Following on from my recent barium swallow demonstrating "mild to moderate dysmobility" in my oesophagus along with "tertiary contractions" (causing severe oesophageal spasm and hold up at the junction between the oesophagus and the stomach) I had a "gastroscopy" this week.
Anyway, the results of the Gastroscopy (I had wondered why it was being done, considering I thought that we had a diagnosis via the barium swallow ) were - to me - a bit shocking.
The Gastroenterologist (Dr Peter Evans) came to see me before discharge and I think that he was even outstanded at the results, considering how non-complaining I am.
I saw the pics, which he was sending to Dr Stephen Watson - my original bariatric surgeon who referred me to him following the result of the barium swallow. And, being a non-Gastronterologist, they were ugly. Really ugly.
Anyhoo, results of FYI:
"Findings Oesophagus: There were broad and thin linear reflux ulcers extending 8 cm above the OG junction. The remainder of the oesophageal mucosa appeared normal. The SC/OG junction was located at 35 cm, above a 3 cm hiatus hernia; there was no Barrett's change.
Stomach: The stomach was tubular consistent with sleeve gastrectomy. The fundus, body and antrum were otherwise normal. Duodenum: The cap and the loop were normal. Conclusion: Severe ulcerative oesophagitis.
Coincidentally I had a double appt with my GP this am, and showed her the copy of the report.
She was somewhat gob-smacked as well!
She's commenced me on Pantaprazole 40 mg twice day for 2/51, then to drop back to one daily.
Weight yesterday fasting, naked 48.71 kg, BMI 20.6 (then I went to the loo twice after).
At GP today fully dressed including shoes, 48.5 kg
Very Low Carbohydrate Diets for Diabetes (ADA 2018)
By Maria Muccioli Ph.D.
June 26th, 2018
A crowd overfilled the ballroom this Sunday afternoon at the ADA 78th Scientific Sessions to hear two presentations about very low carbohydrate diets (VLCD) for diabetes.
In the first presentation, Dr. Jeannie Tay from the University of Alabama at Birmingham summarized the current knowledge on VLCD for type 2 diabetes (T2D) patients and presented new clinical trial results. In the second presentation, Dr. Martin I. de Bock of Princess Margaret Hospital discussed the limited data on VLCD for children with type 1 diabetes (T1D), including the benefits, hypothetical concerns, and areas for additional follow-up.
Study Demonstrates Health Benefits for Patients with T2D
Dr. Tay began her presentation by summarizing the available data on very low carbohydrate diets (VLCD) for patients with T2D. She defined VLCD as that containing between 20-70 grams of carbohydrate per day.
She evaluated results from randomized controlled trials (RCTs) that followed patients for at least six months and highlighted that some data showed greater A1c improvements with the approach. The researcher noted that patients also experience an increase in HDL-C levels, a reduction in triglyceride levels, and improved insulin resistance.
Dr. Tay explained that while some studies showed an increase in LDL-C levels in patients following a VLCD, other studies did not find this. She addressed that LDL-C is becoming a controversial metric to assess cardiovascular disease risk and that context is important when discussing its relevance as a risk factor. Dr. Tay noted that it is generally believed that LDL-C increases may be a result of the higher saturated fat content of some VLCD.
Dr. Tay and colleagues set out to determine how a VLCD that is also low in saturated fat (LCLSF) compares against a high carbohydrate (HC) diet for the metabolic management of patients with T2D.
RCT of HC vs. LCLSF Diet for T2D
The researcher enrolled 115 adults with T2D and obesity with a mean A1c level of 7.3 +/- 1.1% and excluded patients with pre-existing renal conditions. The patients used a variety of methods to control their diabetes, including oral agents and/or insulin. They assigned the participants to either follow a HC diet (53% carbohydrate) or a LCLSF diet (14% carbohydrate, <10% saturated fat). Importantly, the diets were identical in calorie content.
All participants followed the same exercise program and their adherence to the diet was closely followed via food logs, regular meetings with a dietician, as well as urinalysis for ketones and urea/creatinine.
The researchers compared numerous parameters between the groups, including weight, body composition, A1c and markers for cardiovascular disease risk. Furthermore, they also used CGM technology to evaluate post-prandial blood glucose control and glycemic variability. The patients were followed for two years.
Main Study Outcomes
The drop-out rate (~50%) was not significantly different between the two groups, and the researchers confirmed that the remaining participants adhered to the prescribed diets.
While the data showed a comparable reduction in A1c (~1%), weight, and similar body composition, the participants in the LCLSF group:
Lowered their medication use by more than two-fold compared to the HC group
Experienced a greater than two-fold reduction in glycemic variability parameters compared to the HC group
Experienced a greater reduction in triglycerides than the HC group
Both groups experienced comparable decreases in blood pressure, insulin use, insulin resistance, and c-reactive protein levels (a marker of inflammation).
The researchers also performed a very comprehensive evaluation of renal function and cognitive performance in the subjects following the low carbohydrate approach. The researchers found no difference between the HC and LCLSF groups in any of the measured outcomes, demonstrating its safety with regard to renal function and cognitive performance.
Also, the researchers did not observe a significant difference in the LDL-C levels between the groups. Notably, the HC group experienced a significant drop in HDL levels during the study, while the HDL levels remained unchanged in the LCLSF group.
Dr. Tay stated that a very low carbohydrate diet offers a considerable advantage over a high carbohydrate approach for patients with type 2 diabetes.
She noted that reducing medication use is not only cost-effective but can also safeguard from the considerable side effects of some second-line medications. She also explained that achieving less glycemic variability, which may be an independent risk factor for the development of diabetes-associated complications, is “of great clinical importance.”
“It is a good diet to have if you have diabetes, and the data support that,” she concluded.
Endocrinologist Discusses Considerations for Children with T1D
Dr. de Bock began his presentation by describing what he believes to be the current political climate in discussing very low carbohydrate (VLC) approaches for children with T1D. “[It is] thorny, polarizing, and controversial,” he remarked. The speaker went on to explain that while he is no way against VLC approaches for children, the main purpose of his presentation was to identify putative concerns and areas that require additional study.
“I am not a denier. One can get exceptional glycemic control on a very low carbohydrate diet,” he stated, also remarking that frequent blood glucose monitoring and dosing adjustments were key to achieving the results.
Dr. de Bock believes that it is also possible to get “good control” on a high carbohydrate diet. To support this, he presented very limited blood glucose records for one teenage patient who consumes more than 300 g of carbohydrate per day, and also showed some data on pediatric A1c levels. Notably, while the A1c levels were below the average for that age group with T1D, they were still above normal.
Dr. de Bock identified five areas that he believes to be of relevance regarding the potential concerns regarding children eating a VLCD: 1) growth; 2) long-term metabolic profile; 3) bones; 4) exercise and 5) psychosocial impact and conflict. As published data specific to VLCD in children with T1D is limited, the speaker presented some data from animal studies, case studies, and children with epilepsy who followed a ketogenic diet.
Dr. de Bock did not define the specific nutrient distribution of VLCD and the data that he presented on varied greatly in the carbohydrate content, from “ketogenic” to “30% carbohydrate” for one particular case.
Since data on the exact diet composition or on glycemic control for the case study subjects that experienced adverse outcomes was not presented, it was impossible to gauge whether these could be attributed to suboptimal glycemic control or the specific macronutrient distribution.
Dr. de Bock stated that the available data on pediatric growth on a low-carb diet is contradicting and requires further investigation. His main theoretical concern is that those on a VLCD may use less insulin, and insulin is very important for numerous physiological processes, including growth. However, he did not discuss the administration of insulin to account for protein consumption, which is an important consideration. Dr. de Bock also addressed the importance of identifying any nutritional deficiencies, in particular, iron.
Long-Term Metabolic Profile
Dr. de Bock presented some data about elevated LDL-C levels in individuals on a VLCD, although the study results were variable. He stated that for those individuals who experience an uptick in LDL-C, it is unclear whether the improved glycemic control mitigates the LDL-C increase. Notably, the LDL-C metric is a controversial one and needs to be considered in the context of triglycerides, HDL, and other metabolic parameters.
Dr. de Bock pointed to some studies on children with epilepsy who followed the ketogenic diet and exhibited low bone density. He noted that individuals with T1D are prone to low bone density, so it is an important parameter to follow. Dr. de Bock did not mention the relevance of optimizing glycemic control, as chronic hyperglycemia is a relevant factor in low bone density in patients with T1D.
The speaker stated that the exercise capacity of children following a VLCD appears to be variable. He noted that some individuals do not have any problems, while others may experience fatigue. He believes the data on the subject is “inconclusive.” Careful assessment of the specific nutrient distribution of the diet to ensure appropriate nutrient intake may be at the heart of the matter.
Psychosocial Impact and Conflict
The speaker focused heavily on the potential mental and emotional implications of following a “restrictive” diet. He suggested that children (unlike adults) do not yet have the “executive thought” to make a rational decision to eat a VLCD. As such, he believes that children on a VLCD may feel deprived or resentful.
“We are a society that celebrates with food,” de Bock pointed out, as a photograph of excited children gathered around a birthday cake appeared on his presentation slide. He stated that eating cake “may or may not result in a postprandial blood glucose excursion,” depending on the management, and did not discuss that low-carbohydrate dessert recipes are widely available.
He also attempted to draw parallels between the perfectionism and idealism associated with the pursuit of very tight glycemic control on a VLCD and how these qualities are common to individuals who are at an increased risk for developing eating disorders. However, while there is no evidence to support that children on a VLCD are specifically at an increased risk for anxiety and eating disorders, there is evidence to suggest that these issues are more common in people with type 1 diabetes, in general, suggesting that they are likely related to glycemic control.
Dr. de Bock did not address the tangible concerns of suboptimal blood glucose management in pediatric patients, or the potential psychological impacts of increased anxiety, depression, and resentment that may arise from frequently abnormal blood glucose levels and the associated physiological consequences.
Dr. de Bock does not deny that a VLCD for children with type 1 diabetes can help to achieve exceptional glycemic control, as recently demonstrated in a study showing normal average A1c levels in a large cohort of patients. The speaker remarked that the patients in that study had very low glycemic variability.
He believes that more research needs to be conducted to evaluate the relevance of the potential concerns that he outlined. Until then, he advises parents of children who follow a VLCD to work closely with their medical care providers to monitor growth, cardiac, nutritional, and mental/emotional parameters.
Undoubtedly, very low carbohydrate diets for the management of diabetes have been gaining popularity and acceptance in recent years. It is difficult to deny that they constitute an effective and important tool for optimizing glycemic control for both type 1 and type 2 diabetes patients.
This symposium received considerable attention at the meeting and in social media channels. As always, we welcome your comments on the topic and hope that this review has been useful in summarizing the key points and relevant considerations in the broader context of the discussion.
Me - female, 153.5 cm tall (short!), turning 55 next month (how did that happen??).
Sleeved 02.02.2015 by Dr Stephen Watson at SJOG Murdoch Perth, weighed 82.5 kg at my heaviest in 2002 - BMI 35, weighed 74 kg at pre-op appt - BMI 31.4 , and weighed ??70.4 kg BMI 30 immediately pre-op. Lightest I got down to was 41.3 kg, BMI 17.5 in 2015 (I had a gut infection).
I had plastic reconstructive surgery - 1/2 bodylift and arm lift at the end of 2015. My blog is on bandingtogether.com, same username.
Not working, heaps of medical problems not obesity related, on Disability Pension. Health-wise, I do best on a gluten-free, low FODMAP, LCHF diet.
Recent heaviest weight was 22.03.2018 54.88 kg, BMI 23.29. My only consolation is that when I last weighed this, in May 2015, I had more body fat (I have scales which also measure hydration and body fat %). Dietitian's long-term goal for me was 50-53 kg, so I am over my goal weight. My original goal eight was 50 kg. I desperately want to get back to 46 kg, BMI 19.5 - my happy weight.
Following another Campylobacter gut infection last year, i ceased some prescribed medication as I simply could not face taking it. Then inadvertently went through seven months of hideousness with Cymbalta Withdrawal Syndrome, had no energy, was hideously fatigued, no appetite control, and ate and ate and ate. I am now back on Cymbalta for Fibromyalgia/ME/CFIDS nerve and soft tissue pain. For me, a bonus of Cymbalta is one of it's known side effects - diminished appetite! Yay!
Negatives for me are: Still feeling very fatigued and drained with post-exertional malaise (ME/CFS), feel great in the mornings until after I walk the hounds and then it's downhill from there. As far as my "energy/wellness/health budget" go, I either spend it on walking the dogs, or other activities such as housework. Walking the dogs wins out ....
Positives/strategies for me are:
Involvement in a group of like-minded supportive folk, i.e. this forum!
I continue to follow a LCHF diet, and have made the effort over the last couple of days to chew more and to take a break between mouthfuls.
I have found doing the 20, 20, 20 does slow my eating down, and therefore I fill up/reach satiety faster! I am not doing any other activity while I am eating, and quite frankly, it is quite boring, so I don't stretch the time period out more.
I continue to use small crockery and cutlery.
I have been back and looked at the guidelines given to me by my dietitian post-op. I had consulted her at every stage - pre-op, and then at every progression post-op, and have found a very basic guide for a plan for getting in protein when on full diet.
I continue to walk briskly minimum 3.4 km daily with two houndies.
I have identified areas that I personally for me need to work on, these are in italics.
Slow down your eating pace. If you have a gastric band, you may need to wait up to 90 seconds between each swallow.
Chew well and clear the mouth between small forkfuls (spoonfuls). There’s no need to rush when the meal is small.
Skip energy-laden drinks, such as sugar-drinks (soft drinks, cordials, energy drinks) and drinks containing alcohol (beer, wine, spirits, cider, liqueurs).
Choose nutrient rich foods including protein rich foods. Protein is nature’s natural appetite suppressant.
Stick with a smaller serving size that is just enough to take your hunger away without either making you feel over-full or leaving you hungry soon after - a fine balance that takes time to to discover. Serve more and you’ll attempt to eat more - human nature at work! Serve too little and you will slip into a less helpful grazing and snacking pattern.
Learn to recognise the differences between true tummy hunger and head hunger. Head hunger is driven by social occasion, desire, emotions, or mood. Respond to head hunger with something other than food.
Stop grazing and random snacking. Between meal eating and drinking is easy to forget and accounts for stalled weight loss and weight regain in many. http://www.foodtalk.com.au/contents/en-us/d136_The_Pouch_Reset_Test_Diet__does_it_really_work_.html
I am now in the first stages of meal planning and looking at recipes.
I've gone through some of my resources here at home, and had a good browse through "Curb the carb. The safer way to diet. The healthy low-carbohydrate weight loss programme" by Amanda Cross. It's not bariatric, but has good recipes with macros and meal planning. Also goes through three stages of weight loss - fast, slower, maintenance. A lot of the recipes are 1-2 serves for folk who haven't had weight loss surgery, so it's easy enough to split the meal up into servings appropriate for me and know what the macros are for each serve.
I am going to source a LCHF dietitian in Perth - and see them under a Chronic Disease Management Plan. I am really confused about how much my daily protein should be, there is a lot of conflicting info, and also whether or not I should have snacks *sigh*.
Ruben Meerman, researcher,
Andrew J Brown, professor
1School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, 2052, Australia
Correspondence to: R Meerman email@example.com
Accepted 14 November 2014
Ruben Meerman and Andrew Brown explain why the answer might not be what you expect
When somebody loses weight, where does the fat go?
BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g7257 (Published 16 December 2014)Cite this as: BMJ 2014;349:g7257
Considering the soaring overweight and obesity rates and strong interest in this topic, there is surprising ignorance and confusion about the metabolic process of weight loss among the general public and health professionals alike. We encountered widespread misconceptions about how humans lose weight among general practitioners, dietitians, and personal trainers (fig 1⇓). Most people believed that fat is converted to energy or heat, which violates the law of conservation of mass. We suspect this misconception is caused by the “energy in/energy out” mantra and the focus on energy production in university biochemistry courses. Other misconceptions were that the metabolites of fat are excreted in the faeces or converted to muscle. We present a novel calculation to show how we “lose weight.”
Fig 1 Responses of a sample of doctors, dieticians, and personal trainers to the question “When somebody loses weight, where does it go?” (Correct answer CO2)
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Weight we want to “lose”
Excess carbohydrate or protein in the diet is converted to triglyceride and stored in the lipid droplets of adipocytes. Excess dietary fat needs no conversion other than lipolysis and re-esterification. People who wish to lose weight while maintaining their fat-free mass are, biochemically speaking, attempting to metabolise the triglycerides stored in their adipocytes.
The chemical formula for an average triglyceride molecule can be deduced from fatty acid composition studies. In 1960, Hirsch and colleagues published data that yield an “average fatty acid” with the formula C17.4H33.1O2.1This 50 year old result is in remarkable agreement with more recent data.2 Three “average fatty acids” esterified to the glycerol backbone (+3C, +6H) give an “average triglyceride” with the formula C54.8H104.4O6. The three most common fatty acids stored in human adipose tissues are oleate (C18H34O2), palmitate (C16H32O2), and linoleate (C18H32O2),1 2 which all esterify to form C55H104O6.
The complete oxidation of a single triglyceride molecule involves many enzymes and biochemical steps, but the entire process can be summarised as:
Stoichiometry shows that complete oxidation of 10 kg of human fat requires 29 kg of inhaled oxygen producing 28 kg of CO2 and 11 kg of H2O. This tells us the metabolic fate of fat but remains silent about the proportions of the mass stored in those 10 kg of fat that depart as carbon dioxide or water during weight loss.
To calculate these values, we traced every atom’s pathway out of the body. The carbon and hydrogen atoms obviously depart as CO2 and H2O, respectively. The fate of a triglyceride molecule’s six oxygen atoms is a conundrum solved in 1949 by Lifson and colleagues.3 They used labelled heavy oxygen (O18) to show that the oxygen atoms of body water and respiratory carbon dioxide are rapidly exchanged through the formation of carbonic acid (H2CO3). A triglyceride’s six oxygen atoms will therefore be shared by CO2 and H2O in the same 2:1 ratio in which oxygen exists in each substance. In other words, four will be exhaled and two will form water.
The proportion of a triglyceride molecule’s mass exhaled in CO2 is the proportion of its molecular weight (daltons) contributed by its 55 carbon atoms plus four of its oxygen atoms:
(661 Da (C55)+64 Da (O4))/(861 Da (C55H104O6))×100=84%
The proportion of mass that becomes water is:
(105 Da (H104)+32 Da (O2))/(861 Da (C55H104O6))×100=16%
These results show that the lungs are the primary excretory organ for weight loss (fig 2⇓). The water formed may be excreted in the urine, faeces, sweat, breath, tears, or other bodily fluids.
Fig 2 When somebody loses 10 kg of fat (triglyceride), 8.4 kg is exhaled as CO2. The remainder of the 28 kg total of CO2produced is contributed by inhaled oxygen. Lungs are therefore the primary excretory organ for weight loss. (This calculation ignores fat that may be excreted as ketone bodies under particular (patho)physiological conditions or minor amounts of lean body mass, the nitrogen in which may be excreted as urea)
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Lifting the veil on weight loss
At rest, an average 70 kg person consuming a mixed diet (respiratory quotient 0.8) exhales about 200 ml of CO2 in 12 breaths per minute.4 Each of those breaths therefore excretes 33 mg of CO2, of which 8.9 mg is carbon. In a day spent asleep, at rest, and performing light activities that double the resting metabolic rate, each for 8 hours, this person exhales 0.74 kg of CO2 so that 203 g of carbon are lost from the body. For comparison, 500 g of sucrose (C12H22O11) provides 8400 kJ (2000 kcal) and contains 210 g of carbon. Replacing one hour of rest with exercise that raises the metabolic rate to seven times that of resting by, for example, jogging, removes an additional 39 g of carbon from the body, raising the total by about 20% to 240 g. For comparison, a single 100 g muffin represents about 20% of an average person’s total daily energy requirement. Physical activity as a weight loss strategy is, therefore, easily foiled by relatively small quantities of excess food.
Our calculations show that the lungs are the primary excretory organ for fat. Losing weight requires unlocking the carbon stored in fat cells, thus reinforcing that often heard refrain of “eat less, move more.” We recommend these concepts be included in secondary school science curriculums and university biochemistry courses to correct widespread misconceptions about weight loss.
Cite this as: BMJ 2014;349:g7257
Competing interests: I have read and understood BMJ policy on declaration of interests and have no relevant interests to declare
Provenance and peer review: Not commissioned; externally peer reviewed.
This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
Hirsch J, Farquhar JW, Ahrens EH, Jr, Peterson ML, Stoffel W. Studies of adipose tissue in man. A microtechnic for sampling and analysis. Am J Clin Nutr1960;8:499-511.
Abstract/FREE Full TextGoogle Scholar
Hodson L, Skeaff CM, Fielding BA. Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake. Prog Lipid Res2008;47:348-80.
CrossRefPubMedWeb of ScienceGoogle Scholar
Lifson N, Gordon GB, Visscher MB, Nier AO. The fate of utilized molecular oxygen and the source of the oxygen of respiratory carbon dioxide, studied with the aid of heavy oxygen. J Biol Chem1949;180:803-11.
FREE Full TextGoogle Scholar
Ainsworth BE, Haskell WL, Herrmann SD, Meckes N, Bassett DR, Jr, Tudor-Locke C, et al. 2011 Compendium of physical activities: a second update of codes and MET values. Med Sci Sports Exerc2011;43:1575-81.
CrossRefPubMedWeb of ScienceGoogle Scholar
A 4-Week Preoperative Ketogenic Micronutrient-Enriched Diet Is Effective in Reducing Body Weight, Left Hepatic Lobe Volume,and Micronutrient Deficiencies in Patients Undergoing BariatricSurgery: a Prospective Pilot Study
Twelve-month outcomes of a randomized trial of a moderate-carbohydrate versus very low-carbohydrate diet in overweight adults with type 2 diabetes mellitus or prediabetes.
The results are not surprising.
Nutr Diabetes. 2017 Dec 21;7(12):304. doi: 10.1038/s41387-017-0006-9.
Twelve-month outcomes of a randomized trial of a moderate-carbohydrate versus very low-carbohydrate diet in overweight adults with type 2 diabetes mellitus or prediabetes.
Saslow LR1, Daubenmier JJ2, Moskowitz JT3, Kim S4, Murphy EJ4, Phinney SD5, Ploutz-Snyder R6, Goldman V4, Cox RM7, Mason AE4, Moran P4, Hecht FM4.
Dietary treatment is important in management of type 2 diabetes or prediabetes, but uncertainty exists about the optimal diet. We randomized adults (n = 34) with glycated hemoglobin (HbA1c) > 6.0% and elevated body weight (BMI > 25) to a very low-carbohydrate ketogenic (LCK) diet (n = 16) or a moderate-carbohydrate, calorie-restricted, low-fat (MCCR) diet (n = 18). All participants were encouraged to be physically active, get sufficient sleep, and practice behavioral adherence strategies based on positive affect and mindful eating. At 12 months, participants in the LCK group had greater reductions in HbA1c levels (estimated marginal mean (EMM) at baseline = 6.6%, at 12 mos = 6.1%) than participants in MCCR group (EMM at baseline = 6.9%, at 12 mos = 6.7%), p = .007. Participants in the LCK group lost more weight (EMM at baseline = 99.9 kg, at 12 mos = 92.0 kg) than participants in the MCCR group (EMM at baseline = 97.5 kg, at 12 mos = 95.8 kg), p < .001. The LCK participants experienced larger reductions in diabetes-related medication use; of participants who took sulfonylureas or dipeptidyl peptidase-4 inhibitors at baseline, 6/10 in the LCK group discontinued these medications compared with 0/6 in the MCCR group (p = .005). In a 12-month trial, adults with elevated HbA1c and body weight assigned to an LCK diet had greater reductions in HbA1c, lost more weight, and reduced more medications than those instructed to follow an MCCR diet.
Ketogenic diet beats low fat in study of patients with prediabetes and type 2 diabetes
Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors
Calculating a patient’s waist-to-height ratio is the most accurate and efficient way of identifying whether or not they are at risk of obesity, a new study shows.
The research, published in PLOS One, examined the whole-body fat percentage and visceral adipose tissue mass of a group of 81 men and women.
The British authors discovered that 36.5% more adults would be classified as obese using whole-body fat data (one in two participants) rather than BMI (around one in seven participants, or 13.5%).
To conduct their study, they gathered accurate whole-body and abdominal fat data using a total body dual energy X-ray absorptiometry (DXA) scanner — a highly accurate way of measuring body composition and fat content.
They then calculated five predictors of whole-body fat and visceral adipose tissue that could be easily replicated in a GP’s office, and compared the results with those of the DXA scan to determine which simple predictor of obesity was the most accurate.
The five predictors tested were: BMI, waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR) and waist-to-height ratio0.5 (WHtR0.5).
Lead researcher Dr Michelle Swainson, senior lecturer in exercise physiology at Leeds Beckett University, says although there are benefits to the conventional BMI method, there is concern that it is a misleading measurement.
“This is most definitely the case when people have a 'normal’ BMI but high abdominal fat that is often dismissed,” Dr Swainson says.
The results from the study show the best predictor of whole-body fat percentage and visceral adipose tissue in both men and women is WHtR.
This simple method of waist circumference divided by height measurement is not a new obesity classification but, despite evidence supporting its use, it is still not routinely measured in clinical settings, the authors note.
Cut-points for predicting whole body obesity were 0.53 in men and 0.54 in women. The cut-point for predicting abdominal obesity was 0.59 in both sexes
It's my 2nd Surgiversary!
I am 26.8 kg down from when I had my pre-op appts, 34.88 kg down from my all-time heaviest (I have lost a good sized Greyhound )
From my heaviest my BMI was 35, pre op 31.04, currently 20.2, no measurement of body fat% at my heaviest, pre-op 42.5%, currently24.9% I have had plastic reconstructive surgery - abdominoplasty, belt lipectomy and brachioplastys.
"WHAT CAN WE REALLY LEARN 40 YEARS ON FROM THE MINNESOTA CORONARY EXPERIMENT?"
"What a massive week in nutrition science! It was revealed that part of the results from the biggest study ever done to test the diet-heart hypothesis were hidden away and never published. Until now, published in the BMJ by a sort of data archaeologist Christopher Ramsden from the National Institute of Health.
The diet-heart hypothesis says that saturated fat raises cholesterol and thus causes heart disease.
This might not seem like an important question to you, but widespread acceptance of this idea has shaped the way we look and how we eat more than anything else in the history of health and medicine.
It’s still the cornerstone of conventional wisdom and dietary guidelines in virtually every country. It’s still the reason the conventional experts can’t take the biologically obvious leap to embracing low carb healthy fat diets for important treatments like weight loss and diabetes.
So, 40+ years on. Here it is in all its glory, published in the BMJ no less. What did they find?
“Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.”
That’s right, there was no support for their hypothesis in a randomised trial of more than 9500. Replacing saturated fat with Omega 6 fat did reduce cholesterol, but as we’d predict had no effect on heart disease. The one effect they did see was that older subjects who lowered their cholesterol had higher overall mortality.
Yes, cholesterol lowering in older adults caused more death. This is an effect already seen in some population studies.
So what should we take from all this?
It’s hard to say.
It’s hard because we will never know the exact motivations of Ancel Keys the co-principal investigator and infamous diet-heart hypothesis. The guy who shouted down sugar and had the world believe it was butter that was killing us via clogged arteries. If we knew why he decided not to publish these results, and why he waited 16 years to publish the only report on this experiment that did come out during his lifetime, it would be interesting.
If it turned out that the data just didn’t suit his view of the world, then that would be bordering on scientific fraud.
If he just got too busy because of his career success, and ran out of time in the end. Well…is that even plausible for the biggest diet experiment ever conducted? Its hard to imagine Keys being short of resources to help publish a study this important, especially for the time it was published.
How should it change our minds? Well, that depends on who you are really. I’ve never seen the evidence that says that eating saturated fat, in the context of whole food causes harm including more death or even heart disease. The “saturated fat raises LDL cholesterol, and LDL cholesterol is associated with more heart disease in some groups” argument isn’t a cause and effect argument. It’s just a hypothesis.
So I’m perfectly happy to look at this for what it is. Ancel Keys probably behaved unethically, the full extent of which is hard to say. There was never any evidence to demonise saturated fat to the extent that it should become public health enemy number one.
Will convention change?
There is now mounting evidence to advise people to eat less sugar and starch, especially if you are insulin resistant. This is creeping into policy.
But the status quo around fat? Why won’t this change, even with these new (but old) studies being revealed. Even with the evidence of publication bias like this?
I think we all see the word through our own dissonance.
Conventional experts will find problems with Key’s study. I’ve already seen many of these in the rapid response section of the BMJ (we have one there too). Such things as trial length, lack of knowing what they actually ate, low numbers in the autopsy results and so on. These are all issues to be sure, but not such that they’d somehow magically change the outcome to suit the diet-heart hypothesis. All of the diet-heart trials suffer from some of these issues, and usually from others as well (like telling the subjects cutting saturated fat to eat less refined food and more whole food, which at least didn’t happen here, making it a purer test of the hypothesis)
I’d add an issue – they replaced saturated fat with corn oil in high doses (about 19% of calories). Does anyone in modern nutrition science think this is a good idea? Yet they had to do this to lower cholesterol enough to make a difference, in terms of the diet-heart hypothesis.
Predictably, the experts have told us there is no reason to change current dietary advice which is low fat, and saturated fat is to be substituted by polyunsaturated fat.
Why? They cite the results of the meta-analyses of prospective cohorts (following large numbers of people living freely in the population with no actual experiment done). We agree that adding some essential polyunsaturated fats may be a good idea up to the point you get what you need (probably well under 10% of energy). But these studies don’t show that replacing saturated fat is the cause of any benefit, because you see the same small equal benefit of substituting in polyunsaturated fat for carbs.
These cohort studies give us the hypothesis that adding polyunsaturated fats in smallish amounts regardless of what they substitute might have some benefit. The experiments need to be done to find this out for certain.
They cite the Hooper Cochrane review of all the actual diet experiments where saturated fat lowering was part of the diet intervention. In this review there is no effect of these interventions on anything much at all, except one small effect of the interventions on combined coronary events.
OK, so digging deeper what is this effect? This small effect and how it was worked out is critical for the perpetuation of the modern diet-heart hypothesis and mainstream nutrition rejecting low carb eating.
You’ll be surprised about this little effect. When all experiments are added together we see that for the “Reduce saturated fat (treatment)” there were 21 791 people, of which 1774 (or 8.14%) had some sort of cardiovascular event over the study period (52 months). In the “usual diet (control)” there were 31509 people, or which 2603 (or 8.26%) had some sort of cardiovascular event over the same period.
To more directly compare what might happen here we can extrapolate. If we extrapolated and pretend we randomised 20 000 people – 10 000 to a reduced fat diet and 10 000 people their usual diet then we would expect to see 826 CVD events for the usual diet and a reduction to 814 for the reduced saturated fat. That’s a difference in 12 CVD events in 10 000 people over just about 4.5 years, because of eating less saturated fat (compared to doing nothing). And these 12 CVD events that make up the difference do not include either heart attacks or deaths; they include events like angina instead.
That’s a change in absolute risk of 0.12%.
Underwhelmed? Hell yes. So am I, especially because the trials that did show some positive effect like the Oslo diet heart study weren’t just about substituting out saturated fat. They were about more exercise, more vegetables, less processed food, eating fewer calories and often more. In fact, the statistical adjustment the authors make means that these smaller, multifaceted studies end up being given extra weighting because of the chance the bigger studies overwhelm the results.
In the end, it’s hard to see a path, other than a new generation coming through, for the diet-heart hypothesis to go away. It’s hard to see conventional wisdom changing anytime soon.
Remember – in all these studies, there has never been a diet-heart trial of replacing carbohydrate with polyunsaturated and/or monounsaturated fat. There hasn’t even been one that was a test of reducing sugar. All the government funding for long term trials to test the effect of diet on heart health over the years has gone to one team with one idea – to try to lower cholesterol by replacing saturated fat in the diet and see what happens.
Butter or corn oil?
I said before that we all end up with our own dissonance. I’m not naïve enough to think I am excluded from this. I obviously have a bias for low carb healthy fat eating and may see the world that way. That’s why it’s critical for you to take a little time to see the world of nutrition science for what it is and make up your own mind."
A FAT LOAD OF GOOD: WHY IT'S TIME TO BRING FULL FAT BACK
April 13, 2016
Start your day with toast, hold the butter but add margarine if you like. Have it with an egg-white omelette because the yolk is bad and a strong coffee with a splash of fat-free milk and maybe a calorie-free sweetener.
Splenda perhaps – apparently, according to Splenda, "people with diabetes can enjoy up to 4 packets of SPLENDA® No Calorie Sweetener or up to 8 teaspoons of SPLENDA® No Calorie Sweetener, Granulated, because it is considered a 'free food'."
Ten or 15 years ago, this messed-up meal might have been considered a healthy breakfast.
In recent years however, we have learnt that fat is nothing to be afraid of; fat, unlike the message sounded out since the 1950s, does not make us fat. Fake food like margarine and calorie-free sweeteners on the other hand ... well, that's another story.
Another food myth that has been busted is that full-fat dairy and other animal fats – including bacon and egg yolks – lead to heart disease.
In fact, new research has found that those who consume full-fat dairy tend to weigh less and have a reduced risk of diabetes.
Research published in the American Journal of Nutrition analysed the data of 18,438 women in the Women's Health Study, and found that those who consumed the most high-fat dairy products were about 10 per cent less likely to be overweight.
A separate meta-analysis of more than 3000 people over 15 years found that consumers of full-fat dairy had a 46 per cent lower risk of diabetes.
"There is no prospective human evidence that people who eat low-fat dairy do better than people who eat whole-fat dairy," lead researcher Dr Darian Mozaffarian, of Tufts University, told Time.
It makes sense that the fat from full-fat dairy is more satiating, so people are less likely to overeat and the fat is not being swapped for sugar or carbohydrates, but why the association with diabetes?
"They did find that saturated fatty acids in dairy are strongly associated with reducing risk (of diabetes)," explains cardiologist and adviser to the UK's National Obesity Forum, Dr Aseem Malhotra, who was not involved in the study. "When you remove fat you remove the fatty acids."
In a separate paper tellingly titled Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983, researchers concluded that recommendations to reduce fat intake to lessen the risk of heart disease were misguided.
"The present review concludes that dietary advice not merely needs review; it should not have been introduced," concluded the researchers from the University of West Scotland.
It is an issue close to Malhotra's heart.
"The science is quite clear," says Malhotra. "There are two major factors why the low-fat message is perpetuating itself – that fat will increase the risk of heart disease and that fat makes you fat.
"The latest data on saturated fat – over several decades – has revealed that it doesn't increase heart disease and, if it comes from dairy, it is protective against diabetes and heart disease."
He adds fat has the lowest impact on insulin resistance and says that insulin resistance is the greater risk factor in cardiovascular disease. "Good fats – extra virgin olive oil, nuts, butter, coconut oil – are anti-inflammatory and reduce the risk of a heart attack," Malhotra says.
So why is it that the Australian Dietary Guidelines and many doctors and dietitians still advise consuming reduced fat dairy?
"We're unwilling to admit that we were wrong, but science evolves," Malhotra says. "I started off giving that advice [low-fat]. For me, knowing what I know, it would be unethical to give that advice now.
"There is an urgent need to overhaul the dietary guidelines – the guidelines lag behind the science."
As they stand, he says they're a "direct cause" of the obesity epidemic.
Dr Joanna McMillan says we "have to be careful" not to attack the guidelines with every new study.
"Is the dairy making the difference or is it what they're eating instead?" she asks. "What about if you have a diet with plenty of fat from extra virgin olive oil, nuts, seeds, oily fish, avocado and so on, but choose to have skim milk to reduce the kilojoules from your several coffees? Or just because you like it (as I do!)?"
There is also the fact that not all fat is equal of course. "At the end of the day saturated fat from a piece of cheese is not the same as saturated fat from a party pie," McMillan says, adding: "The message overall is to stop buying low fat when it is replaced by refined carbs (not just sugar) – in fact eat more real food that is not manipulated by manufacturing to meet some nutrient criteria."
Indeed Yale's Dr David Katz has argued that the low-fat advice, based largely on the controversial findings from a 1950s study by scientist Ancel Keys and echoed by Preventive Medicine Research Institute founder Dr Dean Ornish, has been warped by the food industry.
"When [Ancel Keys] advised that we should eat less fat, the advice meant eat more spinach," Katz tells Jeff Wilser in his new book The Good News About What's Bad For You. "The food industry said, we can't make a lot of money selling spinach, but we can invent Snackwell Low-Fat Cookies."
"I wouldn't disagree with that," says Malhotra, who eats up to 15 eggs a week and has bacon a couple of times a week. "If you're avoiding fat and eating more vegetables, there's not a problem with that."
His problem is whether fat is being replaced by sugar or refined carbohydrates, and that people still fear fat. McMillan agrees this needs to change.
"I think we will see a revisal of the dairy guidelines in future Australian Dietary Guidelines and that would be a welcome move," she says.
"Eating fat is as likely to make you fat as eating greens is to make you green," Malhotra says. "It's time to bring fat back."
How much fat is OK?
"Force yourself to eat anything in excess and you will probably do harm," Malhotra says. "Eat until you're full. Try to avoid snacking and eat real food."
Read more: http://www.theage.com.au/lifestyle/diet-and-fitness/a-fat-load-of-good-why-its-time-to-bring-full-fat-back-20160412-go4gyc.html#ixzz46Ew9HfiK
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"Very low carbohydrate diets in the management of diabetes revisited".
From Gary Fettke No Fructose
(The combination of Fructose, refined Carbohydrate and Polyunsaturated Oils create inflammation in every blood vessel and eve...ry organ of the body. A Low Carbohydrate and Healthy natural Fat diet (LCHF) can have an enormous benefit to your health. Dr Gary Fettke Orthopaedic Surgeon M.B.,B.S.(University NSW), F.R.A.C.S.(Orthopaedic Surgery), F.A.Orth.A Launceston, Tasmania, Australia www.NoFructose.com www.NutritionForLife.healthcare )
"How does diabetes affect you?
There are only 3 groups of people out there.
You either have diabetes, you are going to get diabetes or you are going to be caught up in the economic or personal costs of diabetes. Pretty simple - so it's worth paying attention to this topic.
Whatever we are recommending for those with diabetes is not working. My New Zealand colleagues have just put this paper together for the New Zealand Medical Journal. Brilliant.
For my patients, LCHF has given them their lives back!!!!
Low Carb in Diabetes management and treatment works better than the current low fat/ high carb recommendations that currently exist.
Eat what you want and chase it with medication is completely unsustainable.
"We’re just continuing to make the point that low carb eating is a very sensible way to go for people with diabetes. The outcomes are better."
"higher-carbohydrate diets for people with diabetes may have played a part in the modern characterisation of type 2 diabetes as a chronic condition with a progressive requirement for multiple medications."
Take the link to read the whole paper."
Humans can derive energy from carbohydrate, fat, or protein. The metabolism of carbohydrate requires by far the highest secretion of insulin. The central pathology of diabetes is the inability to maintain euglycaemia because of a deficiency in either the action or secretion of insulin. That is, because of either insulin resistance often accompanied by hyperinsulinaemia, or insulin deficiency caused by pancreatic beta cell failure. In individuals dependent on insulin and other hypoglycaemic medication, the difficulty of matching higher intakes of carbohydrates with the higher doses of medication required to maintain euglycaemia increases the risk of adverse events, including potentially fatal hypoglycaemic episodes. Thus, mechanistically it has always made sense to restrict carbohydrate (defined as sugar and starch, but not soluble and insoluble fibre) in the diets of people with diabetes. Randomised clinical trials have confirmed that this action based on first principles is effective. The continued recommendation of higher-carbohydrate, fat-restricted diets has been criticised by some scientists, practitioners and patients. Such protocols when compared with very low-carbohydrate diets provide inferior glycaemic control, and their introduction and subsequent increase in carbohydrate allowances has never been based on strong evidence. The trend towards higher-carbohydrate diets for people with diabetes may have played a part in the modern characterisation of type 2 diabetes as a chronic condition with a progressive requirement for multiple medications. Here we will introduce some of the evidence for very low-carbohydrate diets in diabetes management and discuss some of the common objections to their use.
11 February 2016
Improved diabetes control with new diet
Adelaide researchers have developed a diet and exercise program which has proven to be highly effective in reducing the burden of type 2 diabetes, with an average 40 per cent reduction in medication levels.
The diet incorporates an eating pattern that is very low in carbohydrates and higher in protein and unsaturated fats.
The program is based on the findings from a $1.3 million National Health and Medical Research Council (NH&MRC) funded study, which compared the low carbohydrate eating pattern with the current best practice approach of managing type 2 diabetes with a high-unrefined carbohydrate, low fat diet.
"The research results are ground breaking," Associate Professor Grant Brinkworth, principal research scientist at the CSIRO said.
"Health professionals have been divided over the best dietary approach for managing type 2 diabetes, and the ongoing uncertainty is a hotly debated topic amongst clinicians and researchers.
"The most amazing benefit of the low carbohydrate diet was the reduction in the patient’s medication levels, which was more than double the amount than the volunteers following the lifestyle program with the high-carbohydrate diet plan.
"Some of the participants managed to cease their medications altogether, and many described the study as life changing.
"This research shows that traditional dietary approaches for managing type 2 diabetes could be outdated, we really need to review the current dietary guidelines if we are serious about using the latest scientific evidence to reduce the impact of the disease."
The two year research intervention was a collaboration between CSIRO, Adelaide University, Flinders University and the University of South Australia, with the exercise program delivered in partnership with community fitness centres.
Medication requirements were also monitored and supervised with appropriate oversight from physicians.
Professor Campbell Thompson from the University of Adelaide said there were further insights on the clinical outcomes.
"The very low carbohydrate diet presented greater improvements in the blood cholesterol profile, by increasing the levels of good (HDL) cholesterol and decreasing triglyceride levels to a greater extent than the traditional high carbohydrate, low fat diet approach," Professor Thompson said.
"Both diets achieved similar reductions in bad (LDL) cholesterol levels, often a concern with some low carbohydrate diets.
"The variability of blood glucose levels throughout the day is also emerging as a strong independent risk factor for diabetes complications. In our study the very low carbohydrate diet was more effective in reducing the number and levels of blood glucose spikes and dips, flattening the blood glucose profile over a 24-hour period."
Type 2 diabetes is one of the greatest global health challenges of the 21st century, with more than 350 million people suffering from the condition.
Obesity is a major risk factor for type 2 diabetes and given the growing increases in obesity and sedentary lifestyles globally, the world is facing a veritable tsunami of the disease.
In Australia alone, an estimated 800,000 Australian adults have type 2 diabetes with many more undiagnosed. In 2008-09, of the estimated $1507 million spent on the health care of diabetes in Australia, $490 million was spent on diabetes-related medications.
Based on the findings from this study, implementing a lifestyle program that incorporates this effective eating pattern at a national level could save up to $200 million annually through reductions in diabetes-related medication expenditure alone.
My house did not sell.
Mum (in NZ) had to put the unit that she had bought on my behalf (in Orewa) , on the market (obviously, due to financial reasons). https://www.barfoot.co.nz/533537 Mum, and my sister Pam) put a lot of effort into this place, and it had remodelled kitchen, bathroom, repainted, new carpets etc etc etc.
Yes, it looked wonderful.
Yes, the Orewa lifestyle would have been magnificent.
That unit sold. (Settlement was 11th/12th Jan this year, I don't know exact dates).
Current Medication: Before Breakfast:
2 paracetamol/2 Panadol Osteo (depending on what day I have ahead of me...) for... your choice...: ME/CFS, Fibromyalgia, Osteo arthritis hips etc ...I can't stand...feel horrendous, have muscle pain, and "post-exertional malaise" (believe me, that sends you straight to bed) lasting into the next couple of days...
50 mg Lyrica (Fibroymyalgia)
Duloxetine 60 mg (Fibromyalgia/ME/CFS - works wonderfully!) Put on this by my Rheumatologist, Dr Antonia Cole @ Hollywood Specialist Medical Centre, Nedlands. Bless her!!!
Moduretic 50/5 (Menieres Disease, to reduce the fluid in the inner ear)
+/- "Serc" (Menieres Disease - too ferkin' expensive), "Seniere" (also expensive) 16 mg Betahistine dihydrodrochloride as needed
+/- "Panadeine Forte" (prescribed. I haven't used, I believe that I have - thankfully - a pretty high pain tolerance)
+/- "Stemitil" (Prochlorperazine) 5mg (poxy Menieres Disease...)
Post Breakfast (which tends to be about 1030 am:)
1 general multi-vitamin/mineral
6000 mg Gingko Biloba (just recently, as I have given myself haemorrhagic gastritis in the past - this was pathology taken from a gastric endoscopy done September 2013, taking 2000 mg Gingko biloba on an empty stomach) - to increase the blood flow to my inner ears. This was recommended to me by my ENT - Paul Yuen - surgeon in relation to the Menieres Disease...). Benefit - now I am back on it, I have noticed...that my poxy memory has started to improve again. I managed to combine menopause + ME/CFS + Fibromyalgia 2014/2015 lol! And lost my job with DPaW! "Employer Initiated Retirement On The Grounds Of Ill-Health".)
"Nature's Way" "Joint Restore Triple Action" Glucosomine + Chondroitin + MSM, x 1, for Osteo arthritis hips, (+ mainly left hand - c/o Complex Regional Pain Syndrome/ Reflex Regional Sympathy).
+/- OTC Ibuprofen 200 mg + Codeine Phosphate 12.8 mg in view of prospected day ahead...
+/- OTC "Nagestic Forte" Curcumin 6.074 mg if I remember... If I know that I am going to have a REALLY physical day...
+/- Ventolin puffer (prescribed) when I remember, or when I am REALLY having problems...
+/- Becotide puffer (prescribed) when I remember, or when I am REALLY having problems...
+/- And...this is really slack on my behalf..."Flo CRS" Nasal Irrigation followed by (prescribed) "Nasonex" (prescribed) nasal spray...when I remember...when my nose is REALLY bugging me oe O can't breathe through my nose....at all...
"Meniett" machine $2,500.00 to try to relieve poxy Menieres symptoms... when I remember... ( Sleep study showed that "Mandibular Adjustment Splint" - $2,500.00 - become redundant...didn't control UARS/Sleep Apnoea...).
Throughout the day:
[*]+/- OTC Ibuprofen 200 mg + Codeine Phosphate 12.8 mg in view of prospected day ahead... [*]2 paracetamol/2 Panadol Osteo (depending on what day I have ahead of me...)
Night-time: 7.5 mg Mirtazapine (prescribed) - to sleep. The Duloxetine "revs" me up too much. And I don't. Sleep. + WAY TOO MANY sleep behaviour disorders! (Diagnosed on sleep study. STILL have Upper Airway Resistance Syndrome). I sleep "like a good baby" on this lol! 1 x Night-time part of multi-vitamin/mineral ("Nature's Own - Restore Multivitamin Day and Night Formula For Women"). So.
I am still here (24 Ward Cres, Kelmscott WA 6111).
And the unit in Orewa would never had been 'mine' . Mum (turning 85 this coming March!!!) and my sister, had put too much work into it. "Entitling" them to call it "Theirs" and ...dictating... what I could do, and what I couldn't do.
"Things happen for a reason".
My life is no longer "on hold", as it was from January 2015.
Spiritually, I got given, "The timing wasn't right".
I have "Moved On" in many ways.
I have "Taken The Leap Of Faith".
Gone on with 'plans'.
I had plastic reconstructive surgery with Mr Hanh Nguyen & team at Hollywood Hospital 4th December 2015 (arms, abdominoplasty, and "belt lipectomy"). "Sculpt Surgery".
I can not fault them (just only a couple of niggles with Hollywood, but nothing outstanding as at Murdoch SJOGH).
"Sculpt Surgery" - Theresa and Hanh - were fantastic.
And have adopted a boy foster Rescue Greyhound, Zumba, the day before Christmas (I hads fostered him for four months, so knew his personality).
Also, have gone back to fostering Rescue Greyhounds.
I am doing well, and very, very happy that I had had the Gastric Sleeve.
12 Month Measurements
BODY FAT %
Body Fat %
1st January 2016
2nd February 2016
Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base
We present major evidence for low-carbohydrate diets as first approach for diabetes.
Such diets reliably reduce high blood glucose, the most salient feature of diabetes.
Benefits do not require weight loss although nothing is better for weight reduction.
Carbohydrate-restricted diets reduce or eliminate need for medication.
There are no side effects comparable with those seen in intensive pharmacologic treatment
The inability of current recommendations to control the epidemic of diabetes, the specific failure of the prevailing low-fat diets to improve obesity, cardiovascular risk, or general health and the persistent reports of some serious side effects of commonly prescribed diabetic medications, in combination with the continued success of low-carbohydrate diets in the treatment of diabetes and metabolic syndrome without significant side effects, point to the need for a reappraisal of dietary guidelines. The benefits of carbohydrate restriction in diabetes are immediate and well documented. Concerns about the efficacy and safety are long term and conjectural rather than data driven. Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss (although is still best for weight loss), and leads to the reduction or elimination of medication. It has never shown side effects comparable with those seen in many drugs. Here we present 12 points of evidence supporting the use of low-carbohydrate diets as the first approach to treating type 2 diabetes and as the most effective adjunct to pharmacology in type 1. They represent the best-documented, least controversial results. The insistence on long-term randomized controlled trials as the only kind of data that will be accepted is without precedent in science. The seriousness of diabetes requires that we evaluate all of the evidence that is available. The 12 points are sufficiently compelling that we feel that the burden of proof rests with those who are opposed.
LOS ANGELES --Alzheimer's disease was officially recognized a hundred years ago, but there's still no effective treatment for it. Now researchers at UCLA say they've developed a program that shows for the first time memory loss being reversed.
It's not a drug; it's not a procedure; it is a novel, comprehensive and personal approach to treating memory loss associated with Alzheimer's. UCLA researchers spell out exactly what can be done to reverse what the disease does to the brain.
In the report provided by UCLA, Dr. Dale E. Bredesen explains how Alzheimer's is a complex disease affected by sleep, diet, even exercise.
"These all -- and other things -- all contribute to this critical balance in plasticity," said Bredesen.
Ten memory-loss patients, some with brain-scan-confirmed patterns of Alzheimer's, participated in a small UCLA trial called MEND (Metabolic Enhancement for NeuroDegeneration).
In the UCLA protocol, patients made dramatic lifestyle changes. They avoided simple carbs, gluten and processed foods. They increased their fish intake, took yoga and meditated. They were instructed to take melatonin, get adequate sleep, incorporate vitamin B-12, vitamin D-3 and fish oil.
Within six months, nine patients saw a noticeable improvement in memory. One patient, who was in the late stages of Alzheimer's, did not show improvement.
UCLA researchers say the findings suggest at least early on, changing a person's metabolic processes can bring back memory and cognitive function.
Six of the patients of the patients in the study who had to discontinue working were all able to return to their jobs. Study authors say some patients were followed up to two and a half years and the memory improvements remained.
Plans are underway to do larger studies on this therapeutic program.
For more information on the study: Reversal of cognitive decline: A novel therapeutic program
Related Topics: health alzheimers UCLA healthy living Los Angeles
I like this!
It would cover all the incisions from the circumferential abdominoplasty, + also when I have the breast and thigh lift, would be suitable (Ot5herwise I'd want something supportive for the boobies):
ahttp://www.asos.com/au/Motel/Motel-Cinch-Swimsuit/Prod/pgeproduct.aspx?iid=5376714&WT.ac=rec_viewed&CTAref=Recently+Viewed I can't work out the sizing though, and as in no need for swim wear (my boys age 8 Op Shop board shorts +/- bikini top will have to suffice for now, I haven't been at the beach since Jan 2014 anyway )
So, in no hurry to purchase now. But it's the first pair of bathers that I have seen and liked for a long time!
I had a couple of unwell months with diarrhoea and weakness, and had dropped down to 41.82 kg, body fat 18.6% a couple of weeks ago. My GP was starting to get concerned when I got down to 45 kg, which was the level at which Jo Anne Dembo had said that she didn't want me under, and to contact her if I did.
I have to say that I am very disappointed with Jo Anne Dembo. I last saw her in July (I had a total of seven visits to her, five under a Chronic Disease Management Plan) and we discussed the problems with my diarrhoea (she just advised me to increase my fibre and to have smooth peanut butter. We also discussed strategies for me to maintain my weight without losing more, to which she advised me to increase my intake of "healthy" fats such as avocado. I contacted the day after that appt as I have done a huge amount of reading on diets etc, and all my reading indicated that maintaining a low-carb higher fat diet would actually just lead to more weight loss...didn't hear back on that one. I have cut out sugar and other sugar substitutes, and refined carbohydrates (I have been a big proponent of low carb for years, obviously had a big problem with portion control and occasional carb-fests to get me obese lol!). Interesting reading: http://whatthefatbook.com/top-tip-tuesday-20th-oct-profiling-nic-gill-for-wtf-sports-performance/
Anyway, my weight loss continued along with the diarrhoea. I kept advising her by email, and heard nothing from her. I went to my GP last month, did a stool test and grew Campylobacter, for which I was put on antibiotics as my GP did not want me to lose any more weight. The antibiotics worked well, and I have put on a bit of healthy weight, my nausea has gone and food intake has increased. She also wanted me to go back to Jo Anne Dembo, I didn't go as I really didn't think that Jo Anne could offer me anything new, and we had already discussed the issues back in July.
So this is where I am:
Body Fat %
I am very happy with that. I am a mini-me, and have resorted to wearing boys shorts/jeans, ages 8-10.
I've had two consults at Sculpt Surgery for abdominoplasty and bilateral arm lift. They were really lovely there, but came in lots more expensive than who I have decided to go with, Sam Cunneen.
I am booked at Bethesda Nov 17th. And if all goes well, will be looking at having bilateral thigh and breast lifts.