Reductions in Blood Pressure Following Energy Restriction for Weight Loss Do Not Rebound after Re-Establishment of Energy Balance in Overweight and Obese Subjects

Brinkworth, Grant D.; Wycherley, Thomas P.; Noakes, Manny; Clifton, Peter M.

doi:10.1080/10641960802275734

Cited by 22 publications

(19 citation statements)

References 37 publications

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“…In addition potassium intake will be measured using multiple methods to strengthen validity of the data (24-hour urinary excretion, mid-stream sodium-to-potassium ratio, diet history). Weight also directly affects BP [69], so all efforts will be made to keep weight stable during the 6 week trial and weight will be measured at all follow up visits as per Figure 2. GFR may directly affect serum biochemical markers, therefore estimated GFR (eGFR) will be assessed concurrently with other biochemical markers.…”

Section: Discussionmentioning

confidence: 99%

The effect of lowering salt intake on ambulatory blood pressure to reduce cardiovascular risk in chronic kidney disease (LowSALT CKD study): protocol of a randomized trial

et al. 2012

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BackgroundDespite evidence implicating dietary sodium in the pathogenesis of cardiovascular disease (CVD) in chronic kidney disease (CKD), quality intervention trials in CKD patients are lacking. This study aims to investigate the effect of reducing sodium intake on blood pressure, risk factors for progression of CKD and other cardiovascular risk factors in CKD.Methods/designThe LowSALT CKD study is a six week randomized-crossover trial assessing the effect of a moderate (180 mmol/day) compared with a low (60 mmol/day) sodium intake on cardiovascular risk factors and risk factors for kidney function decline in mild-moderate CKD (stage III-IV). The primary outcome of interest is 24-hour ambulatory blood pressure, with secondary outcomes including arterial stiffness (pulse wave velocity), proteinuria and fluid status. The randomized crossover trial (Phase 1) is supported by an ancillary trial (Phase 2) of longitudinal-observational design to assess the longer term effectiveness of sodium restriction. Phase 2 will continue measurement of outcomes as per Phase 1, with the addition of patient-centered outcomes, such as dietary adherence to sodium restriction (degree of adherence and barriers/enablers), quality of life and taste assessment.DiscussionThe LowSALT CKD study is an investigator-initiated study specifically designed to assess the proof-of-concept and efficacy of sodium restriction in patients with established CKD. Phase 2 will assess the longer term effectiveness of sodium restriction in the same participants, enhancing the translation of Phase 1 results into practice. This trial will provide much-needed insight into sodium restriction as a treatment option to reduce risk of CVD and CKD progression in CKD patients.Trial registrationUniversal Trial Number: U1111-1125-2149. Australian New Zealand Clinical Trials Registry Number: ACTRN12611001097932

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Section: Discussionmentioning

confidence: 99%

The effect of lowering salt intake on ambulatory blood pressure to reduce cardiovascular risk in chronic kidney disease (LowSALT CKD study): protocol of a randomized trial

et al. 2012

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“…This attenuation did not occur when the 'established' intervention was combined with the DASH diet, highlighting that dietary composition such as reduced saturated fat and increased potassium and magnesium intakes may enhance the antihypertensive response [51]. A limited number of studies have examined the separate effects of negative energy balance and weight loss on blood pressure [55][56][57]. Laaksonen et al [57] compared the effects of intensive weight loss over 8 weeks (mean weight change À14.4 kg) and weight loss maintenance at 6 months (mean weight change À14.5 kg) in obese metabolic syndrome patients.…”

Section: Effect Modifiersmentioning

confidence: 92%

“…The depressor response to weight loss may be greater in hypertensive than normotensive individuals [44,50,55,56].…”

Section: Effect Modifiersmentioning

confidence: 95%

European Society of Hypertension Working Group on Obesity Antihypertensive effects of weight loss: myth or reality?

Straznicky¹,

Esler²,

Lambert³

et al. 2010

Journal of Hypertension

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Obesity and hypertension are two major cardiovascular risk factors that frequently coexist and contribute increasingly to clinical and public health burden worldwide [1,2]. Overall, 23% of the world's adult population in 2005 was overweight and 10% was obese and these rates are projected to increase markedly over the next two decades [1,3]. For both men and women, arterial hypertension is the most common co-morbidity, with prevalence rates ranging from 34 to 65%, depending on the severity of obesity [4]. Weight loss is regarded as first-line treatment for combating obesity and associated risk factors and is emphasized by all hypertension management guidelines [5][6][7]. Whereas short-term effects of intentional weight loss are well established as being beneficial on blood pressure, the long-term effects remain controversial [8,9]. This state-of-affairs may relate to specific caveats entailed in using weight loss as an intervention: weight loss cannot be prescribed in a fixed dose, instead, individual responses vary widely; weight loss effects on blood pressure may be modified by a number of concurrent factors, including energy balance, dietary composition, physical exercise, co-morbidities, genetic profile and pharmacological co-treatments; and long-term studies of weight loss encompass varying combinations of active weight loss (with nadir weights usually attained at $6 months), weight loss maintenance and subsequent weight regain [10,11]. This position paper of the European Society of Hypertension examines current evidence on the effectiveness of weight loss through lifestyle interventions, surgical and antiobesity drug treatments, as an antihypertensive modality. One of the major limitations when reviewing the evidence is that in most obesity studies, blood pressure reduction was not the primary outcome measure. Obesity hypertension: epidemiology and pathophysiologyPositive associations between various adiposity measures and blood pressure have been recognized since the 1920s [12,13] and subsequently confirmed in many large crosssectional and prospective epidemiological studies [14,15]. For example, recent analysis of the Nurses' Health study indicated that BMI was the most powerful predictor of incident hypertension, with a BMI of 25 or greater having an adjusted population attributable risk of 40% compared with a BMI of less than 25 [16]. The primacy of central obesity in conferring increased incident hypertension risk has been highlighted by the Normative Ageing study [17], the Australian AusDiab study [18] and by a communitybased prospective cohort study in Japanese Americans, in which visceral adiposity was quantified by computed tomography [19]. In Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study participants with the metabolic syndrome, the adjusted 10-year risk of developing new onset hypertension was about three and a half times greater than that in individuals without metabolic syndrome [20]. Conversely, in population studies, high blood pressure predicted future body weight gain [21...

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“…3 Even small reductions in weight significantly improve outcomes of obesity related chronic diseases. 4 Currently life style modifications are main stay treatment of obesity in type 1 diabetes. Whilst pharmacotherapy can augment the effect of life style modifications, 5 its role is limited such that bariatric surgery is often the only effective treatment for morbid obesity.…”

Section: Introductionmentioning

confidence: 99%

The use of liraglutide, a GLP-1 agonist, in obese people with type 1 diabetes

Gillani

Singh

2014

Br J Diabetes

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Aims: Optimisation of glycaemic control in type 1 diabetes often results in unwanted weight gain. glucagon-like peptide-1 (GLP-1) agonist use is associated with weight reduction in type 2 diabetes but its use in type 1 diabetes is little studied. Methods: We developed a protocol for GLP-1 use in people with type 1 diabetes and obesity in which liraglutide was initiated and up-titrated whilst insulin doses were simultaneously titrated according to glycaemic parameters. Results: Of 15 patients offered treatment, 8 proceeded. Baseline parameters were (n=8, mean + SD): (age 50 ± 6 years, BMI 40.4 ± 5.5 kg/m 2 , weight 123.0 ± 23.9 kg, HbA1c 8.5 ± 1.7%, total daily insulin dose 131 ± 112 units/day. By intention to treat analysis (n=8, 12 months), at 3, 6 and 12 months compared to baseline, weight loss was 6.8 ± 4.1 kg, 10.0 ± 5.6 kg and 8.9 ± 8.4 kg (p=0.026). The reductions in insulin dosage were significant over 6 months (n=8, p=0.045) or when analysing only those who completed 12 months of liraglutide therapy (n=6, p=0.044). Conclusions: GLP-1 agonist use in patients with type 1 diabetes may be advantageous where weight reduction becomes both a constraint and a therapeutic objective. Br J Diabetes Vasc Dis 2014;14:98-101

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Reductions in Blood Pressure Following Energy Restriction for Weight Loss Do Not Rebound after Re-Establishment of Energy Balance in Overweight and Obese Subjects

Cited by 22 publications

References 37 publications

The effect of lowering salt intake on ambulatory blood pressure to reduce cardiovascular risk in chronic kidney disease (LowSALT CKD study): protocol of a randomized trial

The effect of lowering salt intake on ambulatory blood pressure to reduce cardiovascular risk in chronic kidney disease (LowSALT CKD study): protocol of a randomized trial

European Society of Hypertension Working Group on Obesity Antihypertensive effects of weight loss: myth or reality?

The use of liraglutide, a GLP-1 agonist, in obese people with type 1 diabetes

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