The best diet for optimal blood sugar control & health
Feature Nutrition
BMJ 2015; 351 doi: http://dx.doi.org/10.1136/bmj.h4962 (Published 23 September 2015) Cite this as: BMJ 2015;351:h4962
We know about the issue of slowed metabolism after weight loss due to the lean muscle mass loss that goes along with fat loss. This is one reason why higher protein/low carb diets work better than low fat diets; because muscle mass is maintained better. Well, new information from Diabetes in Control backs up what some of us know intuitively or may have experienced personally….
The study showed that for every kg of weight they lost, patients consumed an extra 100 calories a day — more than three times what they would need to maintain the lower weight.
This out-of-proportion increase in appetite when patients lost a small amount of weight may explain why maintaining long-term reduced body weight is so difficult.
A validated mathematical method was used to calculate energy intake changes during a 52-week placebo-controlled trial in 153 patients treated with canagliflozin, a sodium glucose co-transporter inhibitor that increases urinary glucose excretion, thereby resulting in weight loss without patients being directly aware of the energy deficit. The relationship between the body weight time course and the calculated energy intake changes was analyzed using principles from engineering control theory.
Previous studies show that metabolism slows when patients lose weight; however, these results suggest that proportional increases in appetite likely play an even more important role in weight plateaus and weight regain.
Knowing that patients with type 2 diabetes who receive the sodium-glucose cotransporter 2 (SGLT-2) inhibitor canagliflozin (Invokana) as part of a glucose-lowering strategy excrete a fixed amount of glucose in the urine (which causes weight loss), they used a mathematical model to calculate energy-intake changes during a 52-week placebo-controlled trial of the drug, in which 153 patients received 300-mg/day canagliflozin and 89 patients received placebo. Using this approach meant that the participants who received canagliflozin consistently excreted 90-g/day glucose but were not aware of the energy deficit.
Previously, the researchers had validated a mathematical model to calculate the expected changes in caloric intake corresponding to changes in body weight (Am J Clin Nutr. 2015;102:353-358). They input the current study data into this model.
At study end, the patients who had received placebo had lost less than 1 kg and those who had received canagliflozin had lost about 4 kg. The weight loss with canagliflozin was less than predicted, due to the patients’ increased appetite. On average, patients who received canagliflozin ate about 100 kcal/day more per kg of weight lost — an amount more than threefold larger than the corresponding energy-expenditure adaptations.
“Our results provide the first quantification of the energy-intake feedback-control system in free-living humans,” the researchers write.
They add that in the absence of “ongoing efforts to restrain food intake following weight loss, feedback control of energy intake will result in eating above baseline levels with an accompanying acceleration of weight regain.”
The findings suggest that “a relatively modest increased appetite might explain a lot of the difficulty that people are having in both losing the weight and maintaining that weight loss over time. From the results it was concluded that, while energy expenditure adaptations have often been considered the main reason for slowing of weight loss and subsequent regain, feedback control of energy intake plays an even larger role and helps explain why long-term maintenance of a reduced body weight is so difficult.
The findings suggest that an increased appetite is an even stronger driver of weight regain than slowed metabolism. “The message to clinicians is to not only push physical activity as a way to counter weight regain but also use medications that impact appetite.”
In summary, the researchers conclude the few individuals who successfully maintain weight loss over the long term do so by heroic and vigilant efforts to maintain behavior changes in the face of increased appetite along with persistent suppression of energy expenditure in an omnipresent obesogenic environment. Permanently subverting or countering this feedback control system poses a major challenge for the development of effective obesity therapies.
Practice Pearls:
Obesity. 2016;24:2289-2295. Abstract
Can Anger and Exercise Trigger a Myocardial Infarction?
Diabetes in Control October 29th 2016
An International study explores the role of physical exertion, anger, and emotional upset in triggering acute myocardial infarction.
In the INTERHEART study, researchers explored the triggering association of acute physical activity and anger or emotional upset with a myocardial infarction (AMI) to quantify the importance of these potential triggers in a large, international population.
INTERHEART was a case-control study of first AMI completed in 262 centers across 52 countries. In this analysis, they included only cases of AMI and used a case-crossover approach to estimate odds ratios for AMI occurring within 1 hour of triggers.
Trained study staff performed a standardized physical examination on participants and administered a structured questionnaire. Participants with AMI (cases) were asked the questions, “Were you engaged in heavy physical exertion?” and “Were you angry or emotionally upset?” in the 1 hour before the onset of symptoms and during the same hour on the previous day.
Control participants were asked, “During the last 24 hours, were you engaged in heavy physical exertion?” and “During the last 24 hours, were you angry or emotionally upset?”
Data were also collected on age, ethnicity, diet, physical activity, tobacco use, education, employment, psychosocial factors, and cardiovascular risk factors. Anthropometric measurements (height, weight, waist, and hip circumference) were measured in a standardized manner.
Medical history (diabetes mellitus, hypertension, angina, stroke, other vascular disease, and depression) and baseline medications were self-reported. Smoking was categorized as never smoking, former smoking, or current smoking. Obesity was defined as body mass index of ≥30 kg/m2.
Countries were grouped into 10 geographical regions: Western Europe, Central and Eastern Europe, Middle East and Egypt, Africa, South Asia, China and Hong Kong, Southeast Asia and Japan, Australia and New Zealand, South America and Mexico, and North America.
Physical activity was categorized as mainly sedentary, mild exercise, or moderate/strenuous activity. Stress was categorized as none or some periods of stress versus several periods or permanent stress. Education was categorized as none, 1 to 8 years, 9 to 12 years, trade school, or college/university.
Of 12,461 cases of AMI, 13.6% (n=1650) engaged in physical activity and 14.4% (n=1752) were angry or emotionally upset in the case period (1 hour before symptom onset).
Physical activity in the case period was associated with increased odds of AMI (odds ratio, 2.31; 99% confidence interval [CI], 1.96–2.72) with a population-attributable risk of 7.7%.
Anger or emotional upset in the case period was associated with increased odds of AMI (odds ratio, 2.44; 99% CI, 2.06–2.89) with a population-attributable risk of 8.5% (99% CI, 7.0–9.6).
There was no effect on modification by geographical region, prior cardiovascular disease, cardiovascular risk factor burden, cardiovascular prevention medications, or time of day or day of onset of AMI. Both physical activity and anger or emotional upset in the case period were associated with a further increase in the odds of AMI.
From the results, it was reported that physical exertion and anger or emotional upset are common in the 1 hour before the onset of symptoms of AMI and that either exposure may act as an external trigger for AMI in all age groups. We report no differences by geographical region, previous cardiovascular disease, cardiovascular prevention medications, cardiovascular risk factors, and INTERHEART risk score.
Circulation. http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.116.023142/-/DC1 and http://dx.doi.org/10.1161/CIRCULATIONAHA.116.023142. 2016;134:1059-1067
This was a 6-month randomized, controlled clinical trial of patients with type 1 and type 2 diabetes with no retinopathy or mild to moderate non-proliferative retinopathy assigned to twice-daily consumption of placebo or a novel, multi-component formula containing xanthophyll pigments, antioxidants and selected botanical extracts.
Measurement of contrast sensitivity, macular pigment optical density, color discrimination, 5-2 macular threshold perimetry, Diabetic Peripheral Neuropathy Symptoms, foveal and retinal nerve fiber layer thickness, glycohemoglobin (HbA1c), serum lipids, 25-OH-vitamin D, tumor necrosis factor α (TNF-α) and high-sensitivity C reactive protein (hsCRP) were taken at baseline and 6 months. Outcomes were assessed by differences between and within groups at baseline and at study conclusion using mean ± SDs and t tests (p<0.05) for continuous variables.
The results showed that there were no significant intergroup differences at baseline. At 6 months, subjects on active supplement compared with placebo had significantly better visual function on all measures (p values ranging from 0.008 to <0.0001), significant improvements in most serum lipids (p values ranging from 0.01 to 0.0004), hsCRP (p=0.01) and diabetic peripheral neuropathy (Fisher’s exact test, p=0.0024). No significant changes in retinal thickness, HbA1c, total cholesterol or TNF-α were found between the groups.
The researchers concluded that this study provides strong evidence of clinically meaningful improvements in visual function, hsCRP and peripheral neuropathy in patients with diabetes, both with and without retinopathy, and without affecting glycemic control.
A. Paul Chous. The Diabetes Visual Function Supplement Study (DiVFuSS). Br J Ophthalmol doi:10.1136/bjophthalmol-2014-306534.
The use of adjuvant drugs for obese, insulin resistant type ones is increasing. What can you expect from therapy with some of the newer add on drugs? This article in Diabetes in Control tells you.
Diabetes management strategies have evolved since the discovery of newer oral agents that provide glycemic control through various pathways. Type 1 diabetes mellitus treatment has changed from traditional insulin regimens to incorporating other agents for improving glycemic control.
Maintaining adequate glycemic control and preventing end-organ damage is of utmost importance when managing diabetes. Uncontrolled blood glucose levels can lead to retinopathy, neuropathy, and nephropathy, which affects overall quality of life in our patients.
Due to these effects and the increased rate of uncontrolled A1c levels in patients with type 1 diabetes, various researchers have devised various treatment approaches for these patients. Recent research efforts have looked into the benefits of SGLT-2 inhibitors and their effect on cardiovascular events and mortality.
Matteo Monami et al., have looked into the benefits of these agents in patients with type 2 diabetes in the EMPAREG OUTCOME study. The findings from this research study highlight the benefit from SGLT-2 inhibitor use. Their use in T2DM was found to reduce the risk of all-cause mortality, cardiovascular mortality, and myocardial infarction, but there was no increase in the risk of stroke. These findings can also provide similar benefits in type 1 diabetes patients; however, more studies are needed to provide stronger evidence.
Previous studies with other SGLT-2 inhibitors (i.e. canagliflozin) showed an increased incidence of diabetic ketoacidosis (DKA) in T1D patients. The incidence of DKA is thought to be associated with an increase in glucagon and free fatty acids that induces insulin resistance, which can also predispose to renal complications.
Conversely, a recent study showed improvements in renal functions in patients taking dapagliflozin through reductions in ischemia and hypoperfusion. These findings are not seen in patients taking liraglutide due to suppression of ketogenesis.
Recently, Nitesh Kuhadiya and colleagues expanded on the use of SGLT-2 inhibitors in type 1 diabetes patients. In this randomized clinical trial, researchers looked at the reduction in glycemia and body weight when adding dapagliflozin to an insulin and liraglutide regimen. Researchers hypothesized that the addition of dapagliflozin to an insulin and liraglutide regimen would provide improvements in glycemia without leading to increased concentrations of glucagon and other ketosis mediators.
Eligible patients were enrolled based on the following characteristics: 18-75 years of age with type 1 diabetes, fasting C-peptide of <0.1nmol/L, on any insulin regimen for more than 12 months with or without history of DKA. All patients had an A1c of <9.2% and were knowledgeable on carbohydrate counting. Additionally, patients needed to be on liraglutide therapy for at least 6 months prior to the start of the trial. 30 patients were assigned in a 2:1 ratio to receive either dapagliflozin 10 mg or placebo for 12 weeks. Consistency of carbohydrate content was documented by a dietitian.
The primary end-point of the study was a change in mean A1c after 12 weeks of dapagliflozin. Each patient’s body weight, systolic blood pressure, carbohydrate intake, and ketosis mediators were measured throughout the study as secondary endpoints. 26 patients completed the study, out of which only 17 were part of the intervention group. Those in the intervention group received dapagliflozin 5 mg daily for one week followed by 10 mg daily for 11 weeks. All insulin doses were targeted to 3.8-8.8 mmol/L.
At the end of the study it was found that triple therapy with liraglutide, insulin, and dapagliflozin decreased A1c by 0.66% when compared to placebo (~0.1%) (p <0.01 vs placebo). No severe hypoglycemic episodes were reported even when weekly glucose concentrations fell by 0.83 + 0.33 mmol/L in patients receiving triple therapy; no significant changes observed in the placebo group (P< 0.05 vs baseline; P=0.07 vs placebo).
When looking at the effects of this regimen and body weight, it was observed that body weight fell by 1.9 + 0.54 kg in the triple therapy group (P<0.05 vs placebo). Furthermore, there was a significant increase in ketosis mediators. It was also seen that total cholesterol and LDL-C level increased by 6% and 8%, respectively. Blood pressure readings remained unchanged in both groups.
In conclusion, a significant decrease in A1c and weight can be obtained by incorporating dapagliflozin for type 1 into an insulin and liraglutide regimen. However, special consideration should be taken when utilizing this approach due to an increase in ketosis mediators that can predispose patients to develop DKA.
Practice Pearls:
Researched and prepared by Pablo A. Marrero-Núñez – USF College of Pharmacy Student Delegate – Doctor of Pharmacy Candidate 2017, reviewed by Dave Joffe, BSPharm, CDE
References:
Chang, Yoon-Kyung, Hyunsu Choi, Jin Young Jeong, Ki-Ryang Na, Kang Wook Lee, Beom Jin Lim, and Dae Eun Choi. “Dapagliflozin, SGLT2 Inhibitor, Attenuates Renal Ischemia-Reperfusion Injury.” PLOS ONE PLoS ONE 11.7 (2016). Web
Kuhadiya, Nitesh D., Husam Ghanim, Aditya Mehta, Manisha Garg, Salman Khan, Jeanne Hejna, Barrett Torre, Antoine Makdissi, Ajay Chaudhuri, Manav Batra, and Paresh Dandona. “Dapagliflozin as Additional Treatment to Liraglutide and Insulin in Patients With Type 1 Diabetes.” The Journal of Clinical Endocrinology & Metabolism (2016). Web.
Monami, Matteo, Ilaria Dicembrini, and Edoardo Mannucci. “Effects of SGLT-2 Inhibitors on Mortality and Cardiovascular Events: A Comprehensive Meta-analysis of Randomized Controlled Trials.” Acta Diabetol Acta Diabetologica (2016). Web.
The incidence of diabetes has been growing and the complications arising from uncontrolled blood glucose has been increasing along with it. It is estimated that more than 80% of deaths in developing countries are associated with life-threatening complications associated with diabetes.
Various treatment approaches have been implemented to avoid these complications and deaths related to diabetes. The mainstay of therapy for diabetes has been diet and exercise in conjunction with glucose-lowering drugs. Each of these agents are implicated with a potential benefit in health outcomes and mortality.
Agents from metformin have proven to be the first-line treatment due to its long-term benefits and improved glycemic control, to thiazolidinediones, which were falling out of favor due to their effects on heart failure and now proves to be beneficial in stroke.
Ongoing research efforts have compared various treatment modalities in head-to-head trials in order to understand glycemic events in diabetes. In a recent meta-analysis conducted by Giovanni F.M. Strippoli, PhD at the University of Bari, it is explained that sometimes these trials fail to dive into the cardiovascular mortality of these medications due to its inability to compare all treatment modalities simultaneously.
Strippoli and colleagues wanted to estimate the relative efficacy and safety of glucose-lowering medications. They extracted data from 301 clinical trials, which took into account 1,417,367 patient-months. All of these trials were 24 weeks of duration or longer. They included biguanides, sulfonylureas, thiazolidinediones, DPP-4 inhibitors, SGLT-2 inhibitors, GLP-1 agonists, basal insulin, meglitinides, and alpha-glucosidase inhibitors.
All of those studies that looked at medication regimens no longer supported by treatment guidelines or that have been withdrawn from the market were excluded from the study.
The primary endpoint of the study was the association of drug treatments with cardiovascular mortality.
Secondary endpoints were stratified into two endpoints, individual safety and individual efficacy. Secondary efficacy endpoints included all-cause mortality, myocardial infarction, stroke, A1c levels, and treatment failure.
Secondary safety endpoints included serious adverse events, hypoglycemia, and body weight.(My comment: the pros and cons that patients and doctors are most interested in)
After randomization, trials were separated into those where patients were given a monotherapy regimen, other drugs were added to metformin, or where other drugs added to metformin and sulfonylureas.
In those trials where drugs were used as monotherapy, there was no significant difference in the drugs used as monotherapy and the odds of death from cardiovascular complications. Nonetheless, these were associated with lower A1c levels. However, there was insufficient data to determine treatment rankings for these effects.
There was a greater risk of hypoglycemia with basal insulin (OR, 17.9 [95% CI, 1.97 to 162]; RD, 10% [95% CI, 0.08% to 20%]) or sulfonylureas (OR, 3.13 [95% CI, 2.39 to 4.12]; RD, 10% [95% CI, 7% to 13%]) as monotherapy. Furthermore, when analyzing those drugs added to metformin there was no significant association between any drug classes and the risk of death, despite 45 cardiovascular deaths reported in 26 trials. Similar findings were seen in all-cause mortality and myocardial infarction when adding other drugs to metformin therapy. However, there was lower risk of stroke in those regimens that included metformin and DPP-4 inhibitors when compared to metformin and sulfonylureas (OR, 0.47 [95% CI, 0.23 to 0.95]; RD, −0.2% [95% CI, −0.4% to −0.04%).
Treatment failure was noted less often in those patients receiving metformin and SGLT-2 inhibitors. In terms of weight and hypoglycemia, the use of metformin and sulfonylureas ranked worse when compared to all different treatment modalities. Furthermore, in the third set of trials that looked at drugs added to metformin and sulfonylureas, there was no association between any of drugs and the risk of cardiovascular death. This same trend was seen with all-cause mortality and serious adverse events; no significant association was observed.
Alpha-glucosidase inhibitors provided the least A1c reduction when added to metformin and sulfonylureas, when compared to the implementation of basal insulin or thiazolidinediones (SMD, 1.42 [95% CI, 0.57 to 2.26]). Treatment failure was more notable in patients receiving DPP-4 inhibitors when compared to those patients where basal insulin was added. Hypoglycemia was observed less in those patients receiving GLP-1 agonists than those receiving thiazolidinediones. All drug classes provided weight reductions except thiazolidinediones and basal insulin.
In conclusion, these findings highlight that the use of glucose lowering agents alone or in combination are not implicated with cardiovascular mortality, all-cause mortality, or serious adverse events. Significant reductions in A1c can be obtained with the use of individual glucose lowering) agents. When these agents are added to metformin, clinically significant reductions can be obtained.
Practice Pearls:
References:
Palmer SC, Mavridis D, Nicolucci A, et al. Comparison of Clinical Outcomes and Adverse Events Associated With Glucose-Lowering Drugs in Patients With Type 2 Diabetes: A Meta-analysis. JAMA. 2016;316(3):313-324. doi:10.1001/jama.2016.9400.
American Diabetes Association. Standards of medical care in diabetes: Summary of revisions-2016, 7: approaches to glycemic treatment. Diabetes Care. 2016;38(suppl):S4-S5
From Diabetes in Control July 17th 2016
The chance of an obese person attaining normal body weight is 1 in 210 for men and 1 in 124 for women, increasing to 1 in 1,290 for men and 1 in 677 for women with severe obesity, according to a study of UK health records led by King’s College London. The findings suggest that current weight management programmes focused on dieting and exercise are not effective in tackling obesity at population level.
The research, funded by the National Institute for Health Research (NIHR), tracked the weight of 278,982 participants (129,194 men and 149,788) women using electronic health records from 2004 to 2014. The study looked at the probability of obese patients attaining normal weight or a 5% reduction in body weight; patients who received bariatric surgery were excluded from the study. A minimum of three body mass index (BMI) records per patient was used to estimate weight changes.
The annual chance of obese patients achieving five per cent weight loss was 1 in 12 for men and 1 in 10 for women. For those people who achieved five per cent weight loss, 53 per cent regained this weight within two years and 78 percent had regained the weight within five years.
Overall, only 1,283 men and 2,245 women with a BMI of 30-35 reached their normal body weight, equivalent to an annual probability of 1 in 210 for men and 1 in 124 for women; for those with a BMI above 40, the odds increased to 1 in 1,290 for men and 1 in 677 for women with severe obesity.
Weight cycling, with both increases and decreases in body weight, was also observed in more than a third of patients. The study concludes that current obesity treatments are failing to achieve sustained weight loss for the majority of obese patients.
Dr. Alison Fildes, first author from the Division of Health and Social Care Research at King’s College London (and now based at UCL), said: ‘Losing 5 to 10 per cent of your body weight has been shown to have meaningful health benefits and is often recommended as a weight loss target. These findings highlight how difficult it is for people with obesity to achieve and maintain even small amounts of weight loss.’
“The main treatment options offered to obese patients in the UK are weight management programmes accessed via their GP. This evidence suggests the current system is not working for the vast majority of obese patients.” “Once an adult becomes obese, it is very unlikely that they will return to a healthy body weight. New approaches are urgently needed to deal with this issue. Obesity treatments should focus on preventing overweight and obese patients gaining further weight, while also helping those that do lose weight to keep it off. More importantly, priority needs to be placed on preventing weight gain in the first place.”
Professor Martin Gulliford, senior author from the Division of Health and Social Care Research at King’s College London, said: “Current strategies to tackle obesity, which mainly focus on cutting calories and boosting physical activity, are failing to help the majority of obese patients to shed weight and maintain that weight loss. The greatest opportunity for stemming the current obesity epidemic is in wider-reaching public health policies to prevent obesity in the population.”
Kings College London News Release
Alison Fildes. American Journal of Public Health. Published online ahead of print July 16, 2015: e1–e6. doi:10.2105/AJPH.2015.302773
Diabetes in Control August 27th 2016
At least an hour of physical activity needed to offset risk for several chronic conditions and mortality
Sedentary behavior has been associated with increased risk of several chronic conditions and mortality. However, it is unclear whether physical activity attenuates or even eliminates the detrimental effects of prolonged sitting. A new study examined the associations of sedentary behavior and physical activity with all-cause mortality.
The meta-analysis of trials involving more than 1 million individuals was reported online July 27 in The Lancet. It is one of a special series of papers on physical activity.
The Lancet notes that its first series on physical activity in 2012 concluded that, “physical inactivity is as important a modifiable risk factor for chronic diseases as obesity and tobacco.” The meta-analysis found that 1 hour of moderate-intensity activity, such as brisk walking or riding a bicycle, can offset the health risks of sitting for 8 hours a day. Twenty-five percent of all individuals in the study reported this level of physical activity. The study also discovered that even shorter periods of 25 minutes a day can be beneficial.
For those of us who work by sitting at a desk, it can be very difficult not to sit while we do our jobs. But, there are still many ways to get moving, like going for a walk during lunch, or even getting up and walking over to an associate to hand them a note instead of sending an email. There are many ways to get in your physical activity.
According to the researchers, the data from more than a million people is the first meta-analysis to use a harmonized approach to directly compare mortality between people with different levels of sitting time and physical activity. They included 16 studies, with data on 1,005,791 individuals (aged >45 years) from the United States, Western Europe, and Australia.
Researchers divided the study participants into four groups based on their reported levels of physical activity: <5 min/day; 25-35 min/day; 50-60 min/day; and 60-75 min/day.
Researchers noted that, “Among the most active, there was no significant relation between the amount of sitting and mortality rates, suggesting that high physical activity eliminated the increased risk of prolonged sitting on mortality.” But as the amount of physical activity decreased, the risk for premature death increased.
Researchers found prolonged sitting associated with an increase in all-cause mortality, mainly due to cardiovascular disease and cancer (breast, colon, and colorectal), noting that, “A clear dose-response association was observed, with an almost curvilinear augmented risk for all-cause mortality with increased sitting time in combination with lower levels of activity.”
Compared with the referent group (i.e., those sitting <4 h/day and in the most active quartile [>35·5 MET-h per week]), mortality rates during follow-up were 12–59% higher in the two lowest quartiles of physical activity (from HR=1·12, 95% CI 1·08–1·16, for the second lowest quartile of physical activity [<16 MET-h per week] and sitting <4 h/day; to HR=1·59, 1·52–1·66, for the lowest quartile of physical activity [<2·5 MET-h per week] and sitting >8 h/day). Daily sitting time was not associated with increased all-cause mortality in those in the most active quartile of physical activity. Compared with the referent (<4 h of sitting per day and highest quartile of physical activity [>35·5 MET-h per week]), there was no increased risk of mortality during follow-up in those who sat for more than 8 h/day but who also reported >35·5 MET-h per week of activity (HR=1·04; 95% CI 0·99–1·10). By contrast, those who sat the least (<4 h/day) and were in the lowest activity quartile (<2·5 MET-h per week) had a significantly increased risk of dying during follow-up (HR=1·27, 95% CI 1·22–1·31). Six studies had data on TV-viewing time (N=465 450; 43 740 deaths). Watching TV for 3 h or more per day was associated with increased mortality regardless of physical activity, except in the most active quartile, where mortality was significantly increased only in people who watched TV for 5 h/day or more (HR=1·16, 1·05–1·28).
In conclusion, the researchers emphasized that high levels of moderate intensity physical activity (i.e., about 60–75 min per day) seem to eliminate the increased risk of death associated with high sitting time. However, this high activity level attenuates, but does not eliminate the increased risk associated with high TV-viewing time. These results provide further evidence on the benefits of physical activity, particularly in societies where increasing numbers of people have to sit for long hours for work and may also inform future public health recommendations.
In another study published online by JAMA Ophthalmology in August, they found that sedentary behavior may be associated with diabetic retinopathy. The analysis included 282 participants with diabetes. The average age was 62 years, 29 percent had mild or worse DR, and participants engaged in an average of 522 min/d of SB. The author found that for a 60-min/d increase in SB, participants had 16 percent increased odds of having mild or worse DR; total PA was not associated with DR. “The plausibility of this positive association between SB and DR may in part be a result of the increased cardiovascular disease risks associated with SB, which in turn may increase the risk of DR. In order to prove a cause and effect of SB and worsening DR s larger study would be needed.”
Practice Pearls
Lancet. Published online July 27, 2016. Abstract Editorial How Much Exercise Compensates for Sitting at a Desk Eight Hours A Day?#848 (1)]–[www_diabetesincontrol_com_how_]-[MTExNjQyNDI1NTE1S0]–
If you are over the age of 60 it’s time to stop fretting about your total cholesterol and low density cholesterol levels. Unless perhaps the levels are on the low side. Indeed total mortality rates are at least the same and usually better if your cholesterol levels are high. Many doctors now believe it is the PATTERN of different lipid levels that is much more important, particularly high triglycerides and low HDL.
This systematic review tells the story:
Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review — Ravnskov et al. 6 (6) — BMJ Open
Almost every patient with stress related mental health problems reports at least one somatic symptom and 45 per cent report six symptoms or more, according to a Swedish study of 228 patients suffering from what is termed as exhaustion disorder.
Here is the chart run down of the most common symptoms:
Almost all: Tiredness and low energy
67% Nausea, gas and indigestion
65% Headaches
57% Dizziness
Men and women reported the same number of symptoms.
Chest pain and sexual problems and pain during sex were more reported in men.
Pain in the arms, legs, joints, knees, hips reported more in the over 40s.
The more severe the mental health problem the higher the number of somatic symptoms.
From Human Givens Volume 21 No 1 2014
(BMC Psychiatry, 2014, 14, 118)
Although the causes of fibromyalgia are insufficiently understood at present and there is dubiety over whether the condition is due to stress or physical factors I have reproduced a chart which does show many psychosomatic symptoms in its presentation.
Diabetes Diet 
I’m delighted that The BMJ has stood by this article and decided against retraction. Two outside reviewers judged that the criticisms of the piece did not merit its retraction, and in the end, the corrections made by The BMJ do not, in my view, materially undermine any of the article’s key claims. This article therefore stands as one of the most serious ever, peer-reviewed critiques of the expert report for the US Dietary Guidelines for Americans (DGAs).
The importance of the DGAs, and therefore of this article, should not be understated (and indeed was recognized by many in the mainstream media when the article was published). The DGAs have long been considered the “gold standard,” informing the US food supply, military rations, US government feeding assistance programs such as the National School Lunch Program which are, altogether, consumed by 1 in 4 Americans each month, as well as the guidelines of professional societies and governments around the world, and eating habits generally.
Yet rates of obesity began to shoot upwards in the very year, 1980, that the DGAs were introduced, and the diabetes epidemic began soon thereafter. A critically important yet little understood issue is why the DGAs have failed, so spectacularly, to safeguard health from the very nutrition-related diseases that they were supposed to prevent.
In documenting fundamental failures in the science behind the DGAs, this article offers new insights; It establishes that a vast amount of nutrition science funded by the National Institutes of Health and other governments worldwide has, for decades, been systematically ignored or dismissed, and that therefore, that the DGAs are not based on a comprehensive reviews of the most rigorous science. Incorporating this long-ignored relevant science would likely lead to fundamentally different DGAs and could very well be an important step in infusing them with the power to better fight the nutrition-related diseases.
A fundamental question is why 170+ researchers (including all the 2015 DGA committee members, or “DGAC”), organized by the advocacy group, the Center for Science in the Public Interest (CSPI), would sign a letter asking for retraction. After all, in the weeks following publication, any person had the opportunity to submit a “Rapid Response” to the article, and both CSPI and the DGAC did so, alleging many errors. I responded to them all in my Rapid Response. This is the normal post-publication process.
Yet after all this, CSPI returned for a second round of criticisms, recycling two of the issues (CSPI points #3 and #10) that I had already addressed in my Rapid Response (and which had required no correction), adding another 9 (one of which, #4, contained no challenge of fact), and demanding that based on these alleged errors, the article be retracted. CSPI then circulated this letter widely to colleagues and asked them to sign on.
This lack of substance in the retraction effort seems to point to the reality that it was first and foremost an act of advocacy—a heavy handed attempt to silence arguments with which CSPI, a longtime supporter of the Dietary Guidelines and its allies disagree.[ footnote 1] And this applies not just to the retraction letter but to other CSPI efforts to stifle alternative viewpoints. Earlier this year, for example, I was dis-invited from the National Food Policy Conference after CSPI, together with the USDA official in charge of the Dietary Guidelines, threatened to withdraw if I were included, details of which are reported here and which a Spiked columnist called an act of “censorship.”
It’s important to note that I am not the only person disturbed by the lack of rigorous science underpinning our dietary guidelines. Numerous scientists around the world have expressed concern about the science. And indeed, this consternation is shared by no less than the US Congress, which held a hearing on Oct 7, 2015 to address its serious doubts about the DGAs. Such was this concern that last year that Congress mandated the first-ever major peer-review of the DGAs, by the National Academy of Medicine. Congress appropriated $1 million for this review, and it additionally stipulated that all members of the 2015 DGA committee recuse themselves from the process.
What is the dangerous information challenging the DGAs that cannot be heard on a conference panel nor published in a peer-reviewed journal?
The major findings of this article are that:
1. The DGAC’s finding that the evidence of a “strong” link between saturated fats and heart disease was not clearly supported by the evidence cited. (Note that as of last year, the Heart and Stroke Foundation of Canada no longer limits saturated fats. Note, also, that Frank Hu, the Harvard epidemiologist in charge of the DGAC review on saturated fats, was an energetic promoter of the retraction letter against my article that critiqued his review, according to emails obtained through FOIA requests);
2. Successive DGA committees have for decades ignored or dismissed a large body of rigorous (randomized controlled trial) literature on the low-fat diet, on more than 50K subjects, collectively finding that this diet is ineffective for fighting obesity, diabetes, heart disease or any kind of cancer;
3. Although the DGAs have for decades recommended avoiding saturated fats and cholesterol to prevent heart disease, no DGA committee has ever directly reviewed the enormous body of rigorous (government-funded, randomized controlled trials) evidence, testing more than 25,000 people, on this hypothesis. Many reviews of this data have concluded that saturated fats have no effect on cardiovascular mortality;
4. The DGAC ignored a large body of scientific literature on low-carbohydrate diets (including several “long term” trials, of 2-years duration) demonstrating that these diets are safe and highly effective for combatting obesity, diabetes, and heart disease;
5. The Nutrition Evidence Library (NEL) set up by USDA to do systematic reviews of the science did not meet its own standards for its review of saturated fats in 2010;
6. Although the DGAC is supposed to consult the NEL to conduct systematic reviews of the science, the 2015 DGAC did so for only 67% of the questions that required systematic reviews;
7. For a number of key reviews, the 2015 DGAC relied on work done in part by the American Heart Association and the American College of Cardiology, which are private associations supported by industry and therefore have a potential conflict of interest;
8. The DGAs, for the first time, introduce the “vegetarian diet” as one of its three, recommended “Dietary Patterns,” yet a NEL review of this diet concluded that the evidence for this its disease-fighting powers is only “limited,” which is the lowest rank of evidence assigned for available data;
9. The DGA’s three recommended “Dietary Patterns” are supported by only limited evidence. The NEL review found only “limited” or “insufficient” evidence that the diets could combat diabetes and only “moderate” evidence that the diets can help people lose weight. The report also gave a strong rating to the evidence that its recommended diets can fight heart disease, yet here, several studies are presented, but none unambiguously supports this claim. In conclusion, the quantity of recommended diets are supported by a small quantity of rigorous evidence that only marginally supports claims that these diets can promote better health than alternatives;
10. The DGA process does not require committee members to disclose conflicts of interest and also that, for the first time, the committee chair came not from a university but from industry;
11. The 2015 DGAC conducted a number of reviews in ways that were not systematic. This allowed for the potential introduction of bias (e.g., cherry picking of the evidence).
This last claim, on the systematic nature of the DGAC reviews, is the subject of the corrections published in The BMJ this week, and refer to CSPI points #1, #2, #7, and #8 (two of which are statements in the text and two of which are in the supporting tables). I am grateful to have had the opportunity to work with The BMJ on developing this notice.
The BMJ has placed a word limit on my response. For the rest of this comment, please see: http://thebigfatsurprise.com/comment-bmj-correction-notice/
Footnote 1
CSPI has fought for decades to eliminate saturated fats from the American food supply (so much so, that throughout the late 1980s, CSPI advocated for replacing saturated fats with trans fats and succeeded in driving up consumption of trans fats to historic levels, as described in The Big Fat Surprise, pp.227-228). CSPI has also long advocated for shifting away from animal foods containing saturated fats, towards a plant-based diet based on grains and industrial vegetable oils. The researchers who joined CSPI in signing the letter are largely adherents to this view; many have participated in generating the science that has been used to support the hypothesis that fat and cholesterol cause heart disease, and it is upon this hypothesis that the Guidelines have been based.
Competing interests: I have read and understood BMJ policy on declaration of interests and declare that I am the author of The Big Fat Surprise (Simon & Schuster, 2014), on the history, science, and politics of dietary fat recommendations. I have received modest honorariums for presenting my research findings presented in the book to a variety of groups related to the medical, restaurant, financial, meat, and dairy industries. I am also a board member of a non-profit organization, the Nutrition Coalition, dedicated to ensuring that nutrition policy is based on rigorous science.