How is Fatty Liver related to Excess Fructose in Diet Intake?

Fatty liver is an extremely common condition that affects 20-30% of all adults. Fatty liver is usually diagnosed on an ultrasound scan of the liver. The liver tests in the blood may or may not be abnormal. Individuals of any age can be affected including young children and adolescents. Most individuals do not have specific symptoms and majority of individuals are often reassured by their doctors of the benign nature of the disease. A certain type of fatty liver is related to excess consumption, but the more common one, which is known as non-alcoholic fatty liver disease or NAFLD affects people who do not drink or drink very little alcohol. Such individuals may have only fatty liver or more commonly suffer from diabetes, high blood pressure, and high cholesterol and triglycerides.

The increasing prevalence of fatty liver is generally linked to overnutrition and sedentary lifestyle. It may be intuitive to believe that a high fat diet can lead to fatty liver; however recent research has highlighted the role of excess carbohydrates in our diet as the cause of fatty liver. Carbohydrates are generally the sweet substances in our diet such as table sugar, fruits, juices, carbonated drinks, candies and related food items. Among the sugars, it is one particular type called fructose that has been found to be most damaging to the liver. Fructose is a simple sugar present in fruits and honey. Table sugar (sucrose) also contain fructose. High fructose corn syrup (HFCS) is a sweetener used in many canned foods. Fructose intake has increased remarkably in the last century and currently it constitutes about 15% of total calorie intake of a typical western diet with higher intakes amongst younger individuals and adolescents.

Non-alcoholic fatty liver disease or NAFLD is strongly related to a condition called metabolic syndrome in which affected individuals are overweight and have diabetes or pre-diabetes, high blood pressure, and elevated triglyceride levels in the blood. An affected individual may actually not be quite overweight; instead he or she may just have a large belly or have what is known as abdominal obesity. This form of obesity is extremely common in Asians and Middle Eastern people.

Scientific studies both in animals and humans have shown that a fructose in diet irrespective of other sugars and fats independently is associated with increased fat accumulation in the liver. It has been shown that it takes about 8-24 weeks on a high fructose diet to develop fatty liver. High fructose intake is also associated with development of high blood pressure and elevation of triglycerides in blood, both of which are components of metabolic syndrome. It has even been shown in studies that despite taking a low calorie diet, an individual can still develop fatty liver if the fructose content of diet is high. Another interesting fact is that diabetics who have high blood glucose levels convert the excess glucose to fructose in their liver and this fructose then damages the liver. There are good observational studies that individuals with high intake of sugar sweetened beverage drinks  have a higher prevalence of fatty liver. This is alarming because NAFLD is now the most common chronic liver disease in adolescents and this may be related to increased use of sweetened beverages in this age group.

The question that comes up is whether fruits also bad for liver since fruit sugar is actually fructose. Whole fruits are less likely to induce metabolic syndrome because of the lower fructose content per fruit (compared to a soft drink) and because they also contain constituents (flavonols, epicatechin, vitamin C, and other antioxidants) that may combat the effects of fructose.

It has been shown further that a diet rich in fats along with fructose is even more damaging to the liver. Similarly excess glucose intake is also converted in the body to fructose. A high salt diet has also been shown to exacerbate fructose induced liver damage.

Fatty liver is of two types. The first type is simple fatty liver, also known as NAFL (non-alcoholic fatty liver). NAFL does not usually progress to more advanced forms of liver disease. The second type of fatty liver is known as NASH (non-alcoholic steatohepatitis). NASH is the progressive form of fatty liver and leads to liver fibrosis and eventually to end stage liver disease or cirrhosis. Excess dietary fructose has been associated with NASH. Diabetes is also associated with NASH.

In summary, there has been a marked rise in sugar and high fructose corn syrup (HFCS) intake that has paralleled the rise of fatty liver disease. Experimentally, the fructose component of sugar and HFCS appears to have a major role in inducing fatty liver by both stimulating fat accumulation and inducing liver damage (inflammation). Clinically the intake of sugar sweetened beverages is strongly linked with NAFLD. Reducing sugar or HFCS intake may have major benefits for patients with fatty liver and specially those suffering from the advanced form of fatty liver known as NASH. While whole fruits can be consumed in good proportions, use of sweetened fruit juices, carbonated sweet beverages and food containing HFCS should be curtailed as much as possible. Special emphasis should be given to the fast food diet of children that is rich in fats and sweetened beverages.

Dr. Kaiser Raja (author) is a Senior Consultant in Liver Diseases and Transplantation associated with the Integrated Liver Care Program of the Aster DM Healthcare Group. He is available for consultation in Aster CMI Hospital, Bangalore, Aster Hospital, Mankhool, Dubai and Aster Medical Centre, Hamdan Street, Abu Dhabi.

Laparoscopic Whipple’s Pancreaticoduodenectomy – My take on it !

Family of Shantha a sixty year old lady was devastated when she was diagnosed to have a pancreatic head tumor. Fortunately, on CT scans she had an early tumor with no evidence of spread elsewhere. Although medically found fit, the complex nature of operation – ‘Whipple Procedure’, possible complications and possibility of prolonged stay provided little comfort. She was referred to me and after careful scrutiny of her reports I suggested a laparoscopic (key hole surgery) Whipple procedure. The course of stay in hospital, undergoing laparoscopic Whipple Procedure came as a pleasant surprise for the patient and family who were feared at the outset about the formidable nature of the operation. She recovered well and was discharged from the hospital on the sixth postoperative day.

The goals of lesser pain, shorter hospital stay and early return to productivity have inspired the believers in minimal access surgery to extend the horizons of laparoscopic surgery. The line between extending the benefits of laparoscopic surgery and questionable advantages with this approach is difficult to draw in complex procedures because of the lack of extensive peer reviewed literature as in the case of ‘laparoscopic Whipple Pancreaticoduodenectomy (LPD).

In a recent surgical meeting a senior surgeon commented that ‘the true benefit for patients with minimal access surgery is when the morbidity with the incision (surgical cut) is obviously more than that of the excision’. The corollary would be that there is less benefit in procedures where the morbidity of excision is more than that of the incision as with LPD.

Till a decade before my work in laparoscopy was limited to removal of a gall bladder, appendix, fundoplication or occasionally a spleen. However, with increasing experience and a desire to extend the benefits of key hole surgery to patients undergoing other gastrointestinal procedures I spent several hours training on the endo-trainer, spent several hours with experts in the country and abroad, on several occasions had the good fortune to join in for operations with them. By the year 2008, most of my foregut (food pipe, stomach) and colorectal work was laparoscopic. The collective experience from having done distal gastric resections, common duct explorations, distal pancreatic resections, choledochal cyst excisions and hepaticojejunostomies and proximal jejunal resections gave me the confidence to proceed to performing my first LPD in 2010.

I have been very selective about patients chosen for LPD selecting mainly with periampullary tumors or cystic neoplasms of pancreas. Patients with serious comorbidities, carcinoma head, previous upper abdominal surgery were excluded. Also in the initial two years patients with an aberrant or replaced right hepatic artery were excluded. To put things in perspective out of forty odd Whipple procedures in the last three years fourteen were done laparoscopically. In the first five the resection and part of reconstruction (hepaticojejunostomy) were completed laparoscopically, the specimen retrieval was done through a 8 cm midepigastric incision. Pancreaticojejunostomy and gastrojejunostomy were completed through this minilaparotomy. In the remaining the entire procedure was completed laparoscopically and specimen was retrieved through a small Pfannenstiel incision. Overall, twenty five percent of patients had morbidity. Although, I need to look at my data critically comparing short term and long term outcomes with the open and the laparoscopic approach, with LPD, I did see most patients recovering faster, having lesser pain, having fewer wound complications and starting adjuvant treatment earlier. In the subgroup of patients with LPD experiencing major morbidity such as bleeding or a Grade B or Grade C pancreatic fistula this benefit was clearly absent. Considering major morbidity was seen in 25% of patients, it would be safe to say that seven out of ten patients undergoing a LPD would have better short term outcomes than the open approach.

LPD is technically feasible for a surgeon with advanced laparoscopic skills with team work from assistant surgeons, anesthetists, scrub nurses and technicians. Also, the procedure requires high definition laparoscopic camera, HD monitors, vessel sealing devices and endostaplers. I am sure with increasing experience, improving technology more centres would adopt LPD as standard of practice in the near future.

Dr G Srikanth, MCh is a Senior GI, HPB & Advanced Laparoscopic Surgeon from Bangalore, Managing Director of Sahasra Hospitals and Visiting Surgeon at Gleneagles Global Hospital, Bangalore. He is certified Consultant Surgeon by Dubai Health Authority (DHA), Offering services at Medeor Hospital 24/7 and Aster Hospital, Dubai.

Ulcerative Colitis – drugs, scope or scalpel

Geetha (name changed) was suffering from ulcerative colitis for nearly eight years. She responded well to medical treatment for the initial five years but had frequent relapses of the disease since.

She had been on prolonged course of mesalamine, steroids, immune modulator drugs, Humira etc. Despite best efforts to control the disease with medications, she needed frequent hospital visits and her symptoms of loose stools with blood continued unabated.  A senior medical gastroenterologist for surgery referred her after best efforts to treat her with all available medical options failed. Her quality of life was seriously compromised and she was in tears during her first out patient consultation for surgery. After two sessions of detailed counseling regarding surgery and preoperative evaluation she underwent a ‘restorative procto-colectomy’ a procedure wherein the entire large intestine was removed and a reservoir (pouch) for stool was constructed from the last one foot of small intestine and connected to the anal canal. The operation removed the entire diseased portion and the pouch performs the function of the large intestine. She made a smooth recovery from surgery and three months after surgery she is glad that her normal life is restored.  The most satisfying part for her was that the operation was performed laparoscopically (key hole) and she made a much faster recovery than she expected.

Surgery is required in about ten percent of patients with Ulcerative colitis. The clear indications for surgery would be

• Non-responders to medical treatment
• Need for prolonged steroids and related complications
• Complications of disease – intestinal obstruction, perforation, development of cancer
• Precursor of cancer detected during long term screening (one out of ten patients with ulcerative colitis stands the risk of developing cancer in the large intestine)

Patients fear surgery for several reasons and the foremost concern with this operation is the perceived need to have a permanent stoma (motion outlet from abdomen wall). Current surgical treatment avoids need for a permanent stoma in nearly all patients. In the last decade I have been performing this entire operation laparoscopically giving the advantages of lesser pain and early recovery, and this has increased the acceptance of the operation by patients, Dr Srikanth said. A temporary stoma may be required for few weeks during recovery from surgery. Risks from surgery are comprehensively evaluated during preoperative workup of patients.

Ulcerative Colitis – At a glance

• Typical symptoms would be loose stools with mucus and blood. Fever, weakness, decreased appetite, joint pains, etc may be present in 15-20% patients
• Diagnosis is established by colonoscopy and biopsy
• Majority (90 %)of patients can be treated with medical therapy and avoid surgery
• Patients not responding to medical therapy or requiring steroids for longer than six months and/or complications of the disease and medications, must have an expert surgical consultation
• Surgical expertise is not available in many centres in the city under one roof. This may cause delay in referral with persistent medical treatment with steroids, immune modulators, the prolonged use of which can have serious side effects and drains the patient of their finances to the extent that they are left in a hopeless situation and in no position to explore the surgical option.