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    • #1332
      Karina Athwal

      Help with 64 year old male client who simply cannot shift weight
      This client came to see me seeking advice to help with weight loss and fatty liver. He also suffered with sleep apnea and plantar facilitis and leg cramps.

      Health history in short:

      • Healthy child
      • Teenage years: started to put on weight and became chubby
      • 20s: Took up sports and became very fit and slim
      • 30s: Generally fine, busy life with children and running a business.
      • 40s: Ran marathon, but started to put on weight again.
      • 50s: Biking accident, fractured hip and no longer able to exercise. Put one more weight. Diagnosed with fatty liver. Suffer sleep apnea.
      • 60s: 2 hip replacements – one due to old injury, the other as a consequence of uneven wear. Put on more weight to reach 16 ½ stone. Developed joint pains, generalised. Had colonoscopy due to changed bowel habits.; diagnosed with diverticulosis. Bowels now fine. Developed plantar facilitis.
      He was already taking magnesium (450mg), turmeric, adrenal support (Core Level Adrenal, Nutri West) and vitamin C when he came to see me.


      He has now followed a GF/DF low carb, moderate protein and reasonably high fat diet eating no grains at all and engaging in intermittent fasting 18-24h twice per week. He portion sizes are appropriate. No snacking between meals, he drinks no alcohol. He participates in moderate exercise mainly as gardening and gentle cycling, but recently also going to the gym.

      He lost 1 ½ stone over 2 months and his bilirubin fell from an initial 31umol/L to 24umol/L whilst his plasma ALT fell from 83IU/L to 40IU/L. His energy and joint pains improved and the plantar facilitis disappeared. His wife reported improvement in his sleep apnea. Supplements included EPA/DHA, choline, magnesium, probiotic and KappArest.

      Even so, he remains stuck at 15st 10lbs and his latest liver results once more showed elevated plasma ALT; 69 and now also a plasma triglyceride level of 2.29mmol/L!


      His diet has remained very clean and I have advised him to increase specific liver foods, ginger, turmeric, onions, garlic, citrus, olive oil, avocado. He eats no sugar, drinks no alcohol. I have advised also on a red meat free diet for a period of time based on the research on NEU5GC and associations with Hashimoto’s. He exercises 3 times per week at the gym for one hour – 20 minutes cardio training and 40 minutes strength training. He gardens on other days. A repeat thyroid test after 3 months showed no change in autoantibodies. Questioning on environmental toxic exposure has not flagged any particular concerns, although he does have mercury fillings. We are planning also to do the adrenal profile again.

      Any advice or ideas to help this client further would be much appreciated.

      Posted By Karina Athwal 8/11/17




    • #1333
      Christine Bailey

      Dear Karina

      Many thanks for your question regarding your client who is now finding it difficult to shift additional weight although I note the improvements he has already experienced following you advice.  In view of the recent liver results I wonder if more attention needs to be given to his liver health and insulin sensitivity which may in turn assist with weight loss.

      I also agree with you that this client may benefit from a more plant based diet and one that includes plenty of soluble and insoluble fibre with care not to include foods that may aggravate the diverticulosis such as seeds and pips etc.  Fatty liver disease has multiple interrelated causes. Primary mechanisms include obesity leading to steadily increasing insulin resistance coupled with an overabundance of circulating fatty acids. These factors fuel one another in a destructive cycle. Together with advanced glycation end-products (AGEs), these events lead to increased oxidant stress and ultimately inflammation, cell death, and fibrous destruction of liver tissue

      Younossi ZM. Review article: current management of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Aliment Pharmacol Ther. 2008 Jul;28(1):2-12. http://tinyurl.com/y7m8r3fl


      An overload of fatty acids and abnormal lipid profiles factor so heavily in the onset of NAFLD that they’re now referred to as “lipotoxicity” because of the ways they directly poison liver tissue

      Musso G, Gambino R, Cassader M. Nonalcoholic fatty liver disease from pathogenesis to management: an update. Obes Rev. 2010 Jun;11(6):430-45. http://tinyurl.com/ydbz422l


      And as fat builds inside liver cells, they begin churning out a storm of fat-related cytokines known as adipokines, which fan the inflammatory flames of the metabolic syndrome and NAFLD

      Polyzos SA, Kountouras J, Zavos C, Tsiaousi E. The role of adiponectin in the pathogenesis and treatment of nonalcoholic fatty liver disease. Diabetes Obes Metab. 2010 May;12(5):365-83. http://tinyurl.com/y8om3jfc


      Ongoing inflammation aggravates the body’s ability to utilise insulin which in turn could make it difficult to lose weight.  Of particular relevance is the amount of fructose in the diet. Fructose promotes formation of new fat molecules in the liver, blocks breakdown of existing fats, stimulates free radical production, and promotes insulin resistance. An increasing number of studies are linking increased fructose consumption with NAFLD, and even with its deadlier consequence, non-alcoholic steatohepatitis (NASH)

      Keeping fruit to a minimum and limiting to low fructose fruit, no fruit juices, smoothies, squash etc would therefore be appropriate

      Abdelmalek MF, Suzuki A, Guy C, et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. Hepatology. 2010 Jun;51(6):1961-71. http://tinyurl.com/y882h6xu


      One of the most effective interventions to consider is vitamin E. One study provided the first evidence that vitamin E can prevent NAFLD before it develops, largely by reducing oxidative stress, inflammation, and liver cell death by apoptosis. Another study demonstrated a vitamin E-related reduction in oxidative damage and tissue levels of the inflammatory mediator TNF-alpha, while beneficially reducing PPAR-gamma activity

      Raso GM, Esposito E, Iacono A, et al. Comparative therapeutic effects of metformin and vitamin E in a model of nonalcoholic steatohepatitis in the young rat. Eur J Pharmacol. 2009 Feb 14;604(1-3):125-31.  http://tinyurl.com/y6wabhfc


      I would also consider the use of fish oil. Increasing the amount of unsaturated fats like omega-3s in cell membranes is associated with improved insulin sensitivity. And supplementation with omega-3 rich fish oil results in activation of the important metabolic sensor, called PPAR-alpha, in liver cells, suppressing production of new fat molecules.

      Omega-3s also contribute to improved insulin sensitivity, a reduction in serum triglycerides, and stimulation of fat utilization in liver tissue and skeletal muscle

      Ukropec J, Reseland JE, Gasperikova D, et al. The hypotriglyceridemic effect of dietary n-3 FA is associated with increased beta-oxidation and reduced leptin expression. Lipids. 2003 Oct;38(10):1023-9.  http://tinyurl.com/yao8l44x

      Larter CZ, Yeh MM, Cheng J, et al. Activation of peroxisome proliferator-activated receptor alpha by dietary fish oil attenuates steatosis, but does not prevent experimental steatohepatitis because of hepatic lipoperoxide accumulation. J Gastroenterol Hepatol. 2008 Feb;23(2):267-75.  http://tinyurl.com/ya785wgp


      A long-term human trial, using 1,000 mg per day of omega-3, revealed significant decreases in serum markers of liver cell damage, triglyceride levels, and fasting glucose. Most impressively, supplemented patients display improvement of their livers’ appearance and blood flow on ultrasound exams, providing graphic evidence of the supplements’ benefits

      In addition, constant exposure to oxidant and toxic stresses makes liver cells especially vulnerable to depletion of glutathione and therefore a supplement such as NAC may be helpful.

      Capanni M, Calella F, Biagini MR, et al. Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with nonalcoholic fatty liver disease: a pilot study. Aliment Pharmacol Ther. 2006 Apr 15;23(8):1143-51. http://tinyurl.com/yaabsovl


      Supporting insulin sensitivity may be also something to consider and watching overall fat intake particularly saturated fat and switching more to oily fish, monounsaturated fat such as olives and avocado would be beneficial.  Clearly if there is a thyroid imbalance and / or adrenal imbalance then this may need specific attention based on test results.


      The following supplements are suggested for you to consider in light of your relevant expertise and intimate understanding of the needs of your client or patient. They may be used in isolation or as part of a multi supplement strategy, but at all times the consideration of their use should be tied into the specific needs of the individual you are responsible for.

      Lowering inflammation

      KappArest (BRC) take 2 with each meal

      Fatty Acids

      EFA-Sirt Supreme (BRC) – take 2 three times daily – http://tinyurl.com/h3czc9x

      Liver health

      NAC Enhanced Antioxidant formula (ARG) take 1 twice daily

      Tocomin SupraBio Tocotrienols (ARG) take 1 twice daily

      Insulin Function

      Glucofit (ARG) take 1 20 minutes before each meal  http://tinyurl.com/gwwkcnk

      Glucobalance (BRC) take 2 with each meal  http://tinyurl.com/jfhvyum

      I hope this helps with your client





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