tought of saying them out loud makes you super uncomfortable!) and be diligent about taking the prescribed dosage with meals.  Know that a lot of research hours and intense investigation, along with scrutiny, accompany your tablets to ensure you are safe and experience only minimal side effects.  It feels daunting at first, taking several pills every time you eat, but the payoff is (hopefully) symptom-free dining and enjoyable living!

Thursday, 23 February 2017

All that glitters is gold!

Malfunction and disease of the pancreas almost inevitably leads to questions about pancreatic cancer.  Does a family history of pancreatic cancer increase the odds that pancreatitis may lead to cancer?  If I develop EPI, will I also develop diabetes and ultimately pancreatic cancer?  What if I already have both diabetes and EPI, am I twice as likely to develop pancreatic cancer?  Five times as likely?  The short answer: We don't really know.  Nobody can predict with perfect accuracy whether or not a cancerous state will develop from a set of symptoms or conditions.  And the problem with statistics is that 80% are made up on the spot ;)  Everybody and every body is unique and comes with a unique set of circumstances including family history, environment, diet and lifestyleFear develops from missing explanations and answers which lead to uncertainties about future prognoses and life expectency. 

What, in part, makes pancreatic cancer so terrifying and ultimately devastating is its relatively calm early stages coupled with a lack of routine testing for high risk populations.  In general, the beginning phases of pancreatic cancer do not present with any defined diagnostic characteristics.  No pain, no swelling, no palpable lumps and bumps, etc.  And again, due to the location of the pancreas (tucked nicely behind the stomach), even if there were palpable masses we would not always be able to assess them.  Imaging techniques in the form of MRI, ultrasound and CT scans have come a very long way in terms of resolution and diagnostic success.  However, early stages of pancreatic cancer (stages I and II) are often not distinguishable because of the organs and bones which envelop the pancreas and distort visualization of the fine structure (think about looking at a flower through a window full of fingerprints, you can see its a flower but can you count how many pedals it has?).  Therefore, pancreatic cancer is most commonly diagnosed in its most advanced stage (stage III), excluding options such as surgical removal or preventative care.  Stage III indicates a systemic disease, typically extending beyond the confines of this tiny gland.

The fear of pancreatic cancer, even when your 'chances' seem low, is justified and not simply misplaced anxiety.  But rest as easily as possible, because cancer research is one of the government's top funding priorities (President Obama signed the 21st Cenury Cures Act in 2015 - hopefully this will not be affected by current legislation) and a recent research report demonstrates a specific advancement in the detection of early stage pancreatic cancer using a simple blood test.  Don't run to the doctor yet, this test is still in the 'proof of concept' phase, but a few major advantages of this test include low cost (relative to similar tests), short processing time, high accuracy and small sample volume.  We are talking a sample volume comparable to having your finger pricked for a blood glucose test...just a drop!  

The components which make up our blood provide a microscopic view of our overall health.  A metabolic blood panel measures values of vitamins and minerals and our bodies absorb from food and supplements; a complete blood count measures the quantity and quality of red and white blood cells; our blood glucose level is measured by a blood test; the list goes on.  Our organs and body systems use circulating blood to send out signaling molecules (known as extracellular vessicles) which help keep all of the processes which occur in the body in sync.  If you were able to listen to the blood it would sound like a crowded stadium after the victory touchdown - loud and indecipherable.  A research group from Arizona State University has developed a method which selectively 'amplifies' the presence extracellular vessicles sent out from pancreatic cancer cells (like turning up the mic at a concert).  Using their technique, even when relatively few pancreatic cancer derived extracellular vessicles are in circulation (such as in the very early stages of disease), visualization of the signaling molecules provides support for a rapid and early diagnosis.  The visualization of the cells occurs with the help of gold nanoparticles, conveniently tagged with a targeting antibody that binds to a specific overexpressed surface protein on the cancer derived vessicle.  Think about a puzzle piece which only has one match out of millions of possibilities - that's how well designed the antibody/antigen for this test is.  With the gold nanoparticles attached (two separate nanoparticles - one nanosphere and one nanorod) each tagged cell will light up - mapping out the presence and quantity of pancreatic cancer derived cells in the blood.  This is almost like intercepting a secret message reading its contents in order to prevent further damage - think of Alan Turing breaking the enigma code 

Blood tests for cancer markers are certainly not new technology, nor is the use of gold nanoparticles as diagnostic tools.  However, this demonstrated use of gold nanoparticles allows for the possibility of a routine screening method for high risk populations, whether through family history or isolated pancreatic diseaseWith all forms of cancer and illness, early detection is key, and with pancreatic cancer, may mean the difference between 5 years and 50 years.  That's a lot of life to be lived.

Friday, 17 February 2017

A split personality

The pancreas is a small pear shaped gland which hides behind the stomach, sneakily out of view and reach for physical exams and routine imaging.  A fully functional pancreas performs an immense service to the body by aiding digestion and regulating blood glucose levels.  These two broad functions have led to two pancreatic 'personalities' ('exocrine pancreas' and the 'endocrine pancreas') based on excretion from the pancreas through a duct (exocrine) or the bloodstream (endocrine).  Pancreatic malfunction may be isolated to the exocrine pancreas or endocrine pancreas individually or may manifest as complete pancreatic disease (both endocrine and exocrine insufficiency).  Luckily, the exocrine pancreas and endocrine pancreas do not work alone - a variety of other glands and organs participate in your exocrine and endocrine systems.  Keeping everything in check can become a challenge when one or the other pancreatic functions is compromised.

The exocrine pancreas works in collaboration with the stomach, small intestine, liver and large intestine (in addition to other organs and processes occuring simultaneously) to break down the fats, carbohydrates, sugars and proteins consumed through food and drink.  The role of the pancreas in this process is twofold: to neutralize stomach acid by excreting a basic bicarbonate solution and supply your intestines with digestive enzymes used to break down components of foods.  For example, lipase produced by acinar cells in the pancreas acts by cleaving lipid bonds in triglycerides to make fatty acids.  Our bodies can more readily absorb these fatty acids and use them in a variety of metabolic pathways, most notably in the regulation of inflammation.  The exocrine pancreas also produces and excretes amylases and proteases to break down carbohydrates and proteins, respectively.  Quite a heavy burden on one single gland, making its malfunction all the more significant.  Exocrine pancreatic insufficiency (EPI) is a digestive condition in which, for a variety of reasons, the pancreas is either not able to produce or not able to excrete the bicarbonate and enzymes required for complete food digestion.  EPI is not a disease of its own, but a symptom often recognized too late for preventative treatment.  The clinical presentation of EPI (postprandial epigastric pain and steatorrhea) does not develop until over 90% of pancreatic enzyme output is lost.  In the meantime, as the acinar cells slowly succumb to damage and cease enzyme production, the remaining organs and glands in the exocrine system make up the deficit (our bodies have incredible reserve capacities!).  A few examples:  salivary amylase (made in the mouth) begins the is initial breakdown of starches as you chew and gastric lipase (made in the stomach) facilitates lipid hydrolysis.  These enzymes differ to those produced by the pancreas and offer only partial resemblance to the role pancreatic enzymes play in digestion.  Treatment regimes for EPI include a low fat diet (max. 20g of fat with no supplemental enzymes) or what is known as PERT - Pancreatic Enzyme Replacement Therapy.  Future posts will discuss the pros and cons of PERT and what products are on the market for EPI treatment.

The endocrine pancreas is a whole different ballgame, and one which enjoys attention from the media as well as the medical community.  The body's relationship with the endocrine pancreas is the key to management of types I and II diabetes (T1D and T2D, respectively).  In addition to the production of digestive enzymes (from the exocrine pancreas), the endocrine pancreas is responsible for the production and distribution of insulin.  Insulin is a hormone, made by islet cells in the pancreas, which regulates metabolism - specifically regarding blood glucose levels - every second of every minute of every hour of every day.  Even when you sleep.  Whilst the exocrine pancreas takes a break between meals, the endocrine pancreas works around the clock to keep you feeling at your best.  Malfunction of the endocrine pancreas is termed 'diabetes,' of which types I and II are the most common (gestational diabetes describes a third type, which occurs rarely during the later stages of pregnancy).  Type I diabetes is an autoimmune disorder in which the islet cells in the pancreas are attacked by the immune system and produce little to no insulin.  Those who have T1D are required to constantly monitor their blood glucose levels and dose with synthetic insulin to control hormone balance - every second of every minute of every hour of every day.  Even when they sleep.  Type II diabetes occurs when the body becomes resistent to insulin, for example, when sugar consumption prompts a constantly high blood glucose level.  The endocrine pancreas is not able to supply the correct amount of hormone to bring these levels back down and the misuse of insulin becomes systemic.  T2D is more common than T1D, and its occurence is growing at a rapid rate as we tend toward to more heavily processed and sugar filled diet.  A variety of management techniques for T2D have been reported, and the condition is reversible, meaning that diet and lifestyle modifications have significant influence on the severity of symptoms - good news!

The pancreas, although hidden deep in the abdominal cavity, has huge influences on our daily lives.  Its dual personality dictates what we are able to eat, which can be challenging in a society which is very food-centric.  But being food driven is not bad.  We find commonality, culture and enjoyment out of food - as we should!  Taking care of your pancreas involves knowing your limits, specifically with respect to alcohol and fast foods, and giving your system a break when requested.  The next time you enjoy a burger, savor the moment and thank your pancreas for the help!