4 Weight Loss Strategies "Preventing Hypertension": 2021AHA Scientific Statement

Compilation: Chen Kang, Department of Endocrinology, Chinese People's Liberation Army General Hospital Foreword: Recently, the American Heart Association (AHA) released a new weight loss strategy for the prevention and treatment of hypertension, and proposed the following ways to achieve weight loss goals: ➤ diet control ➤ sports activities ➤Drug therapy ➤Metabolism surgery obesity, hypertension and cardiometabolic risk epidemiology According to recently published estimates, nearly half (45%) of adults in the United States suffer from hypertension, defined as systolic blood pressure (SBP) ≥130 mm Hg , Diastolic blood pressure (DBP) ≥80 mm Hg, or taking antihypertensive drugs
.

Hypertension is the main cause of increased mortality, chronic kidney disease and cardiovascular disease (CVD), including myocardial infarction, heart failure and stroke
.

Weight gain and obesity are the main risk factors for hypertension and often occur at the same time as hypertension; therefore, intentional weight loss strategies represent ideal goals for reducing the risk of chronic diseases and mortality in individuals with overweight/obesity and hypertension
.

The increase of visceral obesity (rather than subcutaneous obesity) has a great relationship with occasional hypertension
.

As the global prevalence of obesity increases, the prevalence of hypertension is expected to increase
.

According to estimates by the World Health Organization,> 1 billion adults were overweight in 2016, of which> 650 million were obese
.

From 2017 to 2018, the prevalence of severe obesity among American adults was 9.
2%, which has increased by 38% in just 10 years
.

In addition, the prevalence of obesity and overweight in children and adolescents has risen sharply, affecting> 18% globally
.

Therefore, hypertension associated with overweight is a growing problem that will significantly affect the global healthcare system
.

If weight loss continues, deliberate weight loss through dietary intervention or increased physical activity (PA) can produce a clinically significant drop in blood pressure (BP)
.

However, in the long run, these weight loss strategies can be challenging
.

When combined with life>
.

Evidence-based guidelines and scientific statements for obesity treatment have been previously issued
.

The impact of obesity on hypertension Target organ damage Obesity and hypertension are closely related to target organ damage in the vasculature, heart, kidney and brain
.

Evidence from large-scale cohort studies suggests that there is a clear dose-response relationship between more obesity and a higher risk of heart failure, coronary heart disease, and stroke
.

In addition, in a patient-level meta-analysis of participants in 39 cohort studies, Chang et al.
found that a body mass index (BMI) of 40 kg/m2 compared with a body mass index of 25 kg/m2 resulted in decreased renal function or end-stage The risk of kidney disease is 2 times higher
.

Compared with conventional care, significant weight loss due to MS is associated with renal hyperperfusion, proteinuria, and a reduced risk of major adverse CVD events and end-stage renal disease
.

After adjusting for hypertension, the relationship between obesity and the risk of target organ damage disappeared, indicating that hypertension is a key explanatory factor for target organ damage in obesity
.

In a post-mortem analysis of the Systolic Blood Pressure Interven-tion Trial, higher BMI was not associated with the differential effect of enhanced BP control on CVD events
.

Nevertheless, proper management of hypertension is still essential to reduce the adverse effects of obesity on target organs
.

Pathophysiology of obesity hypertension The pathophysiology of obesity hypertension is multifactorial and highly time-dependent (Figure 1)
.

Overfeeding of humans and laboratory animals will quickly activate the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS), even before a significant increase in weight
.

In contrast, in most obese patients (including those with type 2 diabetes), the reduction in calorie intake due to voluntary food restriction or MS will quickly lower BP and reduce metabolic disorders
.

Although the increase in BP accompanied by weight gain is initially mild, for chronic obese patients, target organs will gradually be damaged, thereby aggravating high blood pressure
.

The long-term effect of obesity on BP also depends on where the excess fat is stored.
Visceral fat is more likely to cause high blood pressure than subcutaneous fat
.

Figure 1 The effect of obesity on the increase in blood pressure The effect of obesity on the increase in blood pressure is multifactorial, including neurohormonal changes, physical compression of fat on the kidney, increased renal sodium chloride (NaCl) reabsorption, and inflammation
.

Metabolic abnormalities and inflammation interact with high blood pressure, causing kidney damage and exacerbating blood pressure
.

MC4R represents the melanocortin 4 receptor; MR is the mineralocorticoid receptor
.

Mechanisms that trigger obesity hypertension Obesity causes the extracellular fluid volume expansion and blood flow in many tissues, which leads to venous return and increased cardiac output
.

Volume expansion is mediated by an increase in renal tubular sodium reabsorption, because renal blood flow and glomerular filtration rate initially increase during obesity, that is, before kidney injury
.

There are at least 3 main factors that lead to increased sodium reabsorption: ➤RAAS activation, including mineralocorticoid receptor stimulation; ➤SNS activation, especially increased renal sympathetic nerve activity; ➤Kidney compression through visceral, retroperitoneal and renal sinus fat
.

Several other factors are also considered as potential mediators of obesity hypertension, including insulin resistance, inflammation, natriuretic hormone deficiency, changes in the intestinal microbiota, and increased perivascular fat tissue
.

However, the importance of these mechanisms in causing obese hypertension remains unclear
.

1.
SNS (Sympathetic Nervous System) activation of obesity will lead to SNS activation, which is controlled to varying degrees in various tissues, and is mainly related to the increase in visceral obesity
.

The increase in SNS activity is usually mild, does not reduce tissue blood flow, but is sufficient to increase renal sodium reabsorption and renin release
.

In experimental obesity and treatment-resistant obese patients, denervation can significantly reduce high blood pressure
.

Many factors cause sympathetic nerve activation in obese patients, including: ➤stress reflex dysfunction, ➤hypoxia ➤chemoreceptor activation, especially in sleep apnea patients
.

➤Leptin is a kind of adipokines secreted in proportion to the degree of obesity.
It also stimulates SNS activity in obese hypertension, mainly by activating premelanocortin neurons, which in turn activates melanocortin 4 receptors in the brain
.

2.
RAAS activation A variety of mechanisms related to visceral obesity activate the RAAS effect, including kidney compression and increased SNS activation
.

Experimental and clinical studies have shown that RAAS blockers can effectively reduce the BP of obese subjects, although angiotensin II is only slightly increased, indicating an increased sensitivity to angiotensin II
.

Even if plasma aldosterone is normal or lower than normal levels, mineralocorticoid receptor antagonism can also reduce BP and reduce target organ damage in obese hypertensive patients, which indicates that mineralocorticoid receptor activation is at least partially independent of aldosterone
.

3.
Kidney compression.
With the accumulation of visceral fat, perirenal fat, and renal sinus fat and the increase in intra-abdominal pressure, the kidney becomes compressed, which further activates the RAAS effect, increases the reabsorption of sodium, and promotes the triggering of SNS BP increased
.

4.
Inflammation, metabolic disorders and progressive heart and kidney damage exacerbate obesity, hypertension.
Visceral obesity can trigger inflammatory responses in adipose tissues and organs throughout the body, including the kidneys.
This is due to the activation of resident macrophages and the growth of macrophages.
It is caused by decomposition and secretion of pro-inflammatory cytokines in local and paracrine/endocrine modes
.

Ectopic lipid accumulation in the liver, skeletal muscle, kidneys, blood vessels and other organs leads to "lipotoxicity, inflammation, and a series of metabolic disorders, including dyslipidemia, insulin resistance, glucose intolerance, and type 2 diabetes (over time) )"
.

These chronic inflammation and metabolic diseases interact with increased blood pressure, causing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction in blood vessels, heart, and kidneys
.

In the early stages of obesity, there are mild to moderate renal fibrosis, microalbuminuria, mesangial matrix expansion, glomerular hypertrophy, focal segmental glomerulosclerosis and podocyte damage, accompanied by glomerular filtration Increased rate (increased glomerular filtration rate)
.

As obesity, hypertension, metabolic and inflammatory diseases persist for many years, the glomerular filtration rate decreases, replaced by a decrease in glomerular filtration rate and an increase in BP salt sensitivity associated with nephron loss
.

Obesity can also aggravate the harmful effects of other primary kidney damage, such as unilateral nephrectomy, kidney transplantation, and immunoglobulin A nephropathy [31]
.

As kidney function declines, high blood pressure becomes more serious, proper BP control becomes more difficult, and heart and blood vessel damage throughout the body is also aggravated
.

The impact of diet on sustained weight loss and hypertension control.
Several national guidelines recommend a heart-healthy diet alone or as part of an overall healthy life>
.

Current dietary guidelines emphasize an approach based on dietary patterns, rather than individual foods and nutrients for CVD prevention and control
.

The most mature healthy eating pattern is: ➤Mediterranean diet ➤Dietary Approaches to Stop Hypertension (DASH)
.

These two diets are also rich in fruits, vegetables, legumes, nuts and seeds, eat moderate amounts of fruits, seafood, poultry and dairy products, and consume small amounts of red meat and processed meats and sweets
.

The Mediterranean diet also promotes the use of olive oil in large quantities, and the regular but moderate drinking of wine (especially red wine)
.

1.
The 2019 Cochrane Randomized Controlled Trial Review (RCT) of the Mediterranean diet found that the Mediterranean diet has an effect on SBP (3.
0 mm Hg [95% CI, -3.
5 to -2.
5]) and DBP (-2.
0 mm Hg [95% CI, -2.
3 To -1.
7]) has a significant beneficial effect
.

A meta-analysis of 16 RCTs found that the Mediterranean diet intervention can also reduce weight (-1.
8 kg [95% CI, -2.
9 to -0.
6]).
2.
The DASH diet appears to provide a stronger diet compared with the Mediterranean diet.
The effect of lowering blood pressure
.

In a meta-analysis of 24 dietary pattern intervention RCTs, the DASH diet was effective in reducing SBP disease (-7.
6mm Hg [95% CI, -10.
0 to -5.
3]) and DBP (-4.
2mmHg [95% CI,- 5.
9 to -2.
6]) has a great effect
.

When combined with weight loss and exercise intervention, the DASH diet significantly reduced BP (-16.
1/9.
9mm Hg) compared to the DASH diet alone (-11.
2/7.
5)
.

In the DASH sodium test, compared with the high sodium intake (3450 mg/d) DASH diet, the low sodium intake (1150 mg/d) DASH diet reduced SBP by 0.
9mm Hg (95% CI, -2.
1 to -0.
3), 3.
3mm Hg (95% CI, -4.
7 to -1.
9), 4.
9mm Hg (95% CI, -7.
3 to -2.
6), and 10.
4mm Hg (95% CI-15.
5 to -10.
4)
.

Independent of dietary patterns, low sodium intake is also conducive to BP control
.

In a meta-regression analysis of 133 RCTs, sodium intake decreased by 2300 mg/d and SBP decreased by 7.
7 mmHg (95% CI, -10.
4 to -5.
0) and DBP decreased in people with BP>131/78 mm Hg 3.
0mmHg (95% CI, -4.
6 to -1.
4) is relevant
.

In addition, the results of the meta-analysis showed that the 24-hour urine sodium decreased by 50 mmol (the objective indicator of sodium intake, SBP decreased by 1.
1 mmHg (95% CI, 0.
7-1.
5)
.

The effect of sodium reduction on BP was in older age, hypertension, and blacks.
It seems to be particularly obvious in individuals
.

Increased potassium consumption is also associated with decreased BP, but excessive potassium intake is associated with adverse results
.

3.
Intermittent fasting/light fasting In addition to these widely recommended methods to improve diet composition and quality, some studies have also investigated the time of eating that can reduce weight and control blood pressure
.

A small clinical study of patients with metabolic syndrome showed that intermittent fasting may reduce SBP and DBP moderately, similar to the reduction achieved through other interventions to lose weight
.

A systematic review of 4 randomized controlled trials showed that intermittent fasting is effective for short-term weight loss, but has a weaker effect on BP reduction [51]
.

Another systematic review and meta-analysis of 6 randomized controlled trials showed that intermittent fasting is more effective for weight loss (4.
1 kg [95% CI -2.
0 to -6.
3]) than no treatment, but is associated with continuous energy limitation ( -1.
0kg [95%CI-2.
5 to 0.
4]) There is no significant difference
.

The effect of intermittent fasting on BP control needs further research
.

The effect of PA (physical activity) on sustained weight loss and the hypertension control mechanism that PA lowers blood pressure PA is defined as body movement produced by the contraction of skeletal muscles, which increases energy expenditure above resting levels
.

Exercise is a moderate to vigorous intensity PA, which is planned, structured, and repetitive, designed to improve or maintain health
.

Sedentary behavior, characterized by energy expenditure ≤ 1.
5 metabolic equivalents in sitting or prone position, is considered to be a structure different from the time it takes for moderate or severe PA, because both are related to all-cause mortality Independently related
.

Table 1 shows the proposed mechanism that may be the basis for the benefit of higher PA levels on BP and cardiometabolic risks
.

1.
The effect of PA on obesity hypertension.
Evidence shows that PA and exercise training (ET) can reduce obesity, BP and obesity hypertension
.

Although it has been found that CVD risk factors have improved, with a weight loss of only 2% to 3%, the current recommendation is to lose at least 5% to 10% (clinically significant weight loss) within 6 months because of the main CVD risk factors (including blood lipids).
) And other related cardiometabolic risk factors (including insulin sensitivity, arterial stiffness and resting blood pressure) have more profound improvements
.

ET (exercise training) also has a significant effect on blood pressure, regardless of body weight
.

Recently, Noone et al.
conducted a meta-analysis of 93 RCTs and found that both ET and drug treatment effectively reduced BP
.

Although point estimates are more prone to drug treatment than ET, these differences are not statistically significant
.

Due to its low cost and no major adverse effects or drug interactions, ET should be used for all anti-hypertensive and weight loss work except for the effect of ET on improving the level of cardiopulmonary function (which may be one of the strongest CVD risk markers) Part
.

A weight loss of 5% to 10% can reduce SBP and DBP by> mm Hg and mm Hg, respectively, and a weight loss of 10 kg can reduce SBP by 5-20 mmHg
.

Generally, the weight loss of <150min/wk PA is less than the minimum, 150-225min/wk PA loses 2-3kg, 225-420min/wk PA loses 5-7.
5kg, and requires 200 to 300 minutes/week.
PA is used for long-term weight maintenance
.

Resistance training does not promote clinically significant weight loss, but it does have a mild effect on improving BP and promoting beneficial body composition changes, and resistance training and muscle strength have an effect on reducing CVD mortality, and PA/cardiopulmonary Function is irrelevant
.

2.
Reduce sedentary to lower blood pressure.
There is strong evidence that PA intervention can lower BP
.

A systematic review of 26 studies showed that pedometers increased the PA of adult outpatients and decreased SBP and DBP
.

Increasing evidence from intervention studies suggests that reducing sedentary (ie, reducing or interrupting sitting time for walking or standing rest) leads to a decrease in SBP or DBP by 1 to 16 mmhg
.

Individuals with high blood pressure may have a greater reduction in BP with interruption of sitting time than individuals without high blood pressure
.

Due to the complex relationship between PA and sitting position, the guidelines currently do not recommend a specific prescription to indicate how much sitting time should be reduced in order to observe a decrease in blood pressure
.

High fatigue rate and reduced long-term effects of diet and exercise on blood pressure control Although dietary changes, exercise, and related weight loss are effective strategies for reducing BP, the recurrence rate of hypertension is higher in people who receive such life>
.

Based on the review of prospective trials, the beneficial effects of weight loss on BP were significantly reduced or reversed over time
.

This recidivism is mostly related to the common conditions of weight recovery
.

For example, the TOHP Phase II study (Hypertension Prevention Trial) showed that in adults with moderately elevated blood pressure, weight loss or reduced sodium intake will lower blood pressure, although this effect will diminish over time
.

A post-mortem analysis of TOHP-II in the weight loss group showed that those who maintained weight loss were 65% less likely to develop high blood pressure than participants who were randomly assigned to the routine care control group
.

Several complex physiological adaptations to weight loss promote weight recovery, including increased energy efficiency and decreased energy expenditure due to lower resting metabolic rate, and decreased satiety caused by hormonal changes
.

Therefore, the maintenance of successful weight loss over many years usually requires high levels of PA and limited sedentary time, frequent weight monitoring, and high levels of dietary restrictions
.

In patients receiving life>
.

For example, in response to a daily 800-calorie diet for 9 weeks, the weight of 34 men and women dropped from an average of 101.
7 to 87.
3 kg (–14.
4 kg), and the 24-hour dynamic SBP decreased from 130.
1 mm Hg to 121.
1 mm Hg (– 9mm Hg)
.

However, despite the complete weight loss at 6 months, the average 24-hour SBP rose to 126.
5mm Hg (–3.
6mmHg), which was 40% of the initial response.
Also, although about 88% of the initial weight loss was maintained in the first year (–12.
6 kg), but SBP increased to 127.
9 mm Hg (change from baseline – 2.
2 mm Hg, approximately 24% of the initial BP response)
.

In the course of weight loss, some physiological changes that promote the reduction of BP (including reduction in SNS activity and plasma renin activity) are transient even in subjects who continue to lose weight
.

This suggests that in subjects who achieve weight loss through life>
.

Medication 1.
Weight loss drugs approved by the U.
S.
Food and Drug Administration have limited therapeutic response to life>
.

Anti-obesity drug treatment is intended as an adjunct to diet and exercise
.

The Food and Drug Administration (FDA) of the United States Food and Drug Administration (FDA) has approved four drug therapies that are only used for short-term (up to 12 weeks) obesity treatment: phentermine, diethylaminopropiophenone; Diethylpropion, phendimetrazine, and benzphetamine
.

These drugs have a close structure and mechanism relationship with amphetamine (amphetamine)
.

Currently, there are 5 drug therapies approved by the FDA for long-term weight loss: orlistat, phentermine/topiramate sustained-release, naltrexone/bupropion, liraglutide 3.
0mg and smeglutide (Semaglutide) 2.
4 mg, administered subcutaneously every week
.

The main mechanism of orlistat is to reduce the absorption of fat in the intestines
.

Phentermine/topiramate, naltrexone/bupropion and liraglutide are centrally acting drugs that increase satiety and reduce hunger
.

In RCT, the drugs approved for long-term use (and life>
.

Weight loss in the first 3 to 4 months after starting drug therapy is the most consistent predictor of one-year response to these drugs and can be used as a guide to continue drug therapy rather than switch to alternative weight loss strategies
.

Patients who continue to lose weight and these drugs are well tolerated can benefit from long-term weight recovery or additional gains when these drugs are used continuously for more than 1 year or after they are stopped
.

Due to various factors, including the mechanism of action, weight loss effects, and differences in the study population, the long-term effects of anti-obesity drugs on BP are mixed
.

RCT showed that patients randomly assigned to the orlistat, phentermine/topiramate, and liraglutide groups had a slight decrease in BP at 1 year compared with the placebo group (SBP decreased by 1-3mm Hg on average, DBP decreased by 1-mm Hg; Table 2), which is believed to be mediated by weight loss
.

Alternatively, patients who were randomly assigned to receive naltrexone/bupropion treatment showed a slight increase in BP compared to placebo-treated patients (on average, SBP increased by 2–mm Hg, DBP increased by 1–mm Hg)
.

It is worth noting that in the long-term use of anti-obesity drugs in the RCT, only a portion of the participants had high blood pressure at baseline
.

For weight loss drugs that have been proven to decrease BP, the decrease was slightly larger in the group of subjects with a diagnosis of underlying hypertension (average 1 mm Hg)
.

Recently, as an adjunct to life>
.

This drug, originally developed for the treatment of diabetes, shows the promise of a greater average weight loss and potentially greater cardiometabolic risk improvement, especially when used in combination with life>
.

Table 2 Compared with placebo, the effect of anti-obesity drug treatment on body weight and blood pressure at 1 year *2.
Safety and complications Before use, patients should be informed of the potential adverse effects of anti-obesity drug treatment: ➤Sympathomimetic amine ( The most common side effects such as phentermine are constipation, dizziness, dry mouth and insomnia
.

➤There is also a potential risk of increased blood pressure related to the mechanism of action, including increased levels of catecholamines
.

Although the FDA label warns that drugs that have been approved for long-term weight loss (such as the phentermine/topiramate combination) have this risk, no clinically significant increase in BP has been observed in the RCT of these drugs, which may be due to concomitant Caused by weight loss
.

➤Orlistat has generally good safety due to its peripheral mechanism of action
.

However, when patients do not strictly follow a low-fat diet, their tolerance is usually poor due to the higher incidence of loose stools, urgency of stool, and diarrhea
.

Patients who are prescribed orlistat should take a multivitamin because the absorption of fat-soluble vitamins is reduced
.

➤Lorcaserin has previously been approved by the FDA for long-term weight loss, but during the 5-year follow-up of RCT, the incidence of cancer (including pancreatic cancer, colorectal cancer, and lung cancer) was observed to be higher in patients taking lorcaserin than placebo patients , Therefore voluntarily withdrew from the US market in February 2020
.

➤In the analysis of national electronic medical records data samples, Zhang et al.
observed that among the nearly 2 million eligible patients, <1% received weight-loss drugs
.

Considering the minor effects on BP and the lack of data on the long-term effects of these drugs on target organ damage, the low prescription rate may be due to the belief that the risks outweigh the benefits by many clinicians
.

Metabolic Surgery 1.
Bariatric Surgery In 2016, a total of 216,000 MSs were performed in the United States
.

Sleeve gastrectomy is the most common metabolic surgery (58%), followed by Roux-en-Y gastric bypass (RYGB; 19%), adjustable gastric band (3%), biliary-pancreatic shunt with twelve Diodenal bypass (0.
6%).
At present, >98% of metabolic surgeries are performed under laparoscopy.
The main perioperative morbidity rate of metabolic surgeries is <5%, the mortality rate is <0.
2%, hospitalization for 1 to 2 days, and recovery 2 to 4 weeks
.

Generally speaking, these procedures involve some degree of gastric volume reduction or intestinal bypass
.

It is currently believed that weight loss and metabolic improvement are mainly driven by neuroendocrine mechanisms, which can reduce appetite and increase satiety, and improve insulin sensitivity and secretion
.

In addition, intestinal bypass surgery will reduce the intestinal absorption of calories, thereby further reducing total calorie intake
.

2.
Current indications (U.
S.
) Patients with BMI ≥40 kg/m2 or ≥35 kg/m2 with comorbidities can be candidates for MS if they are mentally stable and have no active substance abuse
.

Patients with type 2 diabetes and BMI ≥ 30 kg/m2 (Asian patients ≥ 27.
5 kg/m2) can be candidates for MS if they have poor blood glucose control while receiving reasonable medication
.

MS should be performed in a center with a multidisciplinary team that includes weight loss surgeons, endocrinologists/diabetes specialists, cardiologists, anesthesiologists, psychologists, and dietitians with expertise in the following areas
.

3.
Metabolic Surgery (Metabolic Surgery) mechanism of lowering blood pressure The mechanism of improving BP control after MS seems to be multifactorial and complex, and it is not yet fully understood
.

The BP reduction occurs as early as 1 week after surgery, that is, before any significant weight loss, which indicates that the neuroendocrine mechanism is working
.

After various types of MS, increased levels of incretin glucagon-like peptide-1 have been observed
.

Glucagon-like peptide-1 stimulates postprandial insulin secretion, inhibits glucagon secretion, and has several central effects, including hypopharyngeal
.

In view of the fact that the posterior area of ​​one of the peripheral organs of the fourth ventricle contains glucagon-like peptide-1 reactive catecholaminergic neurons, SNS may be related to the BP lowering effect of MS
.

Glucagon-like peptide-1 may be important for water and salt homeostasis, and high levels are related to natriuresis
.

Natriuretic peptides may also play a role in the improvement of BP induced by MS; its circulating concentration is lower in obese patients and increases after MS
.

Hypertension may also be affected by changes in polypeptides secreted by white adipose tissue (ie, cytokines (adipokines), systemic and renal inflammation)
.

Finally, centrally obese individuals have increased RAAS activation and may return to normal after surgery
.

4.
Review of clinical research on MS intervention.
A systematic review of observational data shows that MS can improve hypertension
.

An example (136 studies, 22 094 patients) found that the overall hypertension resolution (resolution) 63%, RYGB surgery, adjustable gastric band, and biliary-pancreatic shunt with duodenal switch had a specific surgical percentage of 68, respectively %, 43% and 83%
.

At a median follow-up of 10 years, investigators from the SOS study (Swedish obese subjects) observed that compared with non-surgical control subjects (patients receiving RYGB), patients undergoing RYGB surgery had Both SBP and DBP significantly reduced control subjects, 1.
2 vs -3.
8mmHg; in addition, compared with the control group, the percentage of patients receiving antihypertensive drugs in the RYGB group was significantly reduced (35% vs 53%; P<0.
001)
.

However, the decrease in BP related to the decrease in BMI at 2 years did not exist at 10 years
.

Adams et al.
found that BP was stable for 12 years after RYGB, while a significant increase in BPs over time was observed in the two unoperated control groups (adjusted >6-mm Hg increased SBP and DBP) (all between the RYGB group and the control group) All comparisons are P<0.
05)
.

On the other hand, the RCT, which compares MS with medications for diabetes, did not find that MS has significant long-term benefits for BP compared with medications
.

However, Schauer et al.
noted that the use of antihypertensive drugs after MS has decreased compared with drug therapy
.

5.
GATEWAY trial GATEWAY (Gastric Bypass to Treat Obese Patients With Steady Hypertension) is the only controlled trial involving MS, specifically evaluating BP as the primary endpoint
.

In GATEWAY, 100 patients with a BMI value of 30 to 39.
9 kg/m2, who have received ≥2 maximum doses of antihypertensive drugs or> 2 medium doses of antihypertensive drugs were randomly assigned to receive RYGB+ at a ratio of 1:1 Medication (n=50) or medication alone (n=50)
.

At the 12th month, the main result, which was a reduction of ≥30% in the total number of BP drugs while maintaining office BP <140/90 mm Hg, was more common in the RYGB group than in the control group (83.
7% vs.
12.
8%; rate ratio, 6.
6 [95% CI, 3.
1–14.
0]; P<0.
001)
.

Remission of hypertension (defined as BP <140/90 mm Hg, no medication) is more common after RYGB (51% vs.
0%)
.

At the 3-year follow-up of GATEWAY, 73% of patients in the RYGB group had a primary outcome, compared with 11% in the drug treatment group (relative risk, 6.
52 [95% CI, 2.
50-17.
03]; compared with drug treatment, hypertension was relieved ( 35% vs.
2%) and drug use (median 1 [interquartile range, 0-2] vs.
3 [interquartile range, 2.
8-4]) ​​were beneficial to RYGB (P <0.
001) )
.

The total weight loss of the RYGB group and the drug treatment group were 27.
8% and -0.
1%, respectively
.
In the
RYGB group, 13 patients developed B12 hypovitaminemia, and 2 patients required reoperation
.

6.
Safety and complications Since the introduction of minimally invasive surgery in the 1990s, the perioperative morbidity and mortality associated with MS have dropped significantly
.

The United States National Inpatient Sample Database shows that the overall inpatient morbidity rate is 9%, and the mortality risk is 0.
1%
.

A systematic review reported that the perioperative complication rate of MS patients is between 10%-17%, and the 30-day mortality rate is 0.
08%
.

The perioperative complication rate of MS is roughly the same as that of laparoscopic cholecystectomy or laparoscopic appendectomy or hysterectomy
.

Preventing Obesity Hypertension Preventing weight gain and obesity is essential to prevent cardiometabolic diseases, including hypertension and subsequent heart, kidney, and brain diseases
.

The prevalence of obesity among children and adolescents aged 2-19 years is 18.
5%, and approximately 13.
7 million people were affected between 2015 and 2016 [96]
.

In children and adolescents, the increase in the incidence of BMI is closely related to the increase in blood pressure
.

Compared with children who maintain a healthy weight, obese children have a two-fold increase in the risk of hypertension, and severely obese children have a >4-fold increase in the risk of hypertension
.

Therefore, it is necessary to make a comprehensive and coordinated effort, including a multidisciplinary strategy across the healthcare system, research projects, advocacy, education, media, and consumer organizations [97]
.

Other factors, including maternal and father obesity and hypertension, pregnancy-induced hypertension and genetic causes of early-onset obesity, may play an important role in the occurrence of obesity and hypertension in future life, and are areas that require further research
.

Unanswered questions and future directions Figure 2 and Table 3 illustrate the under-researched areas and unanswered questions, and suggest future directions
.

Figure 2 There are still major deficiencies in the research and implementation of appropriate treatments for obesity hypertension (diet, increase physical activity, reduce sedentary, anti-obesity drug treatment, and metabolic surgery)
.

Conclusion Obesity is the main cause of hypertension and subsequent cardiovascular, kidney and brain damage
.

The mechanism of blood pressure reduction after weight loss may be mainly caused by the reversal of the mechanism that mediates the increase in blood pressure and weight gain
.

However, some of these mechanisms, such as decreased sympathetic nerve activity, appear to be quickly reversed as calorie intake decreases, even before significant weight loss
.

Conscious weight loss strategies, including life>
.

However, these life>
.

Drug therapy and evidence-based treatments such as MS can be used to treat obesity, thereby lowering blood pressure
.

There are short-term and long-term weight loss drugs; however, the prescription rate of these drugs is still low, probably because of limited insurance coverage and low levels of clinicians' treatment of obesity
.

When prescribing anti-obesity medications for individuals at risk of or suffering from hypertension, it is important to consider the mechanism of action when determining the treatment plan
.

MS is an effective long-term method for severely obese individuals to reduce obesity
.

In addition, MS has short-term and important long-term effects on reducing blood pressure in obese patients
.

Additional RCTs are necessary to assess the impact of MS on the risk reduction of downstream obesity-related diseases (such as chronic kidney disease, stroke, and heart failure)
.

References: Hall ME, Cohen JB, Ard JD, et al.
Weight-Loss Strategies for Prevention and Treatment of Hypertension: A Scientific Statement From the American Heart Association[J].
Hypertension, 2021: HYP.
0000000000000202.